Hepatic Malondialdehyde Levels Research Articles

Canagliflozin attenuates thioacetamide-induced liver injury through modulation of HMGB1/RAGE/TLR4 signaling pathways

Thioacetamide (TAA), a classic liver toxic compound, is used to establish experimental models of liver injury via induction of inflammation and oxidative stress. The current study was employed to explore the effects of canagliflozin (CANA), a sodium glucose cotransporter 2 (SGLT-2) inhibitor and antidiabetic agent, on TAA-induced acute liver injury. MethodsA rat model of acute hepatic injury was established using single intraperitoneal injection of TAA (500 mg/kg) and rats received CANA (10 and 30 mg/kg, orally) once daily for 10 days prior to TAA challenge. Liver function, oxidative stress, and inflammatory parameters were measured in serum and hepatic tissues of rats. ResultsElevated levels of liver enzymes, hepatic malondialdehyde (MDA), and serum lactate dehydrogenase (LDH) were significantly attenuated by CANA. CANA also increased hepatic superoxide dismutase (SOD) and glutathione (GSH). Hepatic levels of high-mobility group box 1 (HMGB1), toll like receptor4 (TLR4), receptor for advanced glycation end products (RAGE), and pro-inflammatory cytokines (IL-6, and IL-1β) were normalized with CANA. Additionally, Hepatic expression of p-JNK/p-p38 MAPK was significantly attenuated by CANA compared to TAA-treated rats. CANA also decreased hepatic immunoexpression of NF-κB and TNF-α and attenuated hepatic histopathological alterations via reduction of inflammation and necrosis scores and collagen deposition. Moreover, mRNA expression levels of TNF-α and IL-6 were reduced upon CANA treatment. ConclusionCANA attenuates TAA-prompted acute liver damage, via suppressing HMGB1/RAGE/TLR4 signaling, regulation of oxidative stress and inflammation pathways.

Dietary Chlorella vulgaris effectively alleviates oxidative stress, immunosuppression, and enhances the resistance to Streptococcus agalactiae infection in cadmium-intoxicated Nile tilapia fingerlings

Aquatic pollutants, including cadmium (Cd), cause oxidative stress on aquatic animals. The use of probiotics, including microalgae as a feed additive to alleviate the toxic impacts of heavy metals, is a much more interesting point. Hence, the current study investigated the oxidative stress and immunosuppression in Nile tilapia (Oreochromis niloticus) fingerlings caused by Cd toxicity as well as the preventive function of dietary Chlorella vulgaris against Cd toxicity. Accordingly, fish were fed on 0.0 (control), 5, and 15 g/kg diet of Chlorella up to satiation thrice a day, along with being exposed to 0.0 or 2.5 mg Cd/L for 60 days. Following the experimental procedure, fish from each group were intraperitoneally injected with Streptococcus agalactiae, and their survivability was observed for further ten days. Chlorella-supplemented diets meaningfully (P < 0.05) boosted the antioxidative capability of fish, which was evidenced by higher activities of hepatic superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione-S-transferase (GST) as well as higher levels of reduced glutathione (GSH) along with significant reductions in hepatic malondialdehyde levels. Moreover, the innate immunity indices [phagocytic activity (PA), respiratory burst activity (RBA), and alternative complement activity (ACH50)] were significantly higher in Chlorella-fed fish, particularly in the group of 15 g/kg diet. Additionally, serum of Chlorella-fed fish showed potent bactericidal activities against S. agalactiae, particularly at the treatment of a 15 g/kg diet. Feeding Chlorella diets to Nile tilapia fingerlings upregulated SOD, CAT, and GPx genes expression alongside the down-regulation of IL-1β, IL-8, IL-10, TNF-α, and HSP70 genes expression. Conversely, Cd toxicity caused oxidative stress and suppressed the fish's innate immunity with upregulation of the expression of IL-1β, IL-8, IL-10, TNF-α, and HSP70 genes. Feeding Cd-exposed fish on Chlorella-containing diets attenuated these adverse effects. The current research revealed that supplementing feeds with the treatment of 15 g/kg diet of C. vulgaris supports the antioxidant-immune responses and alleviates the Cd toxicity effects on Nile tilapia fingerlings.

Hepatoprotective effect of water bamboo shoot (Zizania latifolia) extracts against acute alcoholic liver injury in a mice model and screening of bioactive phytochemicals

AbstractIn this study, the hepatoprotective effect of alkali extract (NE) of water bamboo shoot (WBS) against acute alcoholic liver injury (ALI) in mice was evaluated, and its underlying mechanisms were explored. Animal experiment demonstrated that NE exhibited hepatoprotective effect on alcoholic intake‐induced ALI via significantly enhancing the hepatic activities of alcohol dehydrogenase (ADH), acetaldehyde dehydrogenase (ALDH), superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px), and catalase (CAT), whereas significantly attenuated hepatic levels of malondialdehyde (MDA), interleukin‐1β (IL‐1β), interleukin‐6 (IL‐6), and tumor necrosis factor‐α (TNF‐α). The potential molecular mechanism and bioactive compounds of NE against ALI were explored by bioinformatics analysis and isosinensetin was found to be the major bioactive compounds in NE against ALI. The western blot analysis showed that NE inhibited phosphorylation of p65 and IκBα to suppress the NF‐κB pathway. Overall our result indicated that WBS possesses potential hepatoprotective effects against ALI.

Effects of dietary pomegranate peel supplementation on growth performance and biochemical responses of common carp, Cyprinus carpio, to chronic crowding stress

In the present study, the effects of dietary pomegranate peel (PP) at 0 (PP0; control), 5 (PP5), 10 (PP10), 15 (PP15), and 20 (PP20) g/kg were investigated in common carp, Cyprinus carpio (18.1 ± 0.42 g), under normal and stressful conditions. The fish were fed the aforementioned diets over two 4-week periods, one under normal stocking density (5 g/L; basal) and the other under high stocking density (15.5–16.3 g/L; stressed). The results showed that there were no significant differences in growth performance between the PP0 and PP5 treatments. However, PP10, PP15, and PP20 showed deteriorated growth performance, compared to PP0 treatment. The poorest growth parameters have been observed in PP15 and PP20 treatments. Plasma cortisol, glucose, alanine aminotransferase, and aspartate aminotransferase significantly increased after the stress in all treatments. PP5 and PP10 had significantly lower plasma cortisol and PP10 and PP15 had significantly lower plasma glucose and aspartate aminotransferase, compared to PP0 treatment. Increase in dietary PP levels significantly decreased alanine aminotransferase activity. The stress and increase in dietary PP levels significantly decreased the plasma T3 and T4 levels. Dietary PP significantly improved plasma lysozyme (PP5, PP10, and PP15) and complement (PP5 and PP10) activities and mitigated their decrease after the stress (the best effects in PP10), but was not beneficial in mitigating plasma total immunoglobulin decrease after the stress. Dietary PP (5–15 g/kg) significantly decreased hepatic antioxidant enzymes activities and mitigated their elevations after the stress. Hepatic malondialdehyde significantly decreased by dietary PP administration, but increased after the stress. The lowest hepatic malondialdehyde level was observed in PP10 treatment. In conclusion, dietary 5 g/kg PP is recommended as the best supplemental level that improves the fish health, without adverse effects on the fish growth performance.

Activation of AMPK Entails the Protective Effect of Royal Jelly against High-Fat-Diet-Induced Hyperglycemia, Hyperlipidemia, and Non-Alcoholic Fatty Liver Disease in Rats.

This study examined the mechanism underlying the protective effect of royal jelly (RJ) against high-fat-diet (HFD)-mediated non-alcoholic liver disease (NAFLD) in rats. Adult male rats were divided into five groups (n = 8 each): control fed a standard diet, control + RJ (300 mg/kg), HFD, HFD + RJ (300 mg/kg), and HFD + RJ + CC (0.2 mg/kg). The treatment with RJ reduced weight gain, increased fat pads, and attenuated fasting hyperglycemia, hyperinsulinemia, and glucose tolerance in the HFD-fed rats. It also reduced the serum levels of liver function enzymes, interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), and leptin but significantly increased the serum levels of adiponectin. In addition, and with no effect on lipid excretion in stool, RJ significantly decreased the hepatic mRNA expression of SREBP1, serum, hepatic cholesterol, and triglycerides but increased hepatic mRNA levels of PPARα. Furthermore, RJ reduced the hepatic levels of TNF-α, IL-6, and malondialdehyde (MDA) in the livers of these rats. Of note, with no effect on the mRNA levels of AMPK, RJ stimulated the phosphorylation of AMPK and increased the levels of superoxide dismutase (SOD) and total glutathione (GSH) in the livers of the control and HFD-fed rats. In conclusion, RJ attenuates NAFLD via its antioxidant potential and adiponectin-independent activation of liver AMPK.

1,25-Dihydroxycholecalciferol down-regulates 3-mercaptopyruvate sulfur transferase and caspase-3 in rat model of non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) is the commonest cause of liver morbidity and mortality and has multiple unclear pathogenic mechanisms. Vitamin D deficiency was associated with increased incidence and severity of NAFLD. Increased hepatic expression of 3-mercaptopyruvate sulfur transferase (MPST) and dysregulated hepatocyte apoptosis were involved in NAFLD pathogenesis. We aimed to explore the protective effect of 1,25-Dihydroxycholecalciferol (1,25-(OH)2 D3) against development of NAFLD and the possible underlying mechanisms, regarding hepatic MPST and caspase-3 expression. 60 male adult rats were divided into 4 and 12week fed groups; each was subdivided into control, high-fat diet (HFD), and HFD + VD. Serum levels of lipid profile parameters, liver enzymes, insulin, glucose, C-reactive protein (CRP), tumor necrosis factor alpha (TNF-α), and hepatic levels of malondialdehyde (MDA), total antioxidant capacity (TAC), and reactive oxygen species (ROS) were measured. BMI and HOMA-IR were calculated, and liver tissues were processed for histopathological and immunohistochemical studies. The present study found that 1,25-(OH)2 D3 significantly decreased BMI, HOMA-IR, serum levels of glucose, insulin, liver enzymes, lipid profile parameters, CRP, TNF-α, hepatic levels of MDA, ROS, hepatic expression of MPST, TNF-α, 8-hydroxy-2'-deoxyguanosine (8-OHdG), and caspase-3; and significantly increased hepatic TAC in both HFD-fed groups. In conclusion: Administration of 1,25-(OH)2 D3 with HFD abolished the NAFLD changes associated with HFD in 4-week group, and markedly attenuated the changes in 12-week group. The anti-apoptotic effect via decrement of caspase-3 and MPST expression are novel mechanisms suggested to be implicated in the protective effect of 1,25-(OH)2 D3.

Antifatigue effect of sea buckthorn seed oil on swimming fatigue in mice

The effect of sea buckthorn seed oil (SSO) on exercise-induced fatigue in mice was explored. The animals were randomly divided into a normal control group, exercise-induced fatigue group (EFG), SSO low-dose group, SSO medium-dose group, and SSO high-dose group. The mice in all the groups underwent swimming training for 10 days. Those in the treatment groups received different amounts of SSO (0.85, 1.68, and 3.35g/kgBW [body weight]) before the exercise. All the animals were sacrificed on the last day after an exhaustive swimming test, and serum, liver, and brain specimens were collected. In the exhaustive swimming test, the swimming durations in the SSO-treated animals were longer than those in the EFG. Furthermore, SSO reduced serum lactic acid, blood urea nitrogen, and hepatic malondialdehyde levels and increased liver glycogen level, hepatic superoxide dismutase level, hypothalamic dopamine content, and glutathione peroxidase level. The SSO treatment decreased hypothalamic 5-hydroxytryptamine content, lipid hydroperoxide level, NLRP3 inflammasome, and interleukin-1β protein expression in the prefrontal cortex. Furthermore, it promoted the protein expression of nuclear factor erythroid 2-related factor 2 in the liver. SSO exhibited an excellent antifatigue effect, which may be related to its inhibition of oxidative and inflammatory injury and regulation of hypothalamic neurotransmitters. PRACTICAL APPLICATION: In the present study, the effect of sea buckthorn seed oil on fatigue in mice and its potential mechanism were explored. Taken together, the findings provide insight into the potential role of sea buckthorn seed oil in the development of antifatigue drugs.

Capsaicin protects against septic acute liver injury by attenuation of apoptosis and mitochondrial dysfunction

Capsaicin is the main pungent bioactive constituent in red chili with promising therapeutic properties due to its anti-oxidative and anti-inflammatory effects. No evidence exists on the beneficial effect of capsaicin on apoptosis and mitochondrial function in acute liver injury (ALI) under septic conditions. For inducing septic ALI, lipopolysaccharide (LPS, 50 μg/kg) and d-galactose (D-Gal, 400 mg/kg) was intraperitoneally injected and capsaicin was given orally at 5 or 20 mg/kg. Functional markers of liver function and mitochondrial dysfunction were determined as well as hepatic assessment of apoptotic, oxidative, and inflammatory factors. Capsaicin at the higher dose appropriately decreased serum level of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in addition to reducing hepatic level of malondialdehyde (MDA), reactive oxygen species (ROS), nitrite, NF-kB, TLR4, IL-1β, TNF-α, caspase 3, DNA fragmentation and boosting sirtuin 1, Nrf2, superoxide dismutase (SOD) activity, and heme oxygenase (HO-1). These beneficial effects of capsaicin were associated with reversal and/or improvement of gene expression for pro-apoptotic Bax, anti-apoptotic Bcl2, mitochondrial and metabolic regulators PGC-1α, sirtuin 1, and AMPK, and inflammation-associated factors. Additionally, capsaicin exerted a hepatoprotective effect, as revealed by its reduction of liver histopathological changes. These findings evidently indicate hepatoprotective property of capsaicin under septic conditions that can be attributed to its down-regulation of oxidative and inflammatory processes besides its potential to attenuate mitochondrial dysfunction and apoptosis.

Galectin-3 is a key hepatoprotective molecule against the deleterious effect of cisplatin

AimsEvaluate the role of galectin-3 in the liver using an acute model of cisplatin-induced toxicity. Material and methodsModified citrus pectin (MCP) treatment was used to inhibit galectin-3. Rats were distributed into four groups: SHAM, CIS, MCP and MCP + CIS. On days 1–7, animals were treated by oral gavage with 100 mg/kg/day of MCP (MCP and MCP + CIS groups). On days 8, 9 and 10, animals received intraperitoneal injection of 10 mg/kg/day of cisplatin (CIS and MCP + CIS groups) or saline (SHAM and MCP groups). Key findingsCisplatin administration caused a marked increase in hepatic leukocyte influx and liver degeneration, and promoted reactive oxygen species production and STAT3 activation in hepatocytes. Plasma levels of cytokines (IL-6, IL-10), and hepatic toxicity biomarkers (hepatic arginase 1, α-glutathione S-transferase, sorbitol dehydrogenase) were also elevated. Decreased galectin-3 levels in the livers of animals in the MCP + CIS group were also associated with increased hepatic levels of malondialdehyde and mitochondrial respiratory complex I. Animals in the MCP + CIS group also exhibited increased plasma levels of IL-1β, TNF-α, and aspartate transaminase 1. Furthermore, MCP therapy efficiently antagonized hepatic galectin-9 in liver, but not galectin-1, the latter of which was increased. SignificanceReduction of the endogenous levels of galectin-3 in hepatocytes favors the process of cell death and increases oxidative stress in the acute model of cisplatin-induced toxicity.

Hepatoprotective Mechanism of Apigenin via Suppression of Oxidative Inflammatory Signaling and Apoptosis against Hepatotoxicity Induced by CCl4 in Rats

Background: Carbon tetrachloride (CCl4) is a critical hepatotoxicant causing liver injury and fibrosis via hepatic production of reactive oxygen species (ROS). Apigenin (APG) is a natural bioactive compound and flavonoid antioxidant. We, therefore, evaluated whether APG could mitigate CCl4-mediated hepatotoxicity. Methods: Rats were randomly divided and administered APG and/or CCl4 in Control group, CCl4 group, APG + CCl4 groups (APG: 10 and 20 mg/kg bw) and APG groups (APG: 10 and 20 mg/kg bw) 2 times per week for 7 consecutive weeks. Result: Rats exposed to CCl4 demonstrated marked increases in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and monoamine oxidase (MAO) activities and decreased hepatic malondialdehyde (MDA) level compared to control. The hepatic activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) decreased appreciably. The CCl4 intoxication caused significant increases in inflammatory cytokines (IL-6 and TNF-α) and apoptosis markers, while the anti-inflammatory cytokines (IL-4 and IL-10) decreased with evident histopathological lesions compared to control. APG-dose-dependently-prevented these hepatic alterations.

Hepatic regenerative response to long-term consumption of cinnamon-rich diet in aged rats.

The present study aimed to investigate the impact of cinnamon on liver regeneration in a rat model of partial hepatectomy (PH). Thirty-two old male Sprague-Dawley rats (12 weeks old) were randomly divided into two equal groups (n=16). One group was fed with a standard diet (control) while the other group was fed with the same diet containing 1% cinnamon for 41 weeks. Then, all animals were subjected to the PH procedure and their livers were studied on postoperative days 2, 10 and 28. The liver contents of hepatic growth factor (HGF), insulin, malondialdehyde (MDA), nitric oxide metabolites (NOx), superoxide dismutase (SOD) and tumor necrosis factor-alpha (TNF-α) were evaluated. Also, the serum levels of liver function markers (alanine aminotransferase (ALT) and aspartate aminotransferase (AST), MDA, NOx and SOD activity were measured. The regenerated liver weight was significantly higher in cinnamon-treated animals than the controls on both day 10 and 28 post hepatectomy. The hepatic MDA levels in the cinnamon-treated animals were significantly lower than the control rats. Cinnamon led to a significant increase of SOD on day 2 after hepatectomy in serum and liver content. The basal level of HGF in the liver of cinnamon-consuming rats was significantly higher than in the control rats. Hepatic insulin level was significantly increased relative to baseline and control on day 2 in the cinnamon-consuming rats. Hepatic TNF-α levels dramatically decreased on postoperative days (POD) 2 relative to baseline in the control and cinnamon-treated rats. Long-term cinnamon consumption enhanced liver regeneration outcomes in old rats.

Mancozeb-induced hepatotoxicity: protective role of curcumin in rat animal model.

Mancozeb-a widely used fungicide in the agricultural sector-is believed to cause toxicity by increasing oxidative stress. This work investigated the efficacy of curcumin in protecting mancozeb-induced hepatotoxicity. Mature Wistar rats were assigned into 4 equal groups: control, mancozeb (30mg/kg/day, ip), curcumin (100mg/kg/day, po), and mancozeb+curcumin. The experiment lasted for 10days. Our results reported that mancozeb elevated aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase, gamma glutamyltranspeptidase enzyme activities, and total bilirubin level in plasma; and decreased total protein and albumin levels, compared with the control group (P<0.05-0.001). Hepatic tissue levels of malondialdehyde, and advanced oxidation protein products were significantly increased; whereas activities of superoxide dismutase, catalase, glutathione peroxidase, as well as levels of reduced glutathione, vitamin C, and total protein were reduced (P<0.05-0.001). Histopathological examination showed marked histological changes. Co-treatment with curcumin improved the antioxidant activity; reversed oxidative stress and biochemical changes; and restored most of the liver histo-morphological alterations; thus, attenuating the hepatic toxicities induced by mancozeb. These results indicated that curcumin could protect against detrimental hepatic effects induced by mancozeb.

Orthosiphon aristatus (Blume) Miq Alleviates Non-Alcoholic Fatty Liver Disease via Antioxidant Activities in C57BL/6 Obese Mice and Palmitic-Oleic Acid-Induced Steatosis in HepG2 Cells.

Non-alcoholic fatty liver disease (NAFLD) is the most prevalent form of liver disease. Orthosiphon aristatus (Blume) Miq, a traditional plant in South Asia, has previously been shown to attenuate obesity and hyperglycaemic conditions. Eight weeks of feeding C57BL/6 mice with the standardized O. aristatus extract (400 mg/kg) inhibited the progression of NAFLD. Liver enzymes including alanine aminotransferase and aspartate transaminase were significantly reduced in treated mice by 74.2% ± 7.69 and 52.8% ± 7.83, respectively. Furthermore, the treated mice showed a reduction in serum levels of glucose (50% ± 5.71), insulin (70.2% ± 12.09), total cholesterol (27.5% ± 15.93), triglycerides (63.2% ± 16.5), low-density lipoprotein (62.5% ± 4.93) and atherogenic risk index relative to the negative control. Histologically, O. aristatus reversed hepatic fat accumulation and reduced NAFLD severity. Notably, our results showed the antioxidant activity of O. aristatus via increased superoxide dismutase activity and a reduction of hepatic malondialdehyde levels. In addition, the levels of serum pro-inflammatory mediators (IL-6 and TNFα) decreased, indicating anti-inflammatory activity. The aqueous, hydroethanolic and ethanolic fractions of O. aristatus extract significantly reduced intracellular fat accumulation in HepG2 cells that were treated with palmitic-oleic acid. Together, these findings suggest that antioxidant activities are the primary mechanism of action of O. aristatus underlying the anti-NAFLD effects.

Clinico-pathological Evaluation of Hepatoprotective Effect of Dandelion and Ginkgo-biloba Extract against Thioacetamide Induced Liver Damage

This study was carried outto investigatethe ameliorative effect of both of Dandelion and Ginko.biloba extract on liver toxicities induced by thioacetamide (TAA) in male albino rats.Sixty male albino rats were divided into sixgroups (10 rats pereach).Group 1 (Negative control): which received 1 ml of saline orally and 1ml of saline intra-peritoneal (I/P),Group 2: received TAA for induction of hepatic injuryGroup 3:received TAA+ ginkgo biloba extract (50 mg/ b.wt.),Group 4: received TAA+ ginkgo biloba extract (100 mg/ kg b.wt.).Group 5: which received TAA + dandelion extract (250 mg/ kg b.wt).Group 6: which received TAA+ dandelion extract (500 mg/ kg b.wt.).TAA was administrated by I/P route at dose level of 250mg/kg b.wt , extracts were administrated orally, they were administrated 3 times/week for 4 weeks. The obtained results revealed that intoxication with TAAshowed a significant elevation in serum liver enzymes activity, total bilirubinplussignificant decrease in serum levels of total proteins andalbumin, significant increase in total cholesterol and triglycerides.At the same time ,intoxication with TAA exhibited severe oxidative damged stress ,represented by a significant increase in hepatic level of malondialdehyde (MDA)as well asa significant decrease in reduced glutathione (GSH).The characteristic pathological changes were represented by ,(TAA),severe degenerative andnecrotic alterationsin the hepatocytes. The treatment with G.biloba and D- in different treateddosesattenuatedTAA-induced,serum biochemical alterations, oxidative stressand histopathological changes in liver.

Carvacrol Exerts Anti-Inflammatory, Anti-Oxidative Stress and Hepatoprotective Effects Against Diclofenac-Induced Liver Injury in Male Rats.

Diclofenac (DIC) is an NSAID that can cause toxic effects in animals and humans and carvacrol (CAR) is a monoterpene compound that displays effective pharmacological and biological actions. The purpose of this work was to assess the influences of CAR on DIC-induced liver injury and oxidative stress in male rats. The male Wistar rats were segregated into four groups. Group 1, the control group; Group 2 received DIC-only (10 mg/kg BW, p.o); Group 3, received CAR-only (10 mg/kg BW, p.o), and group 4 received DIC plus CAR. The serum levels as well as the activity of several liver-associated markers, and oxidative and anti-oxidant compounds were tested. The expression of pro-inflammatory mediators was also studied using the qRT-PCR analysis. Our results showed that DIC treatment was associated with the elevation in the serum levels of liver-related markers together with the increase in the serum and the hepatic levels of malondialdehyde (MDA) and protein carbonyl (PC). Moreover, DIC reduced the activity of the antioxidant system in the rats and increased lymphocyte infiltration into the hepatocytes. CAR; however, protected the hepatocytes from the toxic effects of DIC by enhancing the activity of antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and Glutathione (GSH). By diminishing the expression of tumor necrosis factor (TNF)-α, CAR was also capable of preventing the inflammatory effects of DIC on liver cells. The findings of this study indicated that the administration of CAR could alleviate the noxious effects of DIC on the antioxidant defense system and liver tissue.

Estimation of Lipid Profile, Hepatic Enzymes, Malondialdehyde, and Uric Acid in Preeclampsia: Implications for Early Intervention

Introduction: Preeclampsia, a serious pregnancy complication, poses significant risks to both maternal and foetal health, potentially leading to morbidity and mortality. This condition is characterised by changes in lipid profiles, hepatic enzymes, Malondialdehyde (MDA), and uric acid levels. Despite significant medical advancements, identifying precise biomarkers for preeclampsia remains complex. Moreover, there is a lack of epidemiological research on preeclampsia within the southern Indian population. Aim: To estimate the levels of serum lipid profiles, hepatic enzyme levels, MDA, and uric acid levels in pregnant women with preeclampsia. Also, to examine the association between MDA and uric acid levels among women with preeclampsia and those with normal pregnancies. Materials and Methods: This cross-sectional study included 162 pregnant patients aged between 18 and 35 years, who attended the Outpatient Department (OPD) or were admitted to a tertiary care hospital in Visakhapatnam, Andhra Pradesh, India between February 2021 and October 2021. The participants were divided into three groups: Group A (54 normotensive pregnant women), Group B (54 pregnant women with non severe preeclampsia), and Group C (54 pregnant women with severe preeclampsia). Lipid profiles, hepatic enzymes, MDA, and uric acid were evaluated in all subjects, and their relationship with preeclampsia severity was assessed. The data were statistically analysed using one-way Analysis of Variance (ANOVA) followed by the Tukey post-hoc test. Results: The study groups (A, B, and C) had comparable age and gestational periods. However, significant variations were observed in lipid profiles, hepatic enzymes, MDA, and uric acid levels among them, which associated with the severity of preeclampsia. Increasing severity was associated with higher cholesterol and triglyceride levels, as well as a decrease in High Density Lipoprotein (HDL) cholesterol. Furthermore, disease progression led to significant elevations in Alkaline Phosphatase (ALP) , uric acid, and MDA levels. In particular, Group A displayed total cholesterol levels of 138.3±20.32 mg/dL, triglycerides of 109.98±15.22 mg/dL, and a negative association with HDLcholesterol at 30.57±3.65 mg/dL. In contrast, Group C exhibited considerably higher levels of total cholesterol, triglycerides, AST, ALT, uric acid, and MDA compared to Group A. Conclusion: As preeclampsia worsens, cholesterol and triglyceride levels increase, while HDL-cholesterol decreases, indicating a deteriorating metabolic profile. Additionally, ALP, uric acid, and MDA levels rise, indicating increased oxidative stress and liver function impact with the progression of the ailment.

Saudi Traditional Fermented Goat Milk Protects against Experimental Non-Alcoholic Fatty Liver Disease by Hypoglycaemic and Antioxidant Potentials

This study examined the effect of fermented goat milk (oggtt) against non-alcoholic fatty liver disease (NAFLD) in rats induced by chronic high-fat diet (HFD) treatments. Both control-fed and HFD-fed adult male rats received the same vehicle or treatment with two doses of freshly collected oggtt (2 mL or 5 mL) for 12 weeks (n = 8/group). The treatment of the control and HFD-fed rats with oggtt in both doses significantly reduced weight gain, but fasting serum glucose and insulin levels as well as HOMA-IR levels were lowered only in the HFD-fed rats. Treatment improved HFD-induced glucose and insulin homeostasis impairment as measured by the oral glucose tolerance test. Both doses of oggtt reduced serum levels of liver function markers and C-reactive protein (CRP) as well as hepatic levels of malondialdehyde (MDA), tumour necrosis factor-α (TNF-α), and in-terlukin-6 (IL-6) in HFD-fed rats. In addition, the oggtt doses reduced serum and hepatic levels of triglycerides (TGs) and cholesterol (CHOL) as well as serum levels of low-density lipoproteins (LDL) in these rats. These biochemical endpoints were reflected by the improvement in liver histology and reduction in the number of fatty vacuolated and pyknotic cells. In both the control and HFD-fed rats, oggtt at both doses stimulated levels of superoxide dismutase (SOD) and glutathione (GSH). All these effects were more profound with the highest dose of oggtt. In conclusion, the finding of this study strongly supports the use of oggtt as a functional food to treat NAFLD, as it has shown hypoglycaemic and antioxidant properties.

Moringa oleifera decreases biomarkers of oxidative stress in a murine NASH model

This study aimed to evaluate the effect of Moringa oleifera aqueous extract on biomarkers of oxidative stress in a murine model of NASH. The characterization of the extract was performed by DPPH and ABTS spectrophotometric assays. Male C57BL/6J mice were randomly separated into two groups. 1) Standard diet (ND) (n = 5) (18% lipid) and 2) High fat (HF) diet (n = 10) (60% lipid and 42 g/L sugar in water of use), for 16 weeks. At the end of eight weeks, five HF group mice were divided into a subgroup, 3) Moringa Oleifera (HF + MO), 290 mg/kg/day p.o. for eight weeks. Malondialdehyde (MDA) levels were determined in liver homogenates and the transcriptome by microarray. Differences between groups were determined by ANOVA/Kruskal-Wallis test. The trial was approved by the research ethics committee. Moringa aqueous extract showed antioxidant capacity; DPPH values were 10081.4 0.3 and 22960.4 0.3 for ABTS. Hepatic MDA levels were increased in the HF group compared to the ND group (p<0.05) and decreased in the moringa-treated group (p<0.05). In the transcriptome, mRNAs involved in endoplasmic reticulum stress were underexpressed. An increase in MDA has been demonstrated in a murine model of NAFLD induced by a high-fat diet. In our study, Moringa administration reduces MDA production and gene expression of molecules involved in oxidative stress. MO treatment is a therapeutic alternative for the NASH spectrum of liver disorders. The resources used in this study were from the hospital without any additional financing The authors declare no potential conflicts of interest.

Effects of fruits and vegetables on gut microbiota in a mouse model of metabolic syndrome induced by high-fat diet.

The aim of this study was to evaluate the effect of fruit and vegetable intake on gut microbiota using a mouse model of metabolic syndrome (MS) induced by a high-fat diet. Forty-eight male mice were randomly divided into four groups, control group (C), high-fat diet-fed model group (H), high fat plus low intake of fruits and vegetables diet-fed group (H.LFV), high fat plus high intake of fruits and vegetables diet-fed group (H.HFV), and each group were fed for 60 days. During the experiment, mouse body weights were recorded and fecal samples were collected. Cetyltrimethyl ammonium bromide (CTAB) method was used to extract fecal bacterial DNA, and the purity and concentration of the DNA were detected by electrophoresis. DNA samples underwent PCR amplification (primers in 16 S V4 (515F and 806R)). Raw sequencing data were processed, and sample complexity and multiple-sample comparisons were investigated. Mouse organ coefficient, serum lipid levels, fecal TC (total cholesterol) and TBA (total bile acid) levels, and hepatic glutathione and malondialdehyde levels were determined. Compared to the H group, the fecal TC and TBA levels decreased significantly in the H.HFV group (p < .05), and hepatic glutathione and malondialdehyde levels decreased significantly in both H.LFV and H.HFV groups (p < .05). Decreased abundance of Firmicutes, Burkholderiales, Syntrophomonas, and Pseudomonadales in gut microbiota was observed in H.LFV and H.HFV groups compared to the H group. The Anosim results showed significant differences in pairwise comparison between groups. The linear discriminant analysis effect size (LEfSe) results showed that k_bacteria not only exhibited statistically differences between H and C groups but also among H.LFV, H.LFV, and H groups, and hence, could be used as a biomarker between groups. To sum up, fruit and vegetable powder could increase the fecal excretion of TC and TBA, and the antioxidant capacity in C57BL/6N mice. Meanwhile, the mechanism that fruit and vegetable powder could prevent MS in C57BL/6N mice was related to the decreased abundance of gut microbiota, including Firmicutes, Syntrophomonadales, and Pseudomonadales. Hence, fruit and vegetable powder could be used as a recommended food to regulate gut microbiota and prevent the occurrence of MS-related diseases.

Effects of dietary methanolic extract of hyssop, Hyssopus officinalis, on growth performance, hepatic antioxidant, humoral and intestinal immunity, and intestinal bacteria of rainbow trout, Oncorhynchus mykiss

The aims of the present study were to assess the effects of Hyssop, Hyssopus officinalis, methanolic extract (HE) on growth performance, hepatic oxidative status, humoral and intestinal immunity, and intestinal bacteria of rainbow trout, Oncorhynchus mykiss. Fish were allocated into twelve tanks for four treatments, receiving diets containing 0, 100, 250, and 500 mg/kg HE for eight weeks. The results showed that dietary HE supplementation induced no significant differences in the growth performance, feed efficiency, and hematological parameters (P &amp;gt; 0.05). HE supplementation significantly increased total leukocyte count and the highest count was observed in 250 mg/kg HE treatment (P &amp;lt; 0.001). Fish in 250 and 500 mg/kg HE treatments exhibited significantly lower lymphocyte (P = 0.001) and higher neutrophil (P = 0.002) percentages; the former exhibited a significantly higher monocyte percentage (P = 0.021). Hepatic superoxide dismutase (100 and 250 mg/kg HE; P &amp;lt; 0.001), glutathione peroxidase (100 and 250 mg/kg HE; P = 0.001), glutathione reducatse (all HE treatments; P &amp;lt; 0.001), and reduced glutathione (250 mg/kg HE; P = 0.046) significantly increased, whereas hepatic malondialdehyde levels (250 and 500 mg/kg HE; P = 0.007) significantly decreased in HE-treated fish. Plasma total protein, albumin, globulin, lysozyme, and alternative complement significantly increased in 250 and 500 mg/kg HE treatments and plasma total Ig significantly increased in 250 mg/kg HE treatment. Quantitative real time PCR found no Streptococcus iniae, Lactococcus garvieae, Aeromonas hydrophila, Yersinia ruckeri, and Vibrio anguillarum in the fish intestines in any treatments. Lactobacillus sp. was detected in the fish intestinal samples, but there were no significant differences among the treatments (P = 0.352). Intestinal defensin (P = 0.044) and interleukin-1 beta (P = 0.0.035) expressions were significantly up-regulated in 100 mg/kg HE; intestinal interleukin-10 (P &amp;lt; 0.001) and tumor necrosis factor-alpha (P &amp;lt; 0.001) expressions were significantly up-regulated in 100 and 500 mg/kg HE; whereas, intestinal interleukin-6 expression was significantly (P = 0.009) up-regulated in 250 mg/kg HE treatments. It is concluded that HE is able to stimulate humoral and intestinal immune responses and hepatic antioxidant capacity. HE effective concentration in rainbow trout may be in the range of 100-250 mg/kg.