AST Levels Research Articles

The Correlation Study Between Seminal Fluid Enzymes and Effects on Men's Fertility

Objective: By analyzing the relationship between ALP, GOT, and LDH action within the seminal plasma of fruitless men and comparing it with ripe men, this study aimed to investigate the physiological conditions that remain unexplained in most cases. Methods: This study collected forty-four semen tests from normospermic men and 20 tests from fertile men, after a period of forbearance (3-5 days). The tests were analyzed within the Babylon Maternity and Children research facility and private research facilities, from January 2024 to April 2024. Results: The results indicated that ALP and AST activity had a negative correlation in both fertile (r = - 0.123) and normospermic men (r = - 0.038). Similarly, ALP and LDH activity had a negative correlation in fertile men (r = -0.334), but a positive correlation that was not significant (P˃0.05) in normospermic men (r= 0.128). Moreover, the results showed that AST and LDH activity positively correlated in both normospermic (r=0.058) and fertile men (r=0.242). Conclusion: The study hypothesized that normal semen components and gland secretory ability may be indicated by ALP, AST, and LDH activity. The levels of ALP, AST, and LDH activity in males who were fertile and those who were not showed any discernible differences.

Therapeutic potential of salvigenin to combat atrazine induced liver toxicity in rats via regulating Nrf-2/Keap-1 and NF-κB pathway

Atrazine (ATR) is the second most extensively used herbicide which adversely affects the body organs including liver. Salvigenin (SGN) is a flavonoid which demonstrates a wide range of biological and pharmacological abilities. This study was planned to assess the protective ability of SGN to avert ATR induced liver damage in rats. Thirty-two rats (Rattus norvegicus) were divided into four groups including control, ATR (5 mg/kg), ATR (5 mg/kg) + SGN (10 mg/kg) and SGN (10 mg/kg) alone supplemented group. ATR exposure reduced the expression of Nrf-2 while instigating an upregulation in Keap-1 expression. Furthermore, the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), heme‑oxygenase-1 (HO-1) and glutathione reductase (GSR) contents were decreased while increasing reactive oxygen species (ROS) and malondialdehyde (MDA) levels after ATR treatment. Moreover, ATR poisoning increased the levels of ALT, AST, and ALP while reducing the levels of total proteins, and albumin in hepatic tissues of rats. Besides, ATR administration escalated the expressions of Bax and Caspase-3 while inducing a downregulation in the expressions of Bcl-2. Similarly, ATR intoxication increased the levels of Interleukin-6 (IL-6), Nuclear factor kappa-B (NF-κB), Interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and the activity of cyclooxygenase-2 (COX-2). Furthermore, ATR disrupted the normal histology of hepatic tissues. However, SGN treatment remarkably protected the liver tissues via regulating antioxidant, anti, inflammatory, anti-apoptotic as well as histology parameters. Therefore, it is concluded that SGN can be used as therapeutic agent to combat ATR-induced hepatotoxicity.

Contribution of ferritin and zinc to adverse infant outcomes among pregnancies with prenatal alcohol exposure in South Africa

Nutritional status during pregnancy can impact fetal development, yet less is known about how alcohol may interact with nutritional status to influence infant outcomes. Pregnant women (n=196) completed 2, 24-hour dietary recalls and provided a venous blood sample to be analyzed for liver enzymes (GGT –gamma-glutamyl transferase; ALT –alanine transaminase; and AST –aspartate transferase), iron, ferritin, and zinc concentrations. Infants were assessed at 6 weeks of age. Women who consumed alcohol had significantly higher ferritin levels compared to non-drinkers (51.8 vs. 34.2). While 44% of women had ferritin <30 ug/L (an indicator of iron deficiency), and 24% of women were low in serum iron, and 72% were low in serum zinc. All six drinking measures for 1st trimester and previous week were significantly correlated with GGT and AST levels while 4 out of 6 alcohol measures were associated with levels of ALT and ferritin. At six weeks of age, nearly all physical measures differentiated infants with alcohol exposure from infants without exposure. Controlling for six covariates, maternal ferritin was significantly and inversely associated with infant head circumference (OFC) centile among infants with alcohol exposure. GGT was inversely associated with infant height and weight centile among unexposed infants. Seventy-four percent (74%) of mothers who consumed alcohol were found to be low in serum zinc, yet higher maternal zinc was associated with more dysmorphology. This may indicate that higher zinc status is not protecting the fetus from the teratogenic effects of alcohol. Prenatal alcohol exposure, ferritin, and zinc status influence infant growth and neurodevelopment.

#2507 Enhancing critical care nephrology: analyzing continuous renal replacement therapy with a citrate-based anticoagulation focus

Abstract Background and Aims Continuous renal replacement therapy (CRRT) is pivotal for managing acute kidney injury (AKI) unstable patients. However, questions persist regarding prescription and the role of anticoagulation. This study aims to examine CRRT practices, focus on citrate-based anticoagulation and clarify contraindications. Method This study comprises a retrospective analysis of a patient cohort requiring CRRT and admitted to the Postoperative Intensive Care Unit and Burn Unit. Inclusion criteria involved the need for CRRT and adult age, with exclusion criteria based on treatment duration (&amp;lt;48 hours), reducing the initial cohort from 256 to 176 patients. Clinical variables, including gender, age, underlying pathology, CRRT modality, and anticoagulation type, were characterized. Subsequently, the association between anticoagulation type and clot formation within 48 hours and in-hospital mortality was investigated. Furthermore, an analysis of citrate-based CRRT was conducted, evaluating laboratory values (Table 1) at the beginning and 48 hours using the Wilcoxon test, and their correlation with clot development and mortality. Additionally, we used a logistic regression model to explore the relationship between AST, ALT, and lactate values with citrate accumulation. Finally, a survival analysis was conducted. Results The sample consisted of 66.5% males and 33.5% females, with an average age of 59.48 years. Reasons for admission are depicted in Fig. 1. CRRT modalities were 20.5% HDVVC, 76.1% HDFVVC, and 3.4% HFVVC. Anticoagulation included 35.2% none, 28.4% heparin, 33.5% citrate, and 2.8% alprostadil. Filter clotting occurred in 29.1% withing 48 hours. Heparin was associated with a 5.4-fold increased risk of clotting compared to citrate. Mortality was 63.3%, with no anticoagulation type showing a significant association. Parameters at CRRT initiation and 48 hours for citrate-based CRRT patients and Wilcoxon test results are presented in Table 1. Only 5.1% had filter clotting &amp;lt;48 hours, and no baseline parameters were significantly associated with an increased clotting risk. There was one case of citrate intoxication due to a programming error, which was not included. 76.81% had CaT/CaI &amp;lt;2.1, and 7.25% had CaT/CaI &amp;gt;2.1, requiring technique adjustments. Aminotransferases and lactate values, often considered as contraindications for citrate, were analyzed: The average AST and ALT values were 188.53 IU/l and 108.08 IU/l, respectively. When AST levels exceeded 5 times the normal range and ALT levels exceeded 3 times the normal range, a statistically significant association with CaT/CaI &amp;gt;2.1 at the 48-hour mark of CRRT utilization was observed (p &amp;lt; 0.001 for both).The average lactic acid value was 1.74 mg/dl. Having a lactic acid level &amp;gt;4 was associated (p &amp;lt; 0.05) with a higher risk of developing CaT/CaI &amp;gt;2.1. 54.2% of the sample died. No baseline parameters were significantly associated with it. At 48 hours, higher bicarbonate levels and metabolic alkalosis were associated with increased mortality (p &amp;lt; 0.05). The median survival time was 11 days (±4.38). Conclusion This study supports the use of citrate-based anticoagulation in CRRT, as no cases of citrate intoxication (CaT/CaI &amp;gt;2.5) were found. Nonetheless, a significantly elevated AST (&amp;gt;5 times normal), ALT (&amp;gt;3 times normal), and lactate (&amp;gt;4 mg/dl), were associated with a higher risk of citrate accumulation (CaT/CaI &amp;gt;2.1). Customized approaches and preventive measures to mitigate the development of metabolic alkalosis are essential for optimizing patient outcomes.

Patrinia villosa (Thunb.) Juss alleviates CCL4-induced acute liver injury by restoring bile acid levels and inhibiting apoptosis/autophagy.

Patrinia villosa (Thunb.) Juss is one of the plant resources of the famous traditional Chinese medicine "Bai jiang cao (herba patriniae)," and it is considered to function at the liver meridian, thereby treating diseases of the liver as demonstrated by the traditional theory of TCM. Unfortunately, the therapeutic mechanism of the whole plant of PV is so far unknown. UPLC QTOF-MS/MS was used to analyze the profile of PV. Male Sprague-Dawley rats were categorized into five groups, and PV groups (125 and 375mg/kg) were administered by oral gavage for seven consecutive days. The model of liver injury was induced by intraperitoneal injection of 40% CCl4 oil solution. H&E staining was performed for histological evaluation. The ELISA method was used to assess the serum level of ALT, AST, and T-BIL. Serum and liver bile acid (BA) profiling was analyzed by LC-MS/MS. TUNEL-stained liver sections were used to monitor apoptosis caused by CCl4. HepG2 cells were used to detect autophagy caused by CCl4. A total of 16 compounds were identified from the 70% methanol extract of PV. PV (125 and 375mg/kg) could reverse the ectopic overexpression of AST, ALT, and T-BIL caused by CCl4 administration. H&E staining indicated that PV (125 and 375mg/kg) could reduce the infiltration of inflammatory cells and restore liver tissue and hepatocyte structures. Six bile acids, including DCA, HDCA, GCA, TCA, TCDCA, and TUDCA, were significantly altered both in the serum and liver tissue after CCl4 administration, and the level of all these six bile acids was restored by PV treatment. Moreover, PV inhibited apoptosis caused by CCl4 stimulation in liver tissue and suppressed autophagy in HepG2 cells treated with CCl4. The results in this paper for the first time reveal the alteration of the bile acid profile in CCl4-induced liver injury and demonstrate that inhibiting apoptosis and autophagy was involved in P. villosa-elicited liver protection, providing a scientific basis for the clinical utilization of P. villosa as a natural hepatic protective agent.

Histopathological and Biochemical Effects of Methanol and Aqueous Extracts of the Leaf of Irvingia Gabonensis (African wild mango) on the liver of Albino Wistar Rat

Background: The use of Irvingia gabonensis locally for different purposes from eating down to drinking its extracts and concoctions for treating various ailments has been a common practice over the ages. The liver is a very vital metabolic organ and the central site for food and drug metabolism and subsequent excretion. In that case, the understanding of the effects of these foods and drugs both orthodox and herbal is ever invaluable both to the clinicians and the patients. This research work aims to investigate the effects of its leaf extract on the liver using histological and biochemical parameters. Methods: The experimental rats (n=20) used were divided into five (5) groups of four (4) each. Group one served as control and received only water and standard pellets. Groups two and three were administered with the methanolic extract of 150 mg/ kg and 300 mg/kg respectively. Groups four and five were administered with the aqueous extract of 250 mg/kg and 500 mg/kg respectively. The liver samples were harvested, fixed and processed in an automated tissue processor. The blood sample obtained through retro-orbital puncture was made to clot. The serum was then used to analyze the ALT, AST, ALP and Bilirubin content of the liver. Results were obtained and analyzed statistically, showing a significant (p &lt; 0.05) increase in the AST and ALP levels in groups three (3) and five (5). The Serum bilirubin and ALT levels showed insignificant (p &gt; 0.05) increases in all the groups. The photomicrograph indicates mild fibrosis and sinusoidal dilations and cellular infiltrations in groups three and five with no visual changes in the rest of the groups. Conclusion: The findings suggest that at high doses of both methanolic and aqueous extracts (300 and 500mg/kg respectively), the leaf extract is mildly toxic to the liver.

Epigallocatechin gallate (EGCG) alleviates inflammation and endothelial dysfunction and improves pregnancy outcomes in preeclampsia (PE)-like rats via eNOS/Nrf2/HO-1 pathway

Background and purposeEpigallocatechin gallate (EGCG), a natural antioxidant, has shown protective effect in many diseases. We explore the effect and potential regulatory mechanisms of EGCG in preeclampsia (PE)-like rats. Methods and materialsPE was mimicked in pregnant rats. EGCG was orally administered at a dosage of 25(Low, L) or 50 mg/kg (High, H) from gestational day (GD) 6–17. The blood pressure signatures, heart rates were monitored. The 24-h proteinuria and serum were analyzed. On GD 18, rats were sacrificed, and pups and placentas were weighed. Kidneys and placentas were analyzed using immunohistochemistry (IHC) and hematoxylin-eosin staining (H&E). Placentas were examined using western blot for sFlt1, eNOS, Nrf2, HO-1, SLC7A11. MDA, GSH, GPx and Fe2+ were measured. ResultsEGCG inhibits systolic blood pressure, BUN, CREA, ALT, AST, UA and proteinuria levels in PE-like rats. EGCG enhances the pup weight and crown-rump length and reduces the rate of fetus growth restriction in PE group. Endothelial dysfunction and infiltration of inflammatory cells were found in kidney cortex and placenta tissues in PE group and were inhibited by EGCG treatment. sFlt1 was activated in placentas in PE group and inhibited by EGCG while eNOS/Nrf2/HO-1 were inhibited in PE group and restored by EGCG. MDA and Fe concentrations were elevated in PE group and reduced by EGCG while the GSH level, SLC7A11 and the GPx activity were inhibited in PE group and restored by EGCG. ConclusionEGCG alleviates inflammation, endothelial dysfunction and placental ferroptosis, improves pregnancy outcomes in PE-like rats via eNOS/Nrf2/HO-1.

Predicting the recurrence of spontaneous intracerebral hemorrhage using a machine learning model.

Recurrence can worsen conditions and increase mortality in ICH patients. Predicting the recurrence risk and preventing or treating these patients is a rational strategy to improve outcomes potentially. A machine learning model with improved performance is necessary to predict recurrence. We collected data from ICH patients in two hospitals for our retrospective training cohort and prospective testing cohort. The outcome was the recurrence within one year. We constructed logistic regression, support vector machine (SVM), decision trees, Voting Classifier, random forest, and XGBoost models for prediction. The model included age, NIHSS score at discharge, hematoma volume at admission and discharge, PLT, AST, and CRP levels at admission, use of hypotensive drugs and history of stroke. In internal validation, logistic regression demonstrated an AUC of 0.89 and precision of 0.81, SVM showed an AUC of 0.93 and precision of 0.90, the random forest achieved an AUC of 0.95 and precision of 0.93, and XGBoost scored an AUC of 0.95 and precision of 0.92. In external validation, logistic regression achieved an AUC of 0.81 and precision of 0.79, SVM obtained an AUC of 0.87 and precision of 0.76, the random forest reached an AUC of 0.92 and precision of 0.86, and XGBoost recorded an AUC of 0.93 and precision of 0.91. The machine learning models performed better in predicting ICH recurrence than traditional statistical models. The XGBoost model demonstrated the best comprehensive performance for predicting ICH recurrence in the external testing cohort.

Effects of compound Anoectochilus roxburghii (Wall.) Lindl. oral liquid on relative metabolic enzymes and various biochemical indices in Wistar rats with isoniazid-induced liver injury

Isoniazid (INH) is the first-line anti-tuberculosis drug in clinical practice, and its main adverse effect is drug-induced liver injury (DILI). This study aimed to investigate the hepatoprotective effect of Compound Anoectochilus roxburghii (Wall.) Lindl. Oral Liquid (CAROL) and to provide a new strategy for the search of potential drugs against INH-induced liver injury in Wistar rats. Animal experiment was based on INH (100 mg/kg) induced liver injury to explore the intervention effects of CAROL at doses of 1.35, 2.70, and 5.40 mL/kg. LC-QTOF-MS/MS was used to identify hepatoprotective components in CAROL and its’ exposed components in rat serum. The hepatoprotective effect of CAROL was evaluated by pathological observation of rat liver tissue and changes in levels of biochemical indices and cytokines in serum or liver tissue. Of the 58 hepatoprotective components identified, 15 were detected in the serum of rats with liver-injured treated by high-dose CAROL. Results of animal experiments showed that the levels of various biochemical indexes and cytokines were significantly reversed with CAROL intervention. In particular, the expression level of cytokeratin-18 and high-mobility group box 1, as specific and sensitive indicators of DILI, was significantly reduced in the serum of rats with CAROL intervention compared with the INH model group. The same reversal was observed in the levels of TBIL, ALP, ALT, and AST in serum, as well as in the levels of TNF-α, IL-6, SOD, and MDA in liver tissue. For INH-metabolizing enzymes, an evident expression inhibition was observed in N-acetyltransferase 2 and glutathione S-transferases with CAROL intervention, which may be the key to controlling INH hepatotoxicity. CAROL has a favorable hepatoprotective effect on INH-induced liver injury. This study takes the first step in studying the hepatoprotective mechanism of CAROL against INH hepatotoxicity and provides reference for wider clinical applications.

Early acute kidney injury in sepsis and septic shock

ABSTRACT Background: Acute kidney injury is one of the severe conditions in hospitalized patients. Acute kidney injury can develop early from admission, usually within the first 24 hours of ICU admission. In Vietnam, there have been limited studies monitoring the progression of acute kidney injury in the early stages. This study aims to investigate the incidence, severity, clinical, laboratory characteristics, and progression of acute kidney injury in patients with sepsis and septic shock within the first 48 hours. Methods: This study is a cross-sectional descriptive analysis of 101 patients who are 15 or older and have been diagnosed with severe infection and septic shock. These patients were treated in the Intensive Care Unit of Hue Central Hospital. The patient had treatment in accordance with a standardized protocol while being closely observed. Samples were collected for diagnostic testing, and the patient’s urine output and blood creatinine levels were diligently checked. Results: The prevalence of acute renal injury (AKI) was 60.40%, with stage 1 accounting for 50.82% of cases, stage 2 accounting for 22.95%, and stage 3 accounting for 26.23%. The cohort of individuals diagnosed with AKI exhibited an advanced age, with a mean age of 60.72 ± 17.41 years, and predominantly consisted of male subjects. Patients diagnosed with acute kidney injury showed a statistically significant decrease in urine output and an increased incidence of shock (p &lt; 0.05). Additionally, these patients demonstrated lower levels of Hct, blood pH, and bicarbonate while exhibiting higher levels of blood urea, blood creatinine, AST, ALT, total bilirubin, PCT, and blood lactate (p &lt; 0.05) compared to individuals without AKI. Patients with AKI had significantly elevated SOFA and APACHE II scores compared to individuals without AKI, as indicated by statistical analysis (p &lt; 0.05). Upon admission, a significant proportion of patients, precisely 81.97%, experienced the development of AKI. Furthermore, a observation was made about the prompt recovery of these patients within the initial 24 and 48 hours following admission. Conclusion: The prevalence of AKI was accounted for 60.40%. Among the cases of AKI, stage 1 accounted for 50.82%, while stage 2 and stage 3 accounted for 22.95% and 26.23%, respectively. There were observed variations in urine output and rates of shock among individuals diagnosed with AKI. Additionally, SOFA and APACHE II scores were elevated. The percentage of AKI was 81.97% of patients upon their initial hospital admission, with a significant proportion seeing early recovery within the first 24 to 48 hours.

Effects of ethyl acetate fraction of Psychotria vogeliana (Benth) leaf on liver function, kidney function, and cytokines level of albino rats induced with rheumatoid arthritis

Plant-based medicines contained bioactive molecules and functions, as reported in our previous study in Psychotria vogeliana leaf using HPLC. This study investigated the effects of Psychotria vogeliana leaf ethyl acetate fractions on liver, kidney, and cytokine levels in albino rats with rheumatoid arthritis. Six groups of eight female albino rats each were constituted from a total of 48. Group A was used as the control group, and they were given simply normal saline. With 0.1 mL of complete Freund's adjuvant (CFA), rheumatoid arthritis (R.A) was induced in Group B (toxic control). Group C received a standard drug (methotrexate) after being infected with R.A. Groups D, E, and F were given ethyl acetate extract fraction of Psychotria vogeliana leaf at 200 mg/kg, 400 mg/kg, and 600 mg/kg body weight, respectively, for 28 days after being induced with R.A using CFA. Biochemical parameters measured in R.A rats revealed increased levels of IL-6, IL-1β, TNF-α, urea, creatinine, BUN, AST, ALT, and ALT compared to the control group. However, albumin and total bilirubin levels decreased. The extracts showed time and dose-dependent ameliorative effects on R.A rats, with anti-arthritic potentials comparable to standard drugs. The extract effectively treated the arthritis by restoring liver, kidney, and cytokine levels against the toxic group. The extracts showed both time and dose-dependent ameliorative effects on arthritic rats, with their anti-arthritic potentials comparable to that of the standard drug. The extract effectively treated arthritis by restoring liver, kidney, and cytokine levels against the toxic group.

Exploring the mechanism of dendrobine in treating metabolic associated fatty liver disease based on network pharmacology and experimental validation

BackgroundThis study investigates the therapeutic mechanisms of dendrobine, a primary bioactive compound in Dendrobium nobile, for Metabolic Associated Fatty Liver Disease (MASLD) management. Utilizing network pharmacology combined with experimental validation, the clinical effectiveness of dendrobine in MASLD treatment was assessed and analyzed.ResultsThe study demonstrates significant improvement in liver function among MASLD patients treated with Dendrobium nobile. Network pharmacology identified key targets such as Peroxisome Proliferator-Activated Receptor Gamma (PPARG), Interleukin 6 (IL6), Tumor Necrosis Factor (TNF), Interleukin 1 Beta (IL1B), and AKT Serine/Threonine Kinase 1 (AKT1), with molecular docking confirming their interactions. Additionally, dendrobine significantly reduced ALT and AST levels in palmitic acid-treated HepG2 cells, indicating hepatoprotective properties and amelioration of oxidative stress through decreased Malondialdehyde (MDA) levels and increased Superoxide Dismutase (SOD) levels.ConclusionDendrobine mitigates liver damage in MASLD through modulating inflammatory and immune responses and affecting lipid metabolism, potentially by downregulating inflammatory mediators like TNF, IL6, IL1B, and inhibiting AKT1 and Signal Transducer and Activator of Transcription 3 (STAT3). This study provides a theoretical basis for the application of dendrobine in MASLD treatment, highlighting its potential as a therapeutic agent.

Toxicological Impact of Brick Kiln Emissions on the Liver of Brick Kiln Workers and Residents

Pakistan is the third-largest brick-producing nation in South Asia, behind China and India. In Pakistan, there are over 20,000 brick kilns and 1.8 million brick kiln employees, 50% of them are in Punjab. Brick kilns in rural Punjabi communities like district Narowal still use antiquated methods and are subject to bad laws, which has a negative impact on people's health. A cross-sectional study was carried out in the Narowal district from January 2021 to January 2022 to examine the toxicological effects of brick kiln emissions on the liver. The participants were divided into three groups based on their demographic profiles in order to examine the relationship between appropriate liver function indices, such as ALT, AST, ALP, and bilirubin, and demographic factors like age, BMI, smoking index, and length of employment among exposed (residents and workers) and control groups. The outcome demonstrated that exposed workers and residents had mean ALT (p, 0.001), AST (p, 0.001), and ALP (p, 0.002) levels that were considerably higher than reference values. Bilirubin, a measure of the liver, remained negligible. Blood chemistry tests cannot establish the presence of liver disorders. Therefore, molecular-based follow-up investigations are required to assess the health concerns related to emissions from brick kilns.

Influences of testosterone undecylate on serological parameters of obese and non-obese rats

This study aimed to assess the impact of testosterone undecylate on renal and hepatic functions by examining serum markers in obese and non-obese rats. The methodology involved treating these animals with testosterone undecylate or a control solution over a period of 28 days and analyzing serum samples for markers such as urea, creatinine, and liver enzymes. The results demonstrated no significant differences in creatinine, AST, ALT, GGT, ALP, and CK levels between the treated and control groups, suggesting that testosterone undecylate does not adversely affect renal or hepatic functions in the conditions tested. The study concludes that testosterone undecylate, within the administered doses, appears safe, presenting a favorable safety profile and good tolerability, making it a viable option for hormonal therapy in clinical and scientific settings.

Unrevealing the therapeutic potential of artesunate against emerging zoonotic Babesia microti infection in the murine model.

Babesiosis, a zoonotic blood protozoal disease, threatens humans and animals and is difficult to treat due to growing antimicrobial resistance. The study aimed to investigate the therapeutic efficacy of artesunate (AS), a well-known derivative of artemisinin, against Babesia microti (B. microti) using a murine infection model. Male BALB/c mice (6 weeks old; 15 per group) were chosen and randomly divided into 1) the control group, 2) the B. microti group, and 3) the B. microti + artesunate treatment groups. AS treatment at 2 mg/kg, 4 mg/kg, and 8 mg/kg of body weight significantly (p < 0.05) reduced the B. microti load in blood smears in a dose-dependent manner. Additionally, AS treatment mitigated the decrease in body weight and restored the normal state of the liver and spleen viscera index compared to the B. microti-infected group after 28 days. Hematological analysis revealed significant increases in RBC, WBC, and PLT counts post-AS treatment compared to the B. microti-infected group. Furthermore, AS administration resulted in significant reductions in total protein, bilirubin, ALT, AST, and ALP levels, along with reduced liver and spleen inflammation and lesions as observed through histopathological analysis. AS also elicited dose-dependent changes in mRNA and protein expression levels of apoptotic, proinflammatory, and anti-inflammatory cytokines in the liver compared to the control and B. microti-infected groups. Immunolabeling revealed decreased expression of apoptotic and inflammation-related proteins in AS-treated hepatic cytoplasm compared to the B. microti-infected group. AS also in dose-dependent manner decreased apoptotic protein and increased Bcl-2. Overall, these findings underscore the potential of AS as an anti-parasitic candidate in combating B. microti pathogenesis in an in vivo infection model, suggesting its promise for clinical trials as a treatment for babesiosis.

The Effect of Benzene Exposure on Liver and Kidney Function in Human

Background: Exposure to benzene in the workplace causes health issues for the workers, it has negative impacts on the blood, liver, and kidney. Also, it is classified as carcinogenic. Methods: This study is cross-sectional; it involved 32 participants; 16 exposed to benzene and 16 non-exposed. The sample was collected by filling out a questionnaire and taking blood samples to test liver and kidney functions. Results: This study found that the means of AST and ALT levels of exposed workers were lower than the control group, while the mean level of ALP was higher. Moreover, it did not find a relationship between qualification, years of experience, age, and level of liver enzymes of exposed participants, however, it reported a positive correlation between smoking and bilirubin level. On the other hand, there are no statistical differences between the two groups in the levels of urea and creatinine, but the mean of urea level was quite higher in the exposed group than non-exposed. Besides, there are no associations between urea and creatinine levels and age, qualification, smoking, and years of experience. Conclusion: This study demonstrated a clear association between exposure to benzene and its effect on the liver. Therefore, suitable precautions should be taken to protect the workers in the gas station.

Protective effects of cupressuflavone against doxorubicin-induced hepatic damage in rats

Doxorubicin (DOX) is a potent chemotherapeutic agent that is used in various sorts of malignancies. However, its uses are restricted owing to its deleterious effects on different organs including the liver. Cupressuflavone (CUP) is a plant-based flavonoid which is well known for its biological as well pharmacological potential. Our investigation aimed to evaluate the ameliorative potential of CUP against DOX provoked liver toxicity in rats. Twenty-four albino rats (Rattus norvegicus) were distributed into four distinct groups such as control, DOX (3 mg/kg), co- administrated DOX (3 mg/kg) + CUP (40 mg/kg) and CUP (40 mg/kg) only. DOX exposure reduced catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), Glutathione reductase (GSR), glutathione-S-transferase (GST) activities and glutathione (GSH) content while escalating the levels of reactive oxygen species (ROS) and malondialdehyde (MDA). Besides, the levels of ALT, AST and ALP were increased in response to DOX exposure. Furthermore, administration of DOX upregulated the levels of Interleukin-6 (IL-6), Nuclear factor kappa-B (NF-κB), Interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and the activity of cyclooxygenase-2 (COX-2). The treatment of DOX reduced the levels of Bcl-2 while escalating the levels of Caspase-3, Caspase-9 and Bax. Similarly, DOX intoxication instigated various histopathological disruptions in hepatic tissues of rats. However, supplementation of CUP notably (p < 0.05) restored abovementioned hepatic dysregulations owing to its anti-oxidative, anti-inflammatory as well as anti-apoptotic potential. Our results manifested that CUP could be used as hepatoprotective agent againt DOX induced liver damage in rats.

Catecholamines-based myocardial injury after acute ischemic stroke and effects of Naoxintong capsule therapy

BackgroundMyocardial injury (MI) after acute ischemic stroke (AIS) poses a significant threat to patient prognosis. However, effective intervention strategies are currently lacking. PurposeTo elucidate the mechanism of MI after AIS and effects of Naoxintong capsule (NXT) therapy. MethodIn vivo, after a rat model of middle cerebral artery occlusion (MCAO)-induced MI was established and assessed. NXT was administered prophylactically to evaluate its pharmacodynamic effects and mechanisms. In vitro, a noradrenaline (NA)-induced damage cell model was constructed. Subsequently, the NXT was applied to the cell models to examine its cardioprotective effects and potential mechanisms. ResultsThe in vivo findings revealed that following MCAO, there was a notable upregulation of TH expression in the rat brain, which subsequently triggered an increase in serum levels of various biomarkers, including AD, NA, AST, cTnT, CK-MB, and NT-proBNP. Histological analysis employing H&E staining and TUNEL assay disclosed significant pathological alterations and an escalation in apoptotic activity within the myocardial tissue. The myocardial tissue exhibited elevated levels of MDA alongside diminished CAT activity. Additionally, a marked increase in the Bax/Bcl-2 ratio, Cytochrome C release, and Caspase-3 activation was observed, all of which are indicative of heightened apoptotic activity. Administration of the NXT intervention successfully attenuated TH expression in the brains of rats subjected to MCAO, consequently leading to a reduction in circulating levels of catecholamines (CAs). NXT also exhibited significant efficacy at ameliorating cardiac oxidative stress and reducing apoptosis. In vitro, stimulation with NA led to an increase in ROS levels and calcium ion concentration in H9c2 cardiomyocytes. However, the administration of NXT has been found to effectively alleviate these adverse effects, thereby protecting H9c2 cardiomyocytes from the deleterious consequences of oxidative stress and calcium dyshomeostasis. ConclusionOverall, this study has demonstrated that increased CAs synthesis in the brain after AIS in experimental rats led to a surge in circulating CAs, ultimately leading to MI. NXT can alleviate MI due to cerebral ischemia by increasing improving brain catecholamine synthesis, cardiac oxidative stress, and apoptosis.

Cu exposure induces liver inflammation via regulating gut microbiota/LPS/liver TLR4 signaling axis

Copper (Cu) serves as an essential cofactor in all organisms, yet excessive Cu exposure is widely recognized for its role in inducing liver inflammation. However, the precise mechanism by which Cu triggers liver inflammation in ducks, particularly in relation to the interplay in gut microbiota regulation, has remained elusive. In this investigation, we sought to elucidate the impact of Cu exposure on liver inflammation through gut-liver axis in ducks. Our findings revealed that Cu exposure markedly elevated liver AST and ALT levels and induced liver inflammation through upregulating pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) and triggering the LPS/TLR4/NF-κB signaling pathway. Simultaneously, Cu exposure induced alterations in the composition of intestinal flora communities, notably increasing the relative abundance of Sphingobacterium, Campylobacter, Acinetobacter and reducing the relative abundance of Lactobacillus. Cu exposure significantly decreased the protein expression related to intestinal barrier (Occludin, Claudin-1 and ZO-1) and promoted the secretion of intestinal pro-inflammatory cytokines. Furthermore, correlation analysis was observed that intestinal microbiome and gut barrier induced by Cu were closely related to liver inflammation. Fecal microbiota transplantation (FMT) experiments further demonstrated the microbiota-depleted ducks transplanting fecal samples from Cu-exposed ducks disturbed the intestinal dysfunction, which lead to impaire liver function and activate the liver inflammation. Our study provided insights into the mechanism by which Cu exposure induced liver inflammation in ducks through the regulation of gut-liver axis. These results enhanced our comprehension of the potential mechanisms driving Cu-induced hepatotoxicity in avian species.

PDE5 inhibition mitigates heart failure in hyperlipidemia

PDE5 inhibitors was reported to play a protective role in both regulating lipid metabolism and reducing heart failure (HF). This study aimed to clarify the effectiveness of PDE5 inhibitors against hyperlipidemia-related HF by combining evidence from population-based study and animal models. The nationwide cohort study found that post-diagnostic use of PDE5 inhibitors was associated with a significantly lower risk of HF compared with patients who used alprostadil, especially among individuals with hyperlipidemia (adjusted HR = 0.56, 95% CI = 0.40–0.78). In animal models, sildenafil significantly recovered the cardiac structure and function induced by AAB surgery, as well as reversed liver dysfunction and ameliorated hyperlipidemia induced by HFD via reducing the level of ALT, AST and serum lipids. Lipidomic analysis identified four lipid metabolites involved in sildenafil administration, including FA 16:3, LPC O-18:1, DG24:0_18:0 and SE28:1/20:4. This study revealed the protective effect of PDE5 inhibitors against HF in hyperlipidemia, indicating the potential of being repurposed as an adjuvant for HF prevention in patients with hyperlipidemia if these findings can be further confirmed in clinical trials.