Serum Aspartate Aminotransferase Levels Research Articles

OTUD7B inhibited hepatic injury from NAFLD by inhibiting K48-linked ubiquitination and degradation of β-catenin

Non-alcoholic fatty liver disease (NAFLD) is the prevalent liver disease. Ovarian tumor domain-containing 7B (OTUD7B) is a deubiquitinating enzyme and its role in NAFLD remains unclear. In high-fat diet (HFD)-induced NAFLD mouse model and palmitic acid (PA)-treated HepG2 cells, OTUD7B expression was decreased. Adenoviral overexpression of OTUD7B in mice resulted in reduced body weight and liver injury, with decreased serum aminotransferase (ALT) and aspartate aminotransferase (AST) levels. OTUD7B overexpression attenuated hepatic lipid deposition (serum TG, TC, LDL-C, HDLC, and FFA levels), which might be through the suppression of lipogenesis and β-oxidation-related genes. The contents of hepatic inflammatory factors (TNF-α, IL-6, and IL-1β) were decreased following OTUD7B overexpression in NAFLD mice. A mechanism study indicated that the protective effect of OTUD7B overexpression might be associated with β-catenin signal activation. OTUD7B overexpression promoted PA-induced β-catenin activity in TopFlash assay, and increased total β-catenin and c-myc levels in cells. The increase in β-catenin levels was contributed to the stabilization via inhibiting K48-linked ubiquitination and proteasomal degradation by OTUD7B. NR4A2 role in NASH has been proved. NR4A2 ChIP-seq and RNA-seq data excluded transcriptional regulation of NR4A2 to OTUD7B, and it was experimentally evidenced that NR4A2 bound to OTUD7B promoter region and positively transcriptionally regulate OTUD7B expression. In summary, OTUD7B overexpression ameliorated hepatic inflammation and steatosis in NAFLD. The possible mechanism of OTUD7B might be through the inhibition of β-catenin degradation by removing K48-linked ubiquitination, which might be regulated by NR4A2.

Ren-Shen-Bu-Qi decoction alleviates exercise fatigue through activating PI3K/AKT/Nrf2 pathway in mice.

Fatigue is a prevalent issue that can lead individuals to a sub-health condition, impacting their work efficiency and quality of life. There are limited effective treatment options available for fatigue. Ren-Shen-Bu-Qi decoction (RSBQD) is a proprietary herbal remedy that is designed to address fatigue. However, the specific pharmacological mechanisms and basis of RSBQD are not yet fully understood. This study aimed to investigate the pharmacological effects and mechanisms of RSBQD in a mouse model of exercise fatigue. UPLC-Q-Orbitrap HRMS was used to analyze the chemical composition of RSBQD. The pharmacological basis and molecular mechanism of RSBQD on exercise fatigue were predicted using network pharmacology analysis. Subsequently, an exercise fatigue mouse model was established and used to analysis the effects of RSBQD. The potential mechanisms were verified by hematoxylin-eosin (HE) staining, real-time fluorescence quantitative PCR (RT-qPCR), Western blot (WB) and molecular docking. The results showed that 88 main components of RSBQD were identified, which have mainly belonged to flavonoids and carboxylic acid compounds. The network pharmacology analysis indicated that RSBQD ameliorate fatigue through PI3K/AKT signaling pathway. Notably, RSBQD prolonged the swimming time and diminished body weight loss of exercise fatigue mice (P < 0.05). Meanwhile, RSBQD significantly alleviated the injury of liver and kidney induced by exhaustive exercise, and decreasing the serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea and BUN levels (P < 0.05). In addition, RSBQD was found could relieve exercise fatigue by decreasing the content of creatine kinase (CK), lactate dehydrogenase (LDH), and lactic acid (LA), but increasing the blood glucose (GLU) and liver glycogen (HG) levels (P < 0.05). RSBQD also significantly increased the hepatic superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) but decreased hepatic malondialdehyde (MDA) levels. Moreover, RSBQD was able to upregulate protein level of activated Nrf2 and PI3K/AKT signaling pathways. RSBQD mitigates exercise fatigue by reversing metabolic changes and reducing oxidative damage through the PI3K/AKT/Nrf2 signaling pathway. This study offers pharmacological support for the utilization of RSBQD in exercise fatigue treatment.

Role of Obeticholic Acid, a Farnesoid X Receptor Agonist, in Nonalcoholic Fatty Liver Disease: A Systematic Review and Meta-analysis.

Background. Obeticholic acid (OCA) has emerged as a promising drug in the management of nonalcoholic fatty liver disease (NAFLD). This meta-analysis aimed to analyse the therapeutic effect of OCA on NAFLD. Methods. Randomized controlled trials (RCTs) involving patients with NAFLD receiving OCA in the intervention arm and placebo in the control arm were searched throughout the electronic databases. The primary outcomes were changes in non-invasive markers of hepatic fibrosis and liver histology. The secondary outcomes included changes in liver enzymes, metabolic parameters from baseline and adverse events (AEs). Results. Four RCTs involving 1,278 subjects met the inclusion criteria. Over 6 weeks to 18 months of clinical use, OCA outperformed placebo in resolving definite nonalcoholic steatohepatitis (odds ratio [OR] 1.60, 95% confidence interval [CI] [1.04-2.48], p=0.03) and improving fibrosis (OR 2.23, 95% CI [1.56-3.20], p<0.0001), hepatocellular ballooning (OR 1.83, 95% CI [1.35-2.47], p<0.0001) and lobular inflammation (OR 1.62, 95% CI [1.13-2.32], p=0.009). OCA did not improve the enhanced liver fibrosis score and steatosis better than placebo, and demonstrated superior efficacy compared with the placebo in reducing serum alanine aminotransferase, aspartate aminotransferase and gamma-glutamyl transferase levels. Although a favourable effect of OCA over placebo was seen in body-weight reduction, the OCA use was associated with adverse changes in lipid parameters. Except for the greater risk of pruritus and constipation, the AE profile was comparable between the OCA and placebo groups. Conclusions. OCA has a favourable efficacy in improving liver histology and liver enzymes. However, the worsening of lipid parameters and other AEs with the OCA use warrants further investigation.

Protective Effect and Mechanism of L-Theanine on Acute Alcoholic Liver Injury in Mice.

Acute alcoholic liver injury (AALI), a global health concern, is exacerbated by excessive episodic drinking. L-theanine (LTA), a compound found in tea leaves, mitigates the AALI-induced liver oxidative stress and inflammation. However, its relationship with alcohol metabolism and its liver-protective mechanism remains unexplored. This study investigates the protective mechanisms of LTA against AALI in mice. The results demonstrate that LTA mitigates liver tissue damage and reduces the serum levels of aspartate aminotransferase and alanine aminotransferase, and liver levels of triglycerides, malondialdehyde, reactive oxygen species (ROS), tumor necrosis factor-α, interleukin-6, and interleukin-1β. However, LTA enhances the activity of ethanol-metabolizing enzymes and decreases ethanol and acetaldehyde serum levels. Mechanistically, LTA accelerates alcohol metabolism by upregulating the hepatic expression of ADH6, ALDH1B1, ALDH2, CAT, and ACSS1 mRNA and protein in AALI mice, LTA downregulates the expression of CYP2E1 mRNA and protein and promoting antioxidative activities thus reducing the accumulation of ROS. This attenuated inflammation by inhibiting the phosphorylation of nuclear factor-kappa B inhibitor alpha (IκBα) and downregulating the hepatic expression of NF-κB p65, TNF-α, IL-1β, IL-6 mRNA, and protein. LTA is a beneficial dietary supplement that protects against AALI by modulating alcohol metabolism and the TNF-α/NF-κB pathway.

Analysis of Clinical and Laboratory Profiles of Patients Hospitalized with Hemorrhagic Fever with Renal Syndrome in Southwestern South Korea.

Hemorrhagic fever with renal syndrome (HFRS) is caused by hantaviruses. Data of 34 patients with HFRS hospitalized at Chosun University Hospital, South Korea, between 2010 and 2021 were retrospectively analyzed. Nested reverse transcription polymerase chain reaction (RT-nPCR) targeting the L segment of hantavirus and sequencing were used for diagnosis. Most cases occurred in men and during the months of October through December. Common symptoms were fever, chills, gastrointestinal symptoms, and myalgia. The common laboratory abnormalities were thrombocytopenia, proteinuria, and elevated levels of serum creatinine, aspartate transaminase, alanine transaminase, and lactate dehydrogenase. Approximately 91.2% of patients had the Hantaan virus with a new genotype cluster, whereas 8.8% had the Seoul virus. Seropositivity based on IgM titer >1:32 on admission was noted in 20.6%, and a 4-fold increase in IgG titer of 1:512 was observed in 11.8%. This study demonstrated that RT-nPCR targeting the L segment of hantaviruses is a more reliable diagnostic method compared to serological testing.

Growth performances of Clarias gariepinus juveniles fed with Jatropha curcas seed meal

Jatropha curcas is an oil producing seed with high nutritional qualities for consumption. However, due to inherent anti-nutritional factors, appropriate processing is necessary to improve its nutrients utilization. This study was aimed at processing J. curcas using solvent-extraction method and evaluating its inclusion effects in the diet for Clarias gariepinus on its growth status. J. curcas meal was extracted using 80 % methanol to remove phorbol esters and other anti-nutrients. Thereafter, five iso-nitrogenous diets (40 % crude protein) were formulated containing J. curcas meal replacements of soybeans meal at 0 % (TRT0), 25 % (TRT25), 50 % (TRT50), 75 % (TRT75) and 100 % (TRT100) and fed to C. gariepinus for 70 days. Results showed that TRT25 fish had the highest mean weight gain and specific growth. The serum alkaline phosphate, alanine aminotransferase, and aspartate aminotransferase levels began to rise significantly (p ≤ 0.05) at 50 % replacement. Likewise, the assessment of gut ecology and morphology indicated that TRT25 had significantly (p ≤ 0.05) the highest gut bacteria colony forming unit (2.60 ×104±0.02cfu/g) and most favorable area of absorption (0.16±0.01 cm2). The histopathological observation of the fish intestine, liver and gills indicated no visible deformity in TRT0 and TRT25 fish. However, various degrees of degenerations were observed in the fish fed with 50 % and higher inclusion of J. curcas. This study showed that methanol-extracted J. curcas meal can be effectively utilized for C. gariepinus at 25 % of replacement.

Lipidomic profiling of serum and liver tissue reveals hepatoprotective mechanism of taxifolin in rats with CCl4-induced subacute hepatic injury based on LC-MS/MS

Currently, the hepatoprotective activity of taxifolin, a flavonoid isolated from Pseudotsuga taxifolia, has been reported in many animal models. However, whether the protective effect of taxifolin on the liver is related to its effect on lipidomics is unclear. Based on the significant therapeutic effect of taxifolin on CCl4 induced subacute hepatic injury, we observed the intervention of taxifolin by lipidomics. The results demonstrate that taxifolin can effectively reverse the damage caused by CCl4, which including hepatocyte vacuolization and necrosis. Lipomic profiling based on liquid chromatography-mass spectrometry showed that taxifolin was able to restore lipidomic changes caused by CCl4, including the levels of lysophosphatidylserine (LPS), phosphatidylcholine (PC), coenzyme (Co), phosphatidylglyceride (PG), phosphatidylserine (PS), dimethylphosphatidylethanolamine (dMePE), ceramide (Cer), sphingosine (So), triglycerides (TG), and monogalactosyl diacylglycerol (MGDG) in the rat liver, and phosphatidylcarbinol (PMe) and phosphatidylethanolamine (PE), plant sphingosine (phSM), glucose ceramide (CerG1), TG, and diglycerides (DG) in serum. Spearman's correlation analysis showed that CerG1, phSM, PE, and PMe in serum, and Cer, dMePE, PG, PS, So, TG, and MGDG in liver were positively correlated with serum levels of aspartate transaminase, alanine transaminase, and liver index; while TG, DG in serum, and Co, LPS, PC in liver were negatively correlated with the parameters. In total, 43 and 34 lipid molecules were altered by taxifolin treatment in the liver and serum, respectively, mainly including glycerophosphoglycerols, glycerophosphocholines, glycerophosphoethanolamines, and linoleic acids and derivatives. Our findings help to provide novel insights into the mechanism of the hepatoprotective effect of taxifolin from a lipidomics approach.

Trimetazidine protects against acute indomethacin-induced gastric mucosal, hepatic, and renal injury in rats

Background: Peptic ulcers are increasingly reported as a challenging disease in clinical settings. Several medications are employed in the management of peptic ulcers. Thus far, there is no medication devoid of any adverse effects that may achieve a 100% curative rate or provide a total remedy for the ailment. Aim: We aimed to examine the healing effects of trimetazidine against indomethacin-induced gastric ulcers in albino rats. Methodology: A total of 25 rats were used, divided into five groups (each group contained five rats): a negative control group that was only treated with distilled water, a positive control group that was only treated with a single dose of indomethacin (30 mg/kg) orally, a group that received indomethacin (30 mg/kg) and low doses of trimetazidine (17.5 mg/kg) orally, a group that received indomethacin (30 mg/kg) and medium doses of trimetazidine (35 mg/kg) orally, and a group that received indomethacin (30 mg/kg) and high doses of trimetazidine (52.5 mg/kg) orally. The induction of gastric ulcers occurred on the first day of the experiment through the administered indomethacin and, subsequently, the rats were treated orally with either trimetazidine or distilled water, three times daily, for 7 days. Serum urea, creatinine, alanine aminotransferase (ALT), aspartate aminotransferase (AST), and albumin levels were measured. Stomachs were excised from the rats’ bodies and opened along the greater curvature; they were then rinsed with saline, extended on a white corkboard, and examined macroscopically. The stomach tissues were also processed in order to generate microscopic slides for microscopical examination. Results: Indomethacin administration caused multiple ulcerations in the gastric mucosa, significant elevations in serum urea, creatinine, AST, and ALT levels, and a significant reduction of the serum albumin levels. The treatment with trimetazidine significantly healed the indomethacin-induced gastric ulcers. Conclusion: The present study indicates that the nonsteroidal anti-inflammatory drug (NSAID) indomethacin can induce substantial gastric ulcers, which may be linked to a direct toxic effect on the histological architecture of the gastric linings in addition to the reduction of blood flow to gastric mucosa; this effect can be treated by administration of trimetazidine. Ultimately, this study suggests that administering the optimal dosage of trimetazidine can be advantageous in treating stomach ulcers caused by NSAIDs. Moreover, the study suggests that the indomethacin-induced liver and renal dysfunction can also be alleviated by the use of trimetazidine.

The impact of hydrogen sulfide on mesenchymal stem cells in rats suffering from liver fibrosis via suppression of TGF-β signaling

Worldwide, liver fibrosis (LF) causes complications and has an elevated death rate. The prevalence of mesenchymal stem cell therapy (MSC) is a result of the lack of liver donors. In recent years, the study of stem cell therapy has advanced into a promising and cutting-edge field of study. The purpose of this study is to assess the possible value of in vitro preconditioning of bone marrow-derived mesenchymal stem cells (BMSCs) with sodium hydrogen sulfide (NaHS), which aims to encourage rats to benefit from stem cell therapy with carbon tetrachloride-induced liver fibrosis. Materials and Methods: Fifty male albino rats (6 weeks old & 120–150 g) were divided equally into 5 groups (10 rats each); the 1st group served as a negative control, the 2nd group was a positive control, in which rats received 2 mL/kg CCl4 (1:1 corn oil) twice a week for five weeks, and the remaining three groups received, in addition to CCL4, a NaHS solution (10 μmol/kg) every 2 days for 6 weeks, one dose of BMSCs (3 × 106 cells per rat) intravenously, and a single dose of BMSCs (3 × 106 cells per rat) in culture with 200 μmol/L NaHS for 24 h. Quantitative gene expression of transforming growth factor-beta (TGF-β), Smad, collagen, α-SMA, MAPK, β-catenin, GSK-3B, and CBS was carried out using real-time polymerase chain reaction; whereas the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and albumin were estimated using colorimetric analysis. Also, the relative expression of MAPK, β-catenin, and GSK-3B by Western blot was done. Histopathological analysis was used to gauge the progression of LF. Results: The liver fibrosis group exhibited significantly increased serum ALT and AST levels, along with decreased serum albumin levels, compared to controls. Additionally, compared to controls, there was a rise in the gene expression of TGF-β, Smad, collagen, α-SMA, MAPK, β-catenin, and GSK-3B, while the gene expression of CBS is decreased. The biochemical parameters indicated above were greatly improved by BMSCs pretreated with H2S, and the liver sections produced from this group demonstrated a notable improvement in histopathology. Conclusion: The study investigated and demonstrated how NaHS affected the efficacy of BMSC therapy in rats with CCl4-induced liver fibrosis.

Protective effect of Zhizi Huangqi Shanzha formula on aflatoxin poisoning in mice and its effect on intestinal flora.

To evaluate the protective effect of Zhizi Huangqi Shanzha formula (, ZHSF) on aflatoxin-induced liver injury. The protective effect of ZHSF on the aflatoxin-induced liver injury was evaluated by histological observation, blood cell analysis, evaluation of liver function and immunity, and gut microbiota analysis. ZHSF can significantly up-regulate the percentage of lymphocytes and eosinophils in the blood of Aflatoxin B1-intoxicated mice, down-regulate the levels of serum aspartate aminotransferase, alanine aminotransferase, and malondialdehyde, and recover the liver tissue structure. Aflatoxin poisoning induces a variation of the intestinal flora of mice, and ZHSF may recover the variation of intestinal flora induced by Aflatoxin B1. Cluster analysis showed that the intestinal flora of mice in the intervention group was more similar to that of the control group. Correlation analysis showed that Lachnospiraceae, Desulfovibrio, and Lactobacillus may be the key flora for the pharmacological effects of ZHSF. ZHSF may protect against aflatoxin-induced liver damage, improve immunity, and inhibit oxidative stress by regulating the composition and relative abundance of intestinal flora, which makes it a promising liver-protective candidate drug.

Immunological, Antioxidant, Growth Responses, and Disease Resistance of Rainbow Trout, Oncorhynchus mykiss, with Feeding Diets Supplemented with Lactobacillus salivarius and Lutein

Abstract The aim of the present study was to assess the effects of dietary supplementation with Lactobacillus salivarius (LS) ATCC 11741 and lutein (LU) on immunological, antioxidant, and growth responses, and resistance against Yersinia ruckeri infection in rainbow trout (Oncorhynchus mykiss). There were seven experimental diets containing un-supplemented diet (CTL), L. salivarius at 1 × 106 (LS6) and 1 × 108 (LS8) CFU/g, lutein at 50 (LU50) and 150 (LU150) mg/kg, L. salivarius at 1 × 106 CFU/g plus lutein at 50 g/kg (LS6+LU50), and L. salivarius at 1 × 108 CFU/g plus lutein at 150 g/kg (LS8+LU150). These diets were provided to the fish (N= 735; 14.0±0.38 g). After 60 days of feeding, all experimental treatments exhibited significantly higher growth performance, compared to the CTL treatment. The intestinal protease activity and the intestinal lactic acid bacteria population in the probiotic-treated fish were significantly higher than in the CTL fish. The intestinal lipase activity was only higher in the LS6+LU50 treatment, compared to the CTL treatment. Compared to the CTL treatment, the intestinal total bacterial count, and serum superoxide dismutase significantly increased in the LS6+LU50 and LS8+LU150 treatments. The serum catalase significantly increased in LU150, LS6+LU50, and LS8+LU150 treatments, and serum glutathione peroxidase significantly increased in the lutein-treated fish. All experimental treatments, particularly LS6+LU50 and LS8+LU150, had significantly lower serum malondialdehyde levels, compared to the CTL treatment. The levels of serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and lactate dehydrogenase in LU50, LS6+LU50, and LS8+LU150 treatments were significantly lower than the CTL. All experimental treatments showed significantly higher serum lysozyme (LYZ), complement, blood respiratory burst activity (RB), and skin mucus alkaline phosphatase (ALP), compared to the CTL treatment. The highest serum LYZ, C4, total immunoglobulin (Ig), blood RB activity, and skin mucus peroxidase, ALP, and Ig were observed in the LS6+LU50 and LS8+LU150 treatments. All the experimental treatments, especially LS6+LU50, exhibited significantly lower mortality after the bacterial challenge compared to the CTL. In conclusion, dietary supplementation with 1 × 106 CFU/g L. salivarius and 50 mg/kg lutein can maximally improve growth performance, digestive enzymes, antioxidant parameters, immune responses, intestinal lactic acid bacteria, and resistance against yersiniosis in rainbow trout.

Effects of including different levels of equal mix of soybean and flaxseed oils in Japanese quail diets on the growth, carcass quality, and blood biomarkers

Corn, the primary ingredient in modern poultry feeds, contains high levels of ω-6 fatty acids but lacks sufficient ω-3 fatty acids, creating an imbalance. Maintaining a balance between ω-6 and ω-3 fatty acids in poultry diets is crucial due to their competition. This study aimed to evaluate the effects of incorporating different concentrations of an equal mix of soybean oil (SO) and flaxseed oil (FO) into quail diets on growth performance, carcass quality, and blood biochemistry. One-week-old Japanese quail birds (n=200) were randomly assigned to four dietary groups, each comprising five replicates with 10 chicks per replicate. Four isonitrogenous/isocaloric basal diets were formulated. Group 1 (control) received a basal diet without SO or FO, while Groups 2-4 received basal diets supplemented with an equal mix of SO+FO at levels of 1.0%, 1.5%, and 2.0%, respectively. The inclusion of oil mixes significantly increased body weight (BW) at five weeks and daily weight gain (DWG) during weeks 3-5 and 1-5. The feed conversion ratio (FCR) improved with the addition of oil mixes throughout the trial period. Supplementing quail diets with oil mixes resulted in reduced serum total cholesterol (TC) and LDL cholesterol, elevated serum HDL cholesterol, and no significant effect on triglycerides (TG) and VLDL cholesterol levels. Quails fed oil-supplemented diets showed lower serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and creatinine levels, while urea and uric acid were significantly affected. Birds fed diets with oil mixes also had increased serum concentrations of immunoglobulin G (IgY), immunoglobulin M (IgM), and superoxide dismutase (SOD). However, serum immunoglobulin A (IgA), malondialdehyde (MDA), and total antioxidant capacity (TAC) levels did not significantly change across experimental groups. Overall, adding up to 2% of the SO and FO mix in growing quail feeds improved growth performance, blood lipid profile, liver and kidney function markers, immune response, and antioxidant defense. The highest level of oil mix (2%) yielded the most beneficial effects.

Effects of fermented oyster extract supplementation on free fatty acid and liver enzymes in older women with obesity.

This study aimed to investigate the effects of a 12-week intake of fermented oyster extract on free fatty acids and liver enzymes in older women with obesity and to provide basic data for improving liver function in older individuals with obesity. A randomized, double-blind, placebo-controlled clinical trial aimed to confirm the effects of fermented oyster extract intake on free fatty acid (FFA) levels and liver function in older women with obesity. The study included 40 older women with obesity with a body mass index ≥ 25 kg/m2. Participants were divided into a fermented oyster intake group (n = 20) and control group (n = 20). Serum FFA, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and gamma-glutamyl transferase (GGT) levels were measured at weeks 0 and 12. Our results showed an interaction effect between the two groups in terms of serum FFA levels (p<0.05), with a post-intervention decrease in the FSO group (p<0.05). AST, ALT, and GGT levels also showed an interaction effect between the two groups (p<0.05), with a significant postintervention decrease in the FSO group (p<0.05). The intake of fermented oyster extract significantly reduced FFA, ALT, AST, and GGT levels. These results suggested that the consumption of fermented oyster extract may improve liver function. However, the findings of this study were limited to elderly women with obesity, and the relatively short intake period and small sample size may limit the generalization of the results.

Comparative Assessment of Beeswax Alcohol and Coenzyme Q10 (CoQ10) to Prevent Liver Aging, Organ Damage, and Oxidative Stress in Hyperlipidemic Zebrafish Exposed to D-Galactose: A 12-Week Dietary Intervention.

The current study was designed to compare in vivo efficacy between beeswax alcohol (BWA) and coenzyme Q10 (CoQ10) to treat fatty liver changes, oxidative stress, and damages in major organs of zebrafish by 12 weeks with high-cholesterol (HC) and galactose (Gal) supplementation. At week 12, the HC control and HC+Gal control groups showed 96% and 92% survivability, respectively, while co-supplementation of the 0.5% BWA and 1.0% BWA groups exhibited 96% and 100% survivability. However, co-supplementation of the 0.5% CoQ10 and 1.0% CoQ10 groups revealed the lowest survivability, around 92% and 89%, respectively. The 0.5% BWA and 1.0% BWA groups showed 21% (p < 0.001) and 41% (p < 0.001), respectively, lower total cholesterol (TC) than the HC+Gal control, while the 1.0% CoQ10 group showed only 15% lower TC than the control. Interestingly, the 0.5% BWA and 1.0% BWA groups showed 22% (p < 0.001) and 38% (p < 0.001), respectively, lower triglyceride (TG) than the HC+Gal control. However, both the 0.5% CoQ10 and 1.0% CoQ10 groups showed similar TG levels as the control, suggesting that CoQ10 supplementation had no effect on lowering serum TG. The 1.0% BWA group showed the highest plasma HDL-C and HDL-C/TC (%) up to 3.2-fold and 5.5-fold, respectively, higher than those of the HC+Gal control, while the 1.0% CoQ10 group showed 2.4-fold and 2.8-fold higher plasma HDL-C and HDL-C/TC (%), respectively, than the control. The plasma aspartate transaminase (AST) and alanine transaminase (ALT) levels were lowest in the 1.0% BWA group, 51% and 72%, respectively, lower than HC+Gal control, suggesting the lowest extent of hepatic damage. In hepatic tissue, neutrophil infiltration and interleukin (IL)-6 production were the lowest in the 1.0% BWA group, around 67% and 85%, respectively, lower than the HC+Gal control. Fatty liver change, cellular apoptosis, and cell senescence in hepatic tissue were remarkably lowered in the 1.0% BWA group, while the CoQ10 group showed much less effect than the BWA group. In kidney, ovary, and testis tissue, the 1.0% BWA group showed the lowest production of reactive oxygen species, the extent of cellular senescence, and cellular apoptosis with the healthiest cell morphology. In conclusion, supplementation of BWA remarkably protected the liver, kidney, ovary, and testis from oxidative damage by cholesterol and galactose consumption, with the least serum AST and ALT levels, inflammatory parameters, and senescence markers.

Evaluation of Fasting Bile Acid Levels in Pregnant Women Diagnosed with Hyperemesis Gravidarum

Background: Hyperemesis gravidarum is a common cause of nausea and vomiting during the early gestational week. At the same time, it can also lead to an increase in liver enzyme values in patients due to or independently of underlying liver disease. This study aimed to evaluate fasting bile acid (FBA) levels, alanine aminotransferase (ALT), aspartate aminotransferase (AST), total and direct bilirubin, and urine ketone levels in pregnant women diagnosed with hyperemesis gravidarum (HG). Additionally, the study sought to investigate the relationship between HG and FBA levels. The diagnosis of HG remains primarily clinical, and identifying markers for disease severity is crucial. Methods: This retrospective cohort study obtained blood samples from 50 women diagnosed with HG and 25 healthy pregnant women. Serum levels of AST, ALT, total bilirubin (TBS), direct bilirubin, urine ketones, and FBA were measured. Statistical analysis was performed using the SPSS software version 28.0. Results: FBA levels were significantly higher in pregnant women diagnosed with HG compared to the healthy control group. Additionally, FBA levels increased simultaneously with ketonuria in the patient group. Our findings suggest that FBA levels can serve as a biomarker for diagnosing HG and indicating early-stage liver damage. Unlike previous studies, our research focused on the relationship between FBA levels and HG, providing valuable insights for future studies. Conclusions: FBA levels show promise as an objective biomarker for diagnosing HG and indicating early-stage liver damage. Further research with larger cohorts is necessary to validate these findings.

A Study on Serum Hepatic Enzymes in Smokers and Nonsmoker’s Adult Male

Background: Cigarette smoking is one of the greatest indirect causes of global death and disease. Cigarette smoke consists of many chemicals, including cytotoxic, carcinogenic and free radicals, therefore it affects many organs including liver either directly or indirectly. Objective: The aim of this study was to find out level of serum hepatic enzymes in smokers and non-smokers adult male. Method: This cross-sectional study was conducted in the Department of Biochemistry, Dhaka Medical College, Dhaka, Bangladesh, from January 2019 to December 2019. Total study subjects were one hundred and twenty with age ranging from 20 to 50 years of male gender, selected from attendance of admitted patients and third &amp; forth class employees of Dhaka Medical College Hospital, Dhaka. Study subjects were grouped smokers as Group A and age and gender matched, nonsmokers as Group B. Group A smokers again divided into three groups. Group A1- heavy smokers (who consume 20 cigarette sticks or more per day) consist of thirty study subjects, Group A2- moderate smokers (who consume 11-19 cigarette sticks per day) consist of thirty study subjects and Group A3- light smokers (who consume 1-10 cigarette sticks per day) consist of thirty study subjects. Serum Alanine Transaminase (ALT), Aspartate transaminase (AST) and Alkaline phosphatase (ALP) level of all study subjects were estimated and recorded. Results: Mean age of the study subjects in group A1, A2, A3 &amp; B were 33.88 years, 34.60 years, 34.60 years and 29.80 years. There was a significant increase in serum ALT, AST and ALP level in heavy, moderate and light smokers when compared to nonsmokers, but the increase was more significant in heavy smokers when compared to moderate smokers, also moderate smokers when compared to light smokers. Conclusion: This study revealed that significantly higher level of serum hepatic enzymes with smokers when compared to that of non smokers. This significantly higher level was also seen in heavy smokers in comparison to moderate smokers, moderate smokers in comparison to light smokers.

Retinal ischemia-reperfusion injury and pretreatment with Lycium barbarum glycopeptide.

To investigate the antioxidant protective effect of Lycium barbarum glycopeptide (LbGP) pretreatment on retinal ischemia-reperfusion (I/R) injury (RIRI) in rats. RIRI was induced in Sprague Dawley rats through anterior chamber perfusion, and pretreatment involved administering LbGP via gavage for 7d. After 24h of reperfusion, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and creatinine (CREA) levels, retinal structure, expression of Caspase-3 and Caspase-8, superoxide dismutase (SOD) activity, and malondialdehyde (MDA) in the retina were measured. The pretreatment with LbGP effectively protected the retina and retinal tissue from edema and inflammation in the ganglion cell layer (GCL) and nerve fiber layer (NFL) of rats subjected to RIRI, as shown by light microscopy and optical coherence tomography (OCT). Serum AST was higher in the model group than in the blank group (P=0.042), but no difference was found in ALT, AST, and CREA across the LbGP groups and model group. Caspase-3 expression was higher in the model group than in the blank group (P=0.006), but no difference was found among LbGP groups and the model group. Caspase-8 expression was higher in the model group than in the blank group (P=0.000), and lower in the 400 mg/kg LbGP group than in the model group (P=0.016). SOD activity was lower in the model group than in the blank group (P=0.001), and the decrease was slower in the 400 mg/kg LbGP group than in the model group (P=0.003). MDA content was higher in the model group than in the blank group (P=0.001), and lower in the 400 mg/kg LbGP group than in the model group (P=0.016). The pretreatment with LbGP did not result in any observed liver or renal toxicity in the model. LbGP pretreatment exhibits dose-dependent anti-inflammatory, and antioxidative effects by reducing Caspase-8 expression, preventing declines of SOD activity, and decreasing MDA content in the RIRI rat model.

Cannabinoids Used for Medical Purposes in Children and Adolescents

Cannabinoids are increasingly used for medical purposes in children. Evidence of the safety of cannabinoids in this context is sparse, creating a need for reliable information to close this knowledge gap. To study the adverse event profile of cannabinoids used for medical purposes in children and adolescents. For this systematic review and meta-analysis, MEDLINE, Embase, PsycINFO, and the Cochrane Library were searched for randomized clinical trials published from database inception to March 1, 2024, for subject terms and keywords focused on cannabis and children and adolescents. Search results were restricted to human studies in French or English. Two reviewers independently performed the title, abstract, and full-text review, data extraction, and quality assessment. Included studies enrolled at least 1 individual 18 years or younger, had a natural or pharmaceutical cannabinoid used as an intervention to manage any medical condition, and had an active comparator or placebo. Two reviewers performed data extraction and quality assessment independently. The Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) reporting guideline and PRISMA-S guideline were used. Data were pooled using a random-effects model. The primary outcome was the incidence of withdrawals, withdrawals due to adverse events, overall adverse events, and serious adverse events in the cannabinoid and control arms. Secondary outcomes were the incidence of specific serious adverse events and adverse events based on organ system involvement. Of 39 175 citations, 23 RCTs with 3612 participants were included (635 [17.6%] female and 2071 [57.3%] male; data not available from 2 trials); 11 trials (47.8%) included children and adolescents only, and the other 12 trials (52.2%) included children, adolescents, and adults. Interventions included purified cannabidiol (11 [47.8%]), nabilone (4 [17.4%]), tetrahydrocannabinol (3 [13.0%]), cannabis herbal extract (3 [13.0%]), and dexanabinol (2 [8.7%]). The most common indications were epilepsy (9 [39.1%]) and chemotherapy-induced nausea and vomiting (7 [30.4%]). Compared with the control, cannabinoids were associated with an overall increased risk of adverse events (risk ratio [RR], 1.09; 95% CI, 1.02-1.16; I2 = 54%; 12 trials), withdrawals due to adverse events (RR, 3.07; 95% CI, 1.73-5.43; I2 = 0%; 14 trials), and serious adverse events (RR, 1.81; 95% CI, 1.21-2.71; I2 = 59%; 11 trials). Cannabinoid-associated adverse events with higher RRs were diarrhea (RR, 1.82; 95% CI, 1.30-2.54; I2 = 35%; 10 trials), increased serum levels of aspartate aminotransferase (RR, 5.69; 95% CI, 1.74-18.64; I2 = 0%; 5 trials) and alanine aminotransferase (RR, 5.67; 95% CI, 2.23-14.39; I2 = 0%; 6 trials), and somnolence (RR, 2.28; 95% CI, 1.83-2.85; I2 = 8%; 14 trials). In this systematic review and meta-analysis, cannabinoids used for medical purposes in children and adolescents in RCTs were associated with an increased risk of adverse events. The findings suggest that long-term safety studies, including those exploring cannabinoid-related drug interactions and tools that improve adverse event reporting, are needed.

β-Caryophyllene, a dietary phytocannabinoid, alleviates high-fat diet-induced hepatic steatosis in mice via AMPK activation.

β-Caryophyllene (BCP), a dietary phytocannabinoid, significantly suppresses palmitate-induced lipid accumulation in human HepG2 hepatocytes via activation of AMP-activated protein kinase (AMPK) signaling. The objective of the preset research was to assess whether oral administration of BCP alleviates obesity-induced hepatic steatosis in mice through AMPK activation. We examined the protective action of supplementation of 0.3% BCP (w/w) in a high-fat diet (HFD) on C57BL/6J mice for 12 weeks. BCP supplementation evidently ameliorated histological hepatic steatosis features, and significantly reduced triglycerides and cholesterol levels in liver, and serum levels of aspartate aminotransferase and alanine aminotransferase as compared with non-supplemented HFD-fed mice. Immunoblotting revealed that BCP supplementation in HFD-fed mice also caused hepatic AMPK activation. Furthermore, treatment with BCP in HFD-fed mice significantly suppressed body weight gain and attenuated obesity-related phenotypes relative to the HFD mice. Our results suggest the usefulness of BCP in the prevention of obesity-related liver steatosis and liver injury.

Association of PM2.5 exposure in early pregnancy and maternal liver function: A retrospective cohort study in Shenzhen, China

ObjectiveStudies have shown that fine particulate matter (PM2.5) has adverse effects on the liver function, but epidemiological evidence is limited, especially regarding pregnant women. This study aims to investigate the association between PM2.5 exposure in early pregnancy and maternal liver function during pregnancy. MethodsThis retrospective cohort study included 13,342 pregnant participants. PM2.5 and Ozone (O3) exposure level, mean temperature, and relative humidity for each participant were assessed according to their residential address. The levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin (TBIL) were measured during the second and third trimesters. Data on PM2.5 and O3 exposure level were sourced from Tracking Air Pollution in China (TAP), while the mean temperature and relative humidity were obtained from the ERA5 dataset. The Generalized Additive Model (GAM) was used to analyze the associations between PM2.5 exposure and maternal liver function during pregnancy, adjusting for potential confounding factors. ResultsAccording to the results, each 10 μg/m3 increase in PM2.5 was associated with an increase of 3.57% (95% CI: 0.29%, 6.96%) in ALT and 4.25% (95% CI: 2.33%, 6.21%) in TBIL during the second trimester and 4.51% (95% CI: 2.59%, 6.47%) in TBIL during the third trimester, respectively. After adjusting for O3, these associations remained significant, and the effect of PM2.5 on ALT during the second trimester was further strengthened. No significant association observed between PM2.5 and AST. ConclusionsPM2.5 exposure in early pregnancy is associated with increasement of maternal ALT and TBIL, suggesting that PM2.5 exposure may have an adverse effect on maternal liver function. Although this finding indicates an association between PM2.5 exposure and maternal liver function, more research is needed to confirm our findings and explore the underlying biological mechanisms.