Hepatotoxicity In Wistar Rats Research Articles

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.

N-acetyl cysteine and zinc sulphate ameliorated crude oil-induced hepatotoxicity in Wistar rats

Even while crude oil offers many advantages, its toxic chemical composition has been shown to negatively interfere with the body's ability to maintain homeostasis. This investigation examined the effects of crude oil on the liver function of Wistar rats as well as the protective effects of N-acetyl cysteine (NAC) and zinc sulphate (ZnSO4). The experimental group and control group consisted of 42 Wistar rats, which were divided into groups of six each. The experimental group had six groups, while the control group only consumed food and water. In the experimental group, three groups received a diet contaminated with crude oil for two, three, and four weeks, respectively. In addition, another three groups received NAC (100 mg/kg), ZnSO4 (0.5 mg/kg), and a combination of NAC and ZnSo4 for three weeks each. Rats' body weights were recorded both before and after the administration of crude oil. Using commercial kits and histological examinations carried out using conventional histopathological methods, the liver's toxicity was assessed. As a result of eating food contaminated with crude oil, the results showed a significant drop (p < 0.05) in body weight. Additionally, there was liver cell injury. The levels of alkaline phosphatase and alanine transaminase considerably increased. Histological analysis revealed abnormal changes to the liver's typical structure. NAC and ZnSO4 therapy reduced the elevated Alanine transaminase and alkaline phosphatase levels. The study's findings highlight the negative impacts of crude oil and the therapeutic effects of NAC and ZnSO4.

Hepatoprotective effect of Pippali Ghrita, an Ayurvedic Formulation against Anti-Tubercular Drug Induced Hepatotoxicity in Wistar Rats

Combination chemotherapy of Isoniazid, Rifampicin, and Pyrazinamide is the preferred regimen for successful treatment of Tuberculosis (TB). The major complication of otherwise useful Anti-tubercular treatment (ATT) drugs is hepatic damage. There is lack of a definite effective treatment for the same in modern medicine. In view of this, the hepatoprotective activity of an Ayurvedic formulation, Pippali Ghrita (PG), was evaluated in anti-tubercular drug induced hepatotoxicity in Wistar rats. ATT drugs, viz., Isoniazid, Rifampicin, and Pyrazinamide were administered for 30 days to induce hepatotoxicity. Co-administration of PG in study group and Silymarin in standard control group was done for same duration. Hepatotoxicity was assessed on basis of ponderal parameters (body and liver weight) and biochemical parameters, viz., liver function parameters (Aspartate transaminase and Alanine transaminase), and oxidative stress parameters (Malondialdehyde and Superoxide dismutase). Results demonstrated significant increase in body weight and significant reduction in the liver weight, in study group and standard control group as compared to ATT control group. Likewise, significant reduction in liver function parameters and Malondialdehyde levels, with increase in Superoxide dismutase activity were observed, when compared to the ATT control group. The results indicated that co-administration of Pippali Ghrita for 30 days along with ATT prevented anti-tubercular drugs induced hepatotoxicity in Wistar rat model.

Protective effect of Bacopa monnieri against Methotrexate induced Hepatotoxicity in Wistar rats

Background: Methotrexate (MTX) is an anticancer drug and its clinical efficacy is limited to the toxicity associated with the liver. In this study, we examine the potential role of aqueous leaf extracts of Bacopa monnieri to counter methotrexate-induced hepatotoxicity. Methods: This study was undertaken by considering 36 numbers. Wistar male rats were randomly segregated into six groups, with six rats per group. Groups 1 and 2 were kept as normal controls and methotrexate was treated on the 9th day. While groups 3 and 4 received an aqueous extract of the leaf of B. monnieri at two varied doses of 150 and 300 mg/kg, respectively, as a treatment, Whereas groups 5 and 6 kept B. monnieri perse and the standard hepatoprotective drug silymarin @ 200 mg/kg and experiment was conducted for 14 days period. After the experimental procedure, AST, ALT, TNF-á and IL-10 were measured and histopathology of the liver was done. Result: The present study revealed significant alterations in AST, ALT, TNF-alfa and IL-10 in methotrexate-treated rats (group 2) when compared to group 1 and treatment groups 4 and 5 revealed significant improvement and these results were validated through imaging in the histopathology of the liver. We conclude that Bacopa monnieri can efficiently reduce methotrexate-induced liver inflammation and can be used in the management of hepatotoxicity in the liver.

EXPLORATION OF MECHANISM OF HYGROPHILA AURICULATA TO TREAT CARBOPLATIN INDUCED TOXICITIES BUILT ON NETWORK PHARMACOLOGY

Hygrophila auriculata is a traditional herb used for several ailments, with an unclear mechanism of action. The present study aimed to detect its efficacy on nephrotoxicity and hepatotoxicity in Wistar rats followed by network pharmacology analysis to explain its mechanism of action. 24 rats were divided into 4 groups (n=6). After baseline blood investigations, group 1 was treated with normal saline on 13th day, groups 2-4 with carboplatin, groups 3, 4 with different strengths of H. auriculata (day 15 to 30). The active components along with targets of H. auriculata were screened and overall network was created using Cytoscape software. We made preliminary predictions about the major active components, targets along with signalling pathways of H. auriculata to treat carboplatin induced hepatotoxicity and nephrotoxicity, which could pave way for clinical application of H. auriculata against carboplatin induced toxicities.

Isolation, characterization, structural elucidation and in vivo hepatoprotective studies of phytoconstituents obtained from the fruits of <i>Cordia obliqua</i> Willd

Purpose: To isolate, characterize, and investigate the hepatoprotective effect of phyto-constituents from fruits of Cordia obliqua Wild in paracetamol-induced hepatotoxicity in Wistar rats.
 Methods: Ethanol and aqueous extracts of C. obliqua fruits were screened for phytochemicals. The extracts were subjected to column chromatography and preparative thin-layer chromatography (TLC) to isolate four novel compounds. Compounds were characterized using infrared spectroscopy (IR), mass spectroscopy (MS), as well as 1H and 13C nuclear magnetic resonance (NMR). The isolated compounds were assessed for acute toxicity, in vivo hepatoprotective and antioxidant potential (dose: 5 mg/kg) in paracetamol-induced (75 mg/kg) hepatotoxicity through oral route in Wistar rats.
 Results: Phytochemical analysis of ethanol (COE) indicated the presence of fatty acids, anthraquinones, glycosides, saponins, alkaloids, tannins, flavonoids, coumarins, phenolics, triterpenes, and sterols. Compounds A, B, and C were identified from COE. Treatment at 50 mg/kg significantly reduced aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transferase (GGTP), and total bilirubin (TB), as well as increased total protein and total alkalinity levels in serum compared to the positive control. Liver histo-architecture showed improvements compared to the positive control, indicating hepatic protection.
 Conclusion: The isolated compounds (A, B and C) from COE exhibit hepatoprotective effects attributed to flavonoids and phenolics with free radical scavenging properties. Further research is needed to identify key mechanisms responsible for hepatoprotective effects.

Economic Importance of Garcinia Kola: Evidences of Shielding Outcome Against Carbon Tetrachloride-Induced Kidney Toxicity in Experimental Models

Introduction: The aim of the study was to evaluate the hepatoprotective effect of aqueous extract of Garcinia kola) seeds on carbon tetrachloride (CCl4) induced liver damage in adult Wistar rats. Thirty adult Wistar rats weighing between 65-145g were randomly divided into six groups of 5 rats each. Group A (control) rats were orally administered with 5ml/kg body weight of distilled water daily for 2 weeks, group B rats were administered distilled water orally daily for 2 weeks (volume per body weight) and carbon tetrachloride (CCl4) 0.4 m1/kg intraperitonially as a single application on day 14 of the experiment. Group C rats were administered 100 mg of silymarin / kg body weight once daily for 2 weeks followed by a single dose of CCl4 (0.4 m1) on day 14 of the experiment. Group D rats were administered 400 mg aqueous extract bitter kola (Garcinia kola) / kg body weight orally once daily for 2 weeks. Group E and F rats were administered 400 mg and 200 mg aqueous extract bitter kola (Garcinia kola) seed) orally once daily for 2 weeks followed by a single dose of CCl4 (0.4 m1) on day 14 respectively. At the end of the experiment. Garcinia kola seed aqueous extract caused significant decrease in the aspartate aminotransferase (AST) levels in the serum of the extract treated groups. Histopathological examinations revealed distortion of histoarchitecture such as, sinusoidal congestion, necrosis, steatosis and fibrosis was observed in group B. The administration of aqueous extract of Garcinia kola seed remarkably inhibited histoarchitectural distortion induced by CCl4 administration. Effects of the extract at dose of 200mg/kg was comparable to the reference drug. Garcinia kola aqueous seed extract showed a remarkable hepatoprotective and antioxidant activity against CCl4 induced hepatotoxicity as observed from the serum marker enzymes and antioxidant levels in liver tissues. CCl4 induced a significant rise in AST, ALT, and ALP with an increase of superoxide dismutase (SOD), catalase (CAT) and reduction lipid peroxidation (MDA). Treatment of the rats with the extract significantly (p<0.05) altered serum marker enzymes and antioxidant levels to near normal compared with CCl4- treated rats (group B). The activity of the extract at dose of 400mg/kg (group F) was comparable to the standard drug confirmed by histopathological examinations of liver sections. Conclusion: Garcinia kola aqueous extract has hepatoprotective and antioxidant properties against CCl4-induced hepatotoxicity in Wistar rats.

Hepatoprotective and antioxidant activity of Persicaria maculosa aqueous extract against carbon tetrachloride induced hepatotoxicity in Wistar rats

Hepatoprotective and antioxidant activity of Persicaria maculosa aqueous extract against carbon tetrachloride induced hepatotoxicity in Wistar rats

Hepatoprotective and in vivo antioxidant effects of granulometric classes and decoction of Ficus dicranostyla Mildbread leaves powders against carbon tetrachloride-induced hepatotoxicity in Wistar rats.

Ficus dicranostyla is a plant from the Moraceae family commonly used in African countries for its nutritional value and its believed medicinal properties. Its antioxidant in vitro capacity and its richness in phenolic compounds have been previously demonstrated. This work aimed at evaluating the hepatoprotective and in vivo antioxidant activities of different granulometric fractions of the F. dicranostyla leaves against carbon tetrachloride-induced hepatotoxicity in rats. Powdery fractions (<125, 250-125, and ≥250 μm), and the unsieved powder, obtained from the F. dicranostyla leaves were water-dissolved and given orally to rats at the same dose (250 mg/kg body weight) before administering carbon tetrachloride intraperitoneally (1 mL/Kg bw). The lipid status parameters (total cholesterol, triglycerides, HDL-cholesterol, and LDL-cholesterol), hepatic toxicity through aspartate aminotransferase (ASAT) and alanine aminotransferase (ALAT) in blood plasma, and antioxidant status by measuring the malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) in liver homogenate were performed. The activities of all parameters registered a significant (p < .05) alteration in CCl4-treated rats, which were significantly recovered toward an almost normal level in coadministered with Ficus dicranostyla leaf powder samples in a particle size-dependent manner. Results suggest that the smaller particle size of the powder fraction, as well as the decoction powder of Ficus dicranostyla, may be used as hepatoprotective and antioxidant agents.

Phytochemical and Hepatoprotective Activity of Prosopis juliflora Barks on Different Models

Liver injury is a common disorder where natural remedies are practiced from ancient time from plant source which shows alternative treatment in a safe manner. The Hepatoprotective activity of methanolic extract of Prosopis juiliflora bark part was taken for evaluation in screening. The model chosen for the study is carbon tetrachloride (0.1ml/kg) and the standard drug silymarin of 20mg/kg was used for the study for 21 days. The hepatoprotective effect of the methanolic extract against the carbon tetrachloride-induced hepatotoxicity in wistar rats has been demonstrated by the substantial and severe reduction of enzymes in the serum.

Antioxidant and anti-inflammatory potential of crocin on the doxorubicin mediated hepatotoxicity in Wistar rats

Doxorubicin (DXR) is widely used in cancer treatment. However, it has not yet been possible to prevent the side effects of DXR. The aim of this study was to investigate the hepatoprotective effect of crocin against DXR used in cancer treatment. For this reason; forty Wistar rats (male-250–300 g) were allocated into four groups (n = 10/group): Control, Crocin, DXR and DXR+Crocin. Control and Crocin groups were administered saline and crocin (40 mg/kg, i.p) for 15 days, respectively. DXR group, cumulative dose 12 mg/kg DXR, was administered for 12 days via 48 h intervals in six injections (2 mg/kg each, i.p). DXR+Crocin group, crocin (40 mg/kg-i.p) was administered for 15 days, and DXR was given as in the DXR group. The results revealed that serum liver markers (alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP) increased significantly after DXR administration but recovered after crocin therapy. In addition, lipid peroxidation (MDA), and inflammatory cytokine (TNF-α) increased after DXR application and the antioxidative defense system (GSH, SOD, CAT) significantly decreased and re-achieved by crocin treatment. Our results conclude that crocin treatment was related to ameliorated hepatocellular architecture and reduced hepatic oxidative stress and inflammation in rats with DXR-induced hepatotoxicity.

Histopathological and Biochemical Effect of Vitamin C and D on Phosphine-Induced Hepatotoxicity in Wistar Rats

Background: Aluminum phosphide is becoming a very common agent for self-poisoning. The lack of specific antidote for phosphide poisoning has aroused the current interest of research. Objectives: This study aimed to investigate the possible protective effect of Vitamin C and D in phosphine-induced hepatotoxicity in Wistar rats. Methods: In this experimental study, 20 Wistar rats were randomly divided into five groups ( n = 12). Group I was apparently normal Control Group. Groups II-V were induced with 2.5 mg/kg ALP. Groups II was without further treatment while Groups III-IV received vitamin C at 100mg/kg/bw and vitamin D at 10mg/kg/bw. Group V was co-administered with vitamin C at 100mg/kg/bw and vitamin at 10mg/kg/bw. The treatments lasted for 28 days. Results: The results showed that Vitamin C and D (P&lt;0.05) increased antioxidant capacity. Combined active constituents of the Vitamin C and Vitamin D raised the GPX antioxidant activities when compared to the phosphine poisoned group treated individually with Vitamin C and D. The combined activities of Vitamin C and Vitamin D showed the highest antioxidant effect as compared with the control Conclusion: The combined activities of Vitamin C and D supplementation improved the antioxidant defense system and histology of the liver in phosphine poisoning. Keywords: Metal phosphide, Carotene, Liver cell damage, Poison

The Preclinical Benefit of Glutamine in bisphenol A-induced Hepatotoxicity in Wistar Rats

Background: Oxidative stress may be a causative factor for bisphenol A (BPA) -induced hepatotoxicity. Glutamine (GM) is an amino acid with the ability to inhibit oxidative stress. Objective: This study evaluated the ability of GM to prevent BPA-induced hepatotoxicity in rats. Methods: Adult Wistar rats of both sexes (n=30) were used. The rats were randomly grouped into six of five rats each. Groups A (Control), B, and C were treated with normal saline (0.2 mL), GM (80 mg/kg), and BPA (50 mg/kg), respectively for 60 days. Groups D-F were treated with GM (20 mg/kg)+BPA (50 mg/kg), GM (40 mg/kg)+BPA (50 mg/kg), and GM (80 mg/kg)+BPA (50 mg/kg), respectively for 60 days. After treatment, blood and liver samples were obtained for biochemical and histological assessments, respectively. Results: Significantly (P&lt;0.01) decreased body weight and significantly (P&lt;0.01) increased liver weight occurred in the BPA-administered group when compared to the control group. The BPA-administered group showed significantly (P&lt;0.001) elevated serum total bilirubin, lactate dehydrogenase, aminotransferases, conjugated bilirubin, gamma-glutamyl transferase, alkaline phosphatase, and liver malondialdehyde concentrations when compared to the control group. Significantly (P&lt;0.001) decreased liver superoxide dismutase, glutathione peroxidase, catalase, and glutathione levels occurred in the PBA-administered group when compared to the control group. BPA caused hepatocyte necrosis, sinusoids, and central vein congestion. BPA-induced hepatotoxicity was reversed by GM; 20 mg/kg (P&lt;0.05), 40 mg/kg (P&lt;0.01), and 80 mg/kg (P&lt;0.001) in a dose-related fashion when compared to BPA. Conclusion: GM may be effective against BPA-associated hepatotoxicity.

Effect of chronic administration of aqueous extract of Neem (Azadirachta indica) leaves on Paracetamol-induced hepatotoxicity in Wistar albino rats

Hepatoprotective drugs are not available for use in modern medicine and different parts of medicinal plants like Neem (Azadirachta indica) are used as hepatoprotectants in traditional medicine. Although there are scientific reports of its hepatoprotective activity on acute administration, we found only one study which had evaluated its hepatoprotective effect on chronic administration. Objectives: To evaluate the effect of chronic oral administration of Neem on paracetamol-induced hepatotoxicity in Wistar rats. Methods: We randomly assigned 72 male and female Wistar albino rats to four groups of 18 animals each and orally administered Distilled water 5ml/kg body weight/day to Groups A (Normal control) and B (Experimental control), 500 mg/kg aqueous Neem leaf extract (Test) to Group C and Silymarin suspension (Standard) 100mg/kg/day to Group D for 30 days. On the 8th day, we induced hepatotoxicity with Paracetamol 2g/kg body weight single dose to groups B, C and D. We performed liver function tests, recorded liver weights and examined liver histology of six rats from each group on 10th, 20th and 30th days. Results: We observed significant difference (P

Therapeutic benefit of ursodeoxycholic acid in tamoxifen-induced hepatotoxicity in Wistar rats

Background. The clinical use of tamoxifen (TAM) may cause hepatotoxicity. Ursodeoxycholic acid (UDCA) has promising liver protective activity. This study assessed the protective effect of UDCA on TAM-induced hepatotoxicity in rats.Material and methods. Thirty five adult female Wistar rats were grouped into 7 of n=5/group. The rats were treated for 10 days as follows: Group 1: Water (10 mL/kg/day; placebo control) per oral [p.o], group 2: Ethanol 1% (1mL/kg/day; vehicle control) intraperitoneally (i.p), group 3: UDCA (40 mg/kg/day/p.o) and group 4: TAM (45 mg/kg/day) i.p. Groups 5-7 were pretreated with UDCA (10, 20 and 40 mg/kg), before daily treatment with TAM (45 mg/kg/day) i.p, respectively. On day 11, blood samples were collected and assessed for serum liver biomarkers. Liver samples were evaluated for oxidative stress markers and histology.Results. Significantly (p&lt;0.05) decreased body weight and significantly (p&lt;0.01) increased liver weight occurred in TAM- treated rats when compared to placebo control. TAM significantly (p&lt;0.001) increased serum alkaline phosphatase, lactate dehydrogenase, gamma-glutamyl transferase, aminotransferases, bilirubin, high density lipoprotein cholesterol levels and liver malondialdehyde levels when compared to control. TAM significantly (p&lt;0.001) decreased liver glutathione, catalase, glutathione peroxidase, superoxide dismutase, serum total protein, albumin total cholesterol, low density lipoprotein cholesterol and triglyceride levels when compared to control. Steatosis and necrotic changes occurred in TAM-treated rats. UDCA pretreatment significantly prevents TAM-induced changes in serum biochemical markers, and oxidative stress indices in a dose-related fashion when compared to TAM. UDCA prevents TAM-induced changes in liver histology.Conclusion. UDCA may be clinically effective for TAM associated hepatotoxicity.

Carum carvi Modulates Acetaminophen-Induced Hepatotoxicity: Effects on TNF-α, NF-κB, and Caspases

Carum carvi is a well-known herb traditionally used as a spice in Asian countries. Acetaminophen is a known marketed drug mainly used as an analgesic. It has been scientifically proven that consumption of acetaminophen (paracetamol) is associated with liver toxicity if taken in high doses without medical supervision. The present study evaluated the in vivo antioxidant and hepatoprotective efficacy of Carum carvi against acetaminophen-induced hepatotoxicity in Wistar rats. Our results demonstrate that Carum carvi, at doses (mg/kg) of 100 (D1) and 200 (D2), showed inhibitory properties for DNA-sugar damage, lipid peroxidation, DPPH scavenging, and increased reducing potential in a concentration-dependent manner. Our results also confirm that liver toxicity associated with paracetamol, such as depletion of reduced glutathione and antioxidant enzyme levels, as well as induction of cytochrome P450, oxidative stress, apoptosis, and inflammatory cytokines, was efficiently restored by Carum carvi treatment in rats. Moreover, the expression of redox-sensitive transcription factors, namely, NF-κB and TNF-α levels, was also modulated by Carum carvi in the rats. In summary, our study confirms that Carum carvi inhibits inflammation and oxidative stress, thereby protecting liver cells from paracetamol prompted hepatotoxicity.

Tamarix articulata Induced Prevention of Hepatotoxicity Effects of In Vivo Carbon Tetrachloride by Modulating Pro-Inflammatory Serum and Antioxidant Enzymes to Reverse the Liver Fibrosis.

This study evaluates the hepatoprotective activity of a Tamarix articulata extract against carbon tetrachloride-mediated hepatotoxicity in Wistar rats. Our results demonstrated that the oral administration of Tamarix articulata extract (50 mg/kg b.w.) significantly restored the serum levels of liver enzymes and antioxidant parameters (superoxide dismutase, catalase, glutathione reductase, and thiobarbituric reactive substances). Histopathology analysis revealed that Tamarix articulata extract significantly reduced hepatic fibrosis by inhibiting the necrosis of hepatocytes. Furthermore, serum pro-inflammatory (tumor necrosis factor-alpha, tumor growth factor-beta, and interleukin-6) markers were significantly restored. However, the anti-inflammatory cytokine adiponectin levels increased to normal levels in the group treated with Tamarix articulata extract. Additionally, we observed diminished reactive oxygen species production and the depolarization of mitochondrial membrane potential in hepatocytes extracted from animal livers treated with Tamarix articulata extract. Our findings suggest that Tamarix articulata extract prevents liver fibrosis induced by carbon tetrachloride and decreases the necrotic population of hepatocytes. These events restored the antioxidant enzymatic activity, serum levels of liver enzymes, and pro-inflammatory markers to their normal levels.

Aqueous Leaf Extract of Chromolaena odorata Attenuates Methotrexate-Induced Hepatotoxicity in Wistar Rats

Methotrexate (MTX) usage, despite its toxicity in body organs, has increased steadily over the years due to its broad applicability for treating different ailments, including various forms of cancer. Certain plant species have been shown to possess therapeutic properties by offering a protective effect against drug side effects. Thus, the current study was carried out to evaluate the potential of aqueous Chromolaena odorata leaf extract (AEOC) to attenuate the effect of MTX-induced hepatotoxicity in Wistar rats. The study divided thirty (30) male Wistar rats into five groups consisting of six each: Group I (control), Group II (AEOC at 250 mg/kg BW), Group III (MTX at 7 mg/kg BW), Group IV (AEOC at 250 mg/kg BW + MTX at 7 mg/kg BW), and Group V (Vitamin C (100 mg/kg BW) + MTX at 7 mg/kg BW). Chromolaena odorata and Vitamin C was administered for ten consecutive days, while MTX was administered on day 8 for three consecutive days. Rats were sacrificed 24hrs after the last administration. Serum collected was used for the determination of Aspartate Aminotransferase (AST), Alanine transaminase (ALT), Albumin (ALB), Total Bilirubin (TB), and Total protein (TP), while liver tissue was used for assessment of Superoxide Dismutase (SOD), Malondialdehyde (MDA) and Catalase (CAT) as well as histopathological analysis. The result showed a significant increase in the level of SOD, CAT and a significant reduction in MDA in Chromolaena odorata or Vitamin C treated groups compared with MTX. Furthermore, Chromolaena odorata or Vitamin C significantly reduced liver function enzymes and Total Bilirubin levels while increasing synthetic molecules compared to the MTX group. Chromolaena odorata attenuated the toxic effect of MTX, which was corroborated by histopathological analysis. In conclusion, Chromolaena odorata attenuated MTX-induced hepatotoxicity by enhancing antioxidant status; thus, scavenging free radicals and reducing oxidative stress.

Protective effect of Euphorbia thymifolia and Euphorbia hirta against carbon tetrachloride-induced hepatotoxicity in Wistar rats

Objectives The present study aims to investigate the protective effect of Euphorbia thymifolia and Euphorbia hirta extracts on in vitro antioxidant activity and in vivo analysis on hepatic marker enzyme levels and histopathological changes in the liver of carbon tetrachloride (CCl4) induced hepatotoxicity rats. Materials and methods This study includes 42 adult male Albino Wistar rats randomly divided into seven treatment groups, including control (basal diet, G1), CCl4-induced single dose (1.5 ml/kg, i.p.) as the negative control (G2), G1 supplemented with 300 mg/kg of ethanol extract of E. thymifolia (G3) and E. hirta (G4), G2 supplemented with 300 mg/kg of ethanol extract of E. thymifolia (G5), E. hirta (G6), and silymarin (25 mg/kg b.w.) used as a standard drug (G7) for 21-days experimental period. Results The ethanolic extracts of E. thymifolia and E. hirta exhibited potential in vitro antioxidant activity in a dose-dependent manner (25 μg/ml, 50 μg/ml, 100 μg/ml, 200 μg/ml and 250 μg/ml). Oxidative stress caused by CCl4-induced the liver damage, including changes in liver marker enzymes (aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase), enzymatic (superoxide dismutase and catalase), non-enzymatic antioxidants (lipid peroxides and glutathione) and hepatocellular alterations such as hydropic degeneration, irregular hepatocytes, and distention of the vein. Administration of E. thymifolia and E. hirta significantly (p < 0.05) restored the enzyme activity along with the histology of the liver. Conclusion The results from the current study demonstrate that E. thymifolia and E. hirta have the property of restoring hepatic redox capacity and antioxidant activities against CCl4-induced acute liver damage.

Evaluation of the effect of total saponins and tannins isolated from Dialium guineense stem bark on CCl4 - Induced hepatotoxicity in wistar rats

The aim of the present study was to evaluate the hepatoprotective effect of total saponins and tannins of Dialium guineense stem bark in Wistar rats exposed to carbon tetrachloride (CCl4). Adult male Wistar rats (n = 25) weighing 160 – 180 g (mean weight = 170 ± 10 g) were randomly assigned to five groups (5 rats per group): normal control, CCl4 control, silymarin, total saponins, and total tannins groups. With the exception of normal control, the rats were exposed to CCl4 (a single oral dose of 1.0 mL/kg body weight, bwt). Rats in the silymarin group were administered 100 mg/kg bwt silymarin (standard hepatoprotective drug), while those in the two treatment groups received 150 mg/kg bwt of total saponins or tannins orally. Treatment lasted 28 days. Activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and Alkaline Phosphatase (ALP), as well as levels of Total Protein (TP), bilirubin, and albumin, were measured in plasma. The results showed that there were no significant differences in the concentrations of TP among the groups (p &gt; 0.05). The activities of the liver enzymes, as well as levels of bilirubin and albumin, were significantly higher in the CCl4 control group than in the normal control group, but they were reduced by extract treatment (p &lt; 0.05). These results indicate that CCl4 negatively impacted the integrity of the liver cells, and total saponins and tannins of D. guineense stem bark conferred some level of protection on the organ.