Hepatotoxicity In Rats Research Articles

Hypoglycemic and hepatoprotective activity of Phellinus fastuosus on streptozotocin-induced diabetic rats and carbon tetrachloride-intoxicated rats, respectively

BackgroundPhellinus fastuosus is a wood-eating medicinal fungus from Western Ghats of India. Therefore, we investigated hypoglycemic and hepatoprotective effects of P. fastuosus aqueous extract on streptozotocin-induced diabetic and carbon tetrachloride (CCl4) induced hepatotoxicity in rats, respectively.ResultAs compared to the diabetic control group, a 400 mg/kg dose had significant hypoglycemic effects, including a reduction in blood glucose (24.44%) and gain in body weight. Aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activity reduced by 31.81% and 32.84%, respectively, were also noted, along with decreases in triglycerides (24.32%) and cholesterol (25.89%) levels. The albumin, bilirubin and creatinine levels were also significantly reduced after administration of P. fastuosus extract in diabetic rats. Administration of P. fastuosus extract showed a substantial decrease in the activity of ALT, AST, alkaline phosphatase (ALP), catalase (CAT) and superoxide dismutase (SOD) in addition a decrease in the level of lipid peroxidation (LPO) as compared to CCl4-intoxicated rats. The cumulative effect of CCl4 increased the erythrocyte membrane peroxidation, whereas P. fastuosus extract reduced the cholesterol and increased phospholipid, thus preventing the alteration of membrane fluidity as compared to CCl4-intoxicated rats. FTIR and HR-LC-MS-based metabolic profiling revealed the presence of various functional groups and bioactive metabolites.ConclusionThe extract showed the hypoglycemic and hepatoprotective effects due to the presence of various bioactive metabolites. Exploration of therapeutic potential of P. fastuosus using bioassay-guided fractionation is needed.

Ameliorating effects of Lactobacillus probiotics on cadmium-induced hepatotoxicity, inflammation, and oxidative stress in Wistar rats

Ameliorating effects of Lactobacillus probiotics on cadmium-induced hepatotoxicity, inflammation, and oxidative stress in Wistar rats

Proteomic analysis of the effects of Dictyophora polysaccharide on arsenic-induced hepatotoxicity in rats

Arsenic (As) is a highly toxic environmental toxicant and a known human carcinogen. Long-term exposure to As can cause liver injury. Dictyophora polysaccharide (DIP) is a biologically active natural compound found in the Dictyophora with excellent antioxidation, anti-inflammation, and immune protection properties. In this study, the Sprague-Dawley (SD) rat model of As toxicity was established using a feeding method, followed by DIP treatment in rats with As-induced liver injury. The molecular mechanisms of As toxicity to the rat liver and the protective effect of DIP were investigated by proteomic studies. The results showed that 172, 328 and 191 differentially expressed proteins (DEPs) were identified between the As-exposed rats versus control rats (As/Ctrl), DIP treated rats versus As-exposed rats (DIP+As/As), and DIP treated rats versus control rats (DIP+As /Ctrl), respectively. Among them, the expression of 90 DEPs in the As/Ctrl groups was reversed by DIP treatment. As exposure caused dysregulation of metabolic pathways, mitochondria, oxidative stress, and apoptosis-related proteins in the rat liver. However, DIP treatment changed or restored the levels of these proteins, which attenuated the damage to the livers of rats caused by As exposure. The results provide new insights into the mechanisms of liver injury induced by As exposure and the treatment of DIP in As poisoning.

Improved Detection of Drug-Induced Liver Injury by Integrating Predicted in vivo and in vitro Data.

Drug-induced liver injury (DILI) has been significant challenge in drug discovery, often leading to clinical trial failures and necessitating drug withdrawals. The existing suite of in vitro proxy-DILI assays is generally effective at identifying compounds with hepatotoxicity. However, there is considerable interest in enhancing in silico prediction of DILI because it allows for the evaluation of large sets of compounds more quickly and cost-effectively, particularly in the early stages of projects. In this study, we aim to study ML models for DILI prediction that first predicts nine proxy-DILI labels and then uses them as features in addition to chemical structural features to predict DILI. The features include in vitro (e.g., mitochondrial toxicity, bile salt export pump inhibition) data, in vivo (e.g., preclinical rat hepatotoxicity studies) data, pharmacokinetic parameters of maximum concentration, structural fingerprints, and physicochemical parameters. We trained DILI-prediction models on 888 compounds from the DILIst dataset and tested on a held-out external test set of 223 compounds from DILIst dataset. The best model, DILIPredictor, attained an AUC-ROC of 0.79. This model enabled the detection of top 25 toxic compounds compared to models using only structural features (2.68 LR+ score). Using feature interpretation from DILIPredictor, we were able to identify the chemical substructures causing DILI as well as differentiate cases DILI is caused by compounds in animals but not in humans. For example, DILIPredictor correctly recognized 2-butoxyethanol as non-toxic in humans despite its hepatotoxicity in mice models. Overall, the DILIPredictor model improves the detection of compounds causing DILI with an improved differentiation between animal and human sensitivity as well as the potential for mechanism evaluation. DILIPredictor is publicly available at https://broad.io/DILIPredictor for use via web interface and with all code available for download and local implementation via https://pypi.org/project/dilipred/.

The ameliorative effect of methanol extract of Ricinodendron heudelotii (Baill.) leaves on paracetamol-induced hepatotoxicity in Wistar rats

Plants are a rich source of antioxidants that are produced naturally. Therefore, this study was aimed to evaluate the effect of the plant Ricinodendron heudelotii (Baill.) in the attenuation of paracetamol (PCM) hepatotoxicity in Wistar rats. Twenty-four male albino Wistar rats weighing between 200 and 250 g were divided into four groups, with six rats each. Group 1 served as the control group, receiving just distilled water. Groups 2 and 3 received orally 250 mg/kg bwt/day PCM and 300 mg/kg bwt/day methanol extract of Ricinodendron heudelotii (Baill.) leaves for two weeks, respectively. For group 4, the Ricinodendron heudelotii (Baill.) leaf extract was pre-administered for 1 week before receiving 300 mg/kg bwt/day Ricinodendron heudelotii (Baill.) leaves extract and 250 mg/kg bwt/day PCM for 2 weeks. As a marker of liver damage, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were measured. Liver tissue reduced glutathione (GSH) concentration, superoxide dismutase (SOD), glutathione-S-transferase (GST), and catalase activities were utilized to determine antioxidant state, while malondialdehyde (MDA) concentration was employed as a lipid peroxidation indicator. When compared to the control group, the activities of serum AST, ALT, SOD, and MDA levels were considerably (p < 0.05) higher in the PCM group, although GSH level and GST and catalase activities were significantly lower. In comparison to the PCM group, co-administration of PCM with Ricinodendron heudelotii (Baill.) extract decreased serum AST and ALT activities. This study shows that the leaf extracts of Ricinodendron heudelotii (Baill.) protects Wistar rats’ livers from PCM-induced oxidative stress by increasing antioxidant enzymes.

Hepatoprotective activity of Peltophorum pterocarpum leaf and bark in the isoniazid and rifampicin-induced hepatotoxic rats

BackgroundIn recent years, various phytomedicines have been used in the treatment of hepatic disorders. The aim of this study is to find out whether Peltophorum pterocarpum bark and leaves can help rats that have been exposed to isoniazid and rifampicin-induced hepatotoxicity. Materials and MethodsThe rats were divided into 10 groups each with 6 rats. The liver damage is induced by isoniazid and rifampicin. The leaf and bark of P. pterocarpum extracted with ethanol are freshly mixed in sterile water (100, 200 and 400 mg/kg body weight), and given to rats orally in the early morning as a single dosage per day until the study period. The animals were sacrificed and the tissue and serum samples were collected for further investigations. ResultsThe liver damage induced by isoniazid and rifampicin altered the various biochemical parameters levels, but after the treatment of P. pterocarpum barks and leaves the levels were significantly altered when compared to the negative control rats. The drug silymarin was used as a standard. ConclusionThe extracts have the protective effect of liver markers and membrane-bound enzymes against the toxin-treated rats. This result highlights the hepatoprotective properties of the leaves and barks of the plant in a similar manner and the formulation (Group 10) have high beneficial effects than other groups.

L.carnitine can attenuate cadmium induced hepatotoxicity in rat: emphasis on TLR4-NFκB axis

L.carnitine can attenuate cadmium induced hepatotoxicity in rat: emphasis on TLR4-NFκB axis

The hepatoprotective effect of 4-phenyltetrahydroquinolines on carbon tetrachloride induced hepatotoxicity in rats through autophagy inhibition

BackgroundThe liver serves as a metabolic hub within the human body, playing a crucial role in various essential functions, such as detoxification, nutrient metabolism, and hormone regulation. Therefore, protecting the liver against endogenous and exogenous insults has become a primary focus in medical research. Consequently, the potential hepatoprotective properties of multiple 4-phenyltetrahydroquinolines inspired us to thoroughly study the influence of four specially designed and synthesized derivatives on carbon tetrachloride (CCl4)-induced liver injury in rats.Methods and resultsSeventy-seven Wistar albino male rats weighing 140 ± 18 g were divided into eleven groups to investigate both the toxicity profile and the hepatoprotective potential of 4-phenyltetrahydroquinolines. An in-vivo hepatotoxicity model was conducted using CCl4 (1 ml/kg body weight, a 1:1 v/v mixture with corn oil, i.p.) every 72 h for 14 days. The concurrent treatment of rats with our newly synthesized compounds (each at a dose of 25 mg/kg body weight, suspended in 0.5% CMC, p.o.) every 24 h effectively lowered transaminases, preserved liver tissue integrity, and mitigated oxidative stress and inflammation. Moreover, the histopathological examination of liver tissues revealed a significant reduction in liver fibrosis, which was further supported by the immunohistochemical analysis of α-SMA. Additionally, the expression of the apoptotic genes BAX and BCL2 was monitored using real-time PCR, which showed a significant decrease in liver apoptosis. Further investigations unveiled the ability of the compounds to significantly decrease the expression of autophagy-related proteins, Beclin-1 and LC3B, consequently inhibiting autophagy. Finally, our computer-assisted simulation dockingonfirmed the obtained experimental activities.ConclusionOur findings suggest that derivatives of 4-phenyltetrahydroquinoline demonstrate hepatoprotective properties in CCl4-induced liver damage and fibrosis in rats. The potential mechanism of action may be due to the inhibition of autophagy in liver cells.

Effects of idebenone and coenzyme Q10 on NLRP3/caspase-1/IL-1β pathway regulation on ethanol-induced hepatotoxicity in rats

Chronic and excessive alcohol consumption leads to liver toxicity. There is a need to investigate effective therapeutic strategies to alleviate alcohol-induced liver injury, which remains the leading cause of liver-related morbidity and mortality worldwide. Therefore here, we looked into and evaluated how ethanol-induced hepatotoxicity was affected by coenzyme Q10 (CoQ10) and its analog, idebenone (IDE), on the NLRP3/caspase-1/IL-1 pathway. Hepatotoxicity induced in rats through the oral administration of gradually increasing dosages of ethanol (from 2 to 6 g/kg/day) over 30 days and the effect of CoQ10 (10 or 20 mg/kg) and IDE (50 or 100 mg/kg) were evaluated. Serum hepatotoxicity markers (ALT, AST, GGT, ALP, and TBIL), tissue oxidative stress markers and the mRNA expressions of IL-1β, IL-18, TGF-β, NF-κB, NLRP3, and caspase-1 were evaluated. Masson’s trichrome staining was also used to visualize fibrosis in the liver tissue. The results indicated that ethanol exposure led to hepatotoxicity as well as considerable NLRP3/caspase-1/IL-1β pathway activation. Moreover, CoQ10 or IDE treatment reduced measured parameters in a dosage-dependent manner. Thus, by inhibiting the NLRP3/caspase-1/IL-1 pathway, CoQ10 and IDE can prevent the hepatotoxicity caused by ethanol, although CoQ10 is more effective than IDE. This study will provide insight into new therapeutic avenues that take advantage of the anti-inflammatory and antioxidant properties of CoQ10 and IDE in ethanol-induced liver diseases.

Pericopsis laxiflora (Baker) stem bark extract is protective against carbon tetrachloride-induced acute liver damage by modulation of oxidative stress and inflammation

The present study aimed to investigate the hepatoprotective activity of the hydroethanolic (HSE) and methanolic extracts (MSE) of Pericopsis laxiflora stem bark on carbon tetrachloride-induced hepatotoxicity in rats. The stem bark of P. laxiflora was extracted with 50% ethanol and methanol. Hepatoprotective activities were assessed using the CCl4 model and tested against extracts at 100, 250, and 500 mg/kg bwt. Biochemical, antioxidant enzymes and proinflammatory cytokines in liver homogenate were assayed. Treatment with HSE and MSE resulted in a significant increase in SOD, CAT, and GSH levels and a significant decrease in MDA and MPO levels in livers of CCl4 treated rats. There was also restoration of liver biomarkers and pro-inflammatory cytokines to near-normal levels. The present investigation suggests P. laxiflora extracts possess good hepatoprotective properties. This could be attributed in part to the inhibitory effect of the extracts on oxidative stress and the suppression of proinflammatory cytokines.

Effect of Polyphenols (Kolaviron and Quercetin) on Hepatic indices of Testosterone Propionate Induced-Benign prostatic Hyperplasia in Wistar rats

This research examined the impact of polyphenols (kolaviron and quercetin) on hepatic indices in Wistar rats with testosterone propionate-induced benign prostatic hyperplasia. Forty-two animals weighing between 250 and 300g were utilized, divided into six groups, each comprising seven animals. Group one served as the normal control and received 0.5ml Canola oil, while group two- six underwent BPH induction via an intraperitoneal injection of 5mg/kg body weight testosterone for four weeks. Following BPH induction, group two got 0.5mL of Canola oil, while groups three, four, five, and six were treated with 150mg/kg body weight Kolaviron, 15mg/kg body weight Quercetin, 150mg/kg body weight kolaviron plus 15mg/kg body weight quercetin and 5mg/70kg body weight finasteride for twenty-eight days. Following the experimental duration, the rats were euthanized, and liver samples were collected for biochemical analyses. BPH induction led to a decrease in liver weight in rats compared to the control group, whereas treatment with Kolaviron, Quercetin, and Kolaviron + Quercetin resulted in an increase in liver weight compared to the BPH group. Moreover, BPH induction elevated hepatic concentrations of ALT, AST, ALP, total protein, albumin, globulin, total bilirubin, and conjugated bilirubin in comparison to the normal control group. Conversely, treatment with KV, QC, and KV+QC decreased the concentrations of ALP, AST, ALT, total protein, albumin, globulin, total bilirubin and conjugated bilirubin compared to the BPH group. In conclusion, our study demonstrated that quercetin and kolaviron significantly reduced the hepatotoxicity in rats induced by testosterone propionate and could be a cheap and non-invasive treatment alternative for hepatic toxicity brought on by benign prostatic hyperplasia in men.

Combined hepatoprotective potentials of medicinal plants on CCl4-induced hepatotoxic Wistar rats

Combined hepatoprotective potentials of medicinal plants on CCl4-induced hepatotoxic Wistar rats

Evaluation of propolis hepatotoxicity in male rats

Background: Propolis is a natural resinous combination that honeybees produce from the materials they gather from plant parts, buds, and exudates. Numerous favorable pharmacological qualities have been demonstrated for propolis. Objectives: This study aimed to investigate the hepatotoxic effects of ethanolic propolis extract on the liver of male rats. Methods: In this research, 40 male rats were divided randomly into five groups: 1. Control 2. Sham (solvent), and 3. Three experimental groups (ethanolic propolis extract at doses of 50,100 and 200 mg/kg). All materials were administered by oral gavage once daily for 13 consecutive days. On the 14th day, blood sampling was performed to measure serum levels of liver function enzymes and triglycerides. After deep induction of anesthesia, the liver of the rats was removed for histopathological studies. Data were analyzed using ANOVA and Tukey’s test (p &lt;0.05). Results: The data showed that the administration of propolis significantly increased the serum levels of aminotransferases in a dose-dependent manner and decreased triglycerides, accompanied by pathological changes. Conclusions: The results of this study indicate that the administration of propolis is associated with liver toxicity, and it seems that it should be consumed more carefully. Keywords: Alanine aminotransferase, Aspartate aminotransferase, Propolis, Hepatotoxicity Triglycerides

Hepatoprotective effects of safranal on acetaminophen-induced hepatotoxicity in rats

Abstract This research aimed to explore the protective and therapeutic properties of safranal in mitigating inflammation and oxidative stress induced by elevated acetaminophen (APAP) doses in a rat model. The protective and therapeutic effects of safranal were determined by histopathologically and examining some biochemical parameters such as aspartate transaminase (AST), alanine transaminase (ALT), glutathione, glutathione peroxidase, catalase, malondialdehyde, interleukin-6, tumor necrosis factor-α, and interleukin-1β. Male Wistar–Albino rats were subject to random allocation, forming five groups, each comprising seven rats (n = 7) in the study. Group 1 was the control group. APAP was administered in Group 2 to induce hepatotoxicity. Rats in Groups 3, 4, and 5 received intraperitoneal injections of safranal at doses of 0.025, 0.05, and 0.1 mL/kg/day for 14 days, respectively. On the 15th day, to induce APAP-induced hepatotoxicity, four groups (Groups 2, 3, 4, and 5) acquired a single intraperitoneal injection of 600 mg/kg APAP. The presence of APAP-induced hepatotoxic effect was proven by elevated AST and ALT levels, which are typical biomarkers of liver function in addition to the demonstration of histopathological changes. The findings suggest that pre-treatment with safranal may offer a protective effect against hepatotoxicity by attenuating oxidative stress and the inflammatory response.

Comparative versatility and diverse biological applications of eco-friendly zinc oxide and cobalt oxide nanoparticles using Punica granatum L. peel extract

A fundamental element of nanotechnology today is the advancement of sustainable, environmentally friendly and economically viable approaches to green synthesis of nanomaterials. In this study, fresh aqueous extract of pomegranate peels was used as reducing and stabilizing agents in a rapid and eco-friendly approach for the synthesis of zinc oxide nanoparticles (ZnO-NPs) and cobalt oxide nanoparticles (Co3O4-NPs). X-ray diffraction (XRD), Scanning Electron Microscopy (SEM), Transmission electron microscope (TEM), Energy Dispersive Analysis of X-rays (EDX), and Fourier-transform Infrared Spectroscopy (FT-IR) were used to analyze the biosynthesized ZnO-NPs and Co3O4-NPs. XRD analysis confirmed the crystalline structures of ZnO-NPs and Co3O4-NPs as approximately 33.4 and 11.9 nm, respectively. SEM images showed distinct morphologies, while EDX and elemental mapping confirmed compositional integrity. FT-IR validated the characteristic functional groups present in both nanoparticles. TEM analysis provide the average particle size of ZnO-NPs and Co3O4-NPs were observed at 41.25 and 17.19 nm, respectively. The zeta potential of green synthesized ZnO-NPs and Co3O4-NPs were found to have a distinct peak at −12.5 and −16.3 mV, respectively. Both NPs have shown potent antimicrobial activity against four common pathogens, with increased antimicrobial activity against increasing concentrations of NPs. In vivo studies show a protective role for both ZnO-NPs and Co3O4-NPs against doxorubicin (DOX)-induced toxicity. In addition, Co3O4-NPs were effective against hepatotoxicity, nephrotoxicity, and endocrine disruption in male albino rats. Multi-technique investigation in this study offers a comprehensive understanding and indicates promising biological applications of ZnO-NPs and Co3O4-NPs.

Alleviation of the arsenic induced hepatotoxicity in rats by ginger or omega-3: a histological and biochemical study

Background: Millions of individuals worldwide are unintentionally exposed to arsenic through food and water. Arsenic bioaccumulates in the human body and causes organ toxicity, especially hepatotoxicity, through apoptosis, inflammation, and the production of oxidative stress markers. Aim of the study: We aimed to determine whether Ginger (Zingiber officinale) or omega-3 could mitigate the hepatotoxicity that rats experienced from long-term exposure to arsenic in drinking water. Methods: Rats were randomly assigned into four groups (10/group): a control group, an arsenic exposed group (20 mg/kg body weight) only, or an arsenic exposed group in the presence of either Zingiber officinale (12 mg/kg of body weight) or omega-3 (100 mg/kg b.w.) daily for 28 days. We used different biochemical parameters to assess liver functions, such as oxidative stress parameters, inflammatory markers, and histological and immunohistochemical stains. Results: Arsenic exposure to rats in drinking water results in hepatotoxicity, proved by increased liver enzymes and structural pathological changes in the liver, those mediated by increased oxidative stress, antiapoptotic effects, and inflammatory parameters, while supplementation of either Zingiber officinale or omega-3- to arsenic exposed rats significantly (P &lt; 0.05) improved liver function biomarkers and alleviated oxidative stress induced by arsenic as well as, liver protection as confirmed by our histological and findings. Conclusion: Ginger or omega-3 are safe and effective antioxidants to ameliorate arsenic-induced hepatotoxicity. Keywords: Arsenic; Oxidation; Inflammation; Ginger; Omega-3.

Histopathological alterations in the vital organs of Indian major carp Labeo rohita exposed to monosodium glutamate (MSG)

BackgroundMonosodium glutamate (MSG E621) is one of the most popular flavouring agents of modern times and is widely used in many commercially packed food and even in house hold cooking. Previous studies revealed that excessive intake of MSG in diet causes obesity, metabolic defects, nephrotoxicity, neurotoxicity and hepatotoxicity in rats, but no reports are available in the literature about the ecotoxicological assessment of MSG by using fishes as a bioindicators. Since fishes are important consumer in aquatic food chain and directly linked with human health status, the present study was aimed to investigate the impact of MSG in freshwater fish Labeo rohita by using histological biomarkers.ResultsNinety-six h-LC50 of MSG to Labeo rohita was determined (1.5 g/L), and fish exposed to sub-lethal concentration of MSG (1/10th of 96 h-LC50 concentration of MSG (150 mg/L)) showed distinguished behavioural changes like erratic movement, loss of appetite and excessive mucous secretion all over the body as an adaptive syndrome to avoid the direct exposure to MSG in the medium. Histopathological analysis clearly depicts severe damages in the vital organs of fish. In gills, epithelial necrosis, hypertrophy, hyperplasia, primary and secondary gill lamellae degeneration, oedema, fusion of adjacent secondary lamellae and rupture of gill epithelium were observed. The intensity of tissue damage was increased as the exposure period was extended. The liver displayed vein congestion, vacuole formation, degeneration in parenchymal cells and bile stagnation, whereas MSG-treated kidney tissue showed high interstitial inflammation. Among the vital organs gill and liver displayed the highest histopathological alterations.ConclusionsThe present study clearly demonstrated that MSG is toxic to fish and able to cause significant damages in the vital organs as the exposure period was extended. Since the studies on the toxicity of MSG to fish are rare, the present investigation may contribute to the scarce literature on sub-lethal toxicity of MSG to freshwater fishes.

Sophorin mitigates flutamide-induced hepatotoxicity in wistar rats

Flutamide is frequently used in the management of prostate cancer, hirsutism, and acne. It is a non-steroidal anti-androgenic drug and causes hepatotoxicity. The current study's objective is to evaluate sophorin's hepatoprotective effectiveness against flutamide-induced hepatotoxicity in Wistar rats. Sophorin is a citrus flavonoid glycoside, also known as rutin, which is a low molecular weight polyphenolic compound with natural antioxidant properties and reported to have promising hepatoprotective efficacy. In this study, sophorin was used at a dose of 100 mg/kg body weight in purified water via oral route for 4 week daily whereas, flutamide was used at a dose of 100 mg kg/b.wt for 4 weeks daily in 0.5% carboxy methyl cellulose (CMC) through the oral route for the induction of hepatotoxicity. Flutamide administration leads to enhanced reactive oxygen species (ROS) generation, an imbalance in redox homeostasis and peroxidation of lipid resulted in reduced natural antioxidant level in liver tissue. Our result demonstrated that sophorin significantly abrogate flutamide induced lipid peroxidation, protein carbonyl (PC), and also significantly increasesed in enzymatic activity/level of tissue natural antioxidant such as reduced glutathione(GSH), glutathione reductase(GR), catalase, and superoxide dismutase(SOD). Additionally, sophorin reduced the activity of cytochrome P450 3A1 in liver tissue which was elevated due to flutamide treatment. Furthermore, sophorin treatment significantly decreased the pro-inflammatory cytokines (TNF-α and IL-6) level. Immunohistochemical analysis for the expression of inflammatory proteins (iNOS and COX-2) in hepatic tissue was decreased after sophorin treatment against flutamide-induced hepatotoxicity. Moreover, sophorin suppressed the infiltration of mast cells in liver tissue which further showed anti-inflammatory potential of sophorin. Our histological investigation further demonstrated sophorin's hepatoprotective function by restoring the typical histology of the liver. Based on the aforementioned information, we are able to come to the conclusion that sophorin supplementation might benefit wistar rats with flutamide-induced hepatic damage by reducing oxidative stress and hepatocellular inflammation.

Metabolic profiling of Verbena bonariensis L. extract by LC/MS and evaluation of the hepatoprotective potential with isoniazid- and rifampicin-induced hepatotoxicity in rats.

The study explored the hepatoprotective activity and metabolic profile of Verbena bonariensis L. methanol extract (VBM) and fractions using isoniazid as well as rifampicin-triggered liver toxicity in Wistar albino rats. Metabolite profiling of VBM using HPLC-PDA-ESI-MS identified 12 compounds, mainly iridoids, phenylpropanoids, and flavonoids, where verbascoside represents the major compound. Different biochemical parameters such as aspartate transaminase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP), bilirubin, and total protein levels were used to assess liver functions. All the evaluated samples exhibited hepatoprotective potential, but VBM exhibited maximum activity and a notable decline in ALP (p < 0.05, significant), even better than the standard drug (silymarin). VBM significantly reduced the elevated ALT, AST, ALP, and total bilirubin. It also triggered a significant elevation in total proteins compared with diseased animals. This was further consolidated by histopathological studies. Verbena bonariensis L. could serve as a potent hepatoprotective agent and may alleviate liver ailments.

Protective effect of Enicostemma axillare - Swertiamarin on oxidative stress against nicotine-induced liver damage in SD rats

The current investigation was aimed to determine the hepatoprotective benefits of Swertiamarin (ST) administration against nicotine-induced hepatotoxicity in SD rats. A total of 48 adult male SD rats were allocated into six groups using a fully randomised approach. As a control, group I was given oral (PO) normal saline. For 65days, the animals in groups II, III, IV, V and VI received 2.5mg/kg/day of nicotine intraperitoneally (IP), 100mg/kg/day of ST orally (PO), 200mg/kg/day of ST orally (PO), 2.5mg/kg/day of nicotine (IP)+100mg/kg/day of ST (PO), and 2.5mg/kg/day of nicotine (IP)+200mg/kg/day of ST (PO), respectively. Animals were killed on 66thday, liver tissue was removed and used for histopathological analysis as well as biochemical testing (oxidative stress parameters and liver function enzymes). When compared to control animals, the animals in group II showed a substantial rise in their aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea, and creatinine levels (P˂0.001). Furthermore, compared to control animals, these animals displayed enhanced hepatic oxidative stress as indicated by significantly higher Malondialdehyde (MDA) levels (P˂0.001) and lower levels of Catalase (CAT), Glutathione (GSH), Glutathione peroxidase (GSH-Px) and Superoxide dismutase (SOD) (P˂0.001). Further, more histological anomalies were seen in the liver of nicotine-treated rats compared to control rats, including significant vacuolization, poor tissue architecture, the growth of pycnotic nuclei, and dilated sinusoids. Contrary to nicotine-treated rats, the co-administration of ST and nicotine was observed to prevent the abnormalities caused by nicotine (groups V and VI). The results of the current study show that nicotine can seriously harm liver tissue and that swertiamarin can prevent the harmful effects of nicotine on rat liver. Future research is necessary to delve deeply into the mechanisms behind swertiamarin protective impact against nicotine-induced hepatotoxicity.