The ethanol extract of Bacopa monnieri Linn. (Schrophulariaceae) aerial parts (EBM) was investigated for any in vitro and in vivo antioxidant and hepatoprotective effects. EBM was prepared and estimation of total phenolics was carried out. Further, the antioxidant activity of EBM was studied using four in vitro models. The amount of total phenolics was estimated to be 47.7g of pyrocatechol equivalent per mg of extract. The reducing power of the extract was found to be concentration dependant. The antioxidant activity, nitric oxide scavenging activity and superoxide radical scavenging activity were also concentration dependant with IC50 value being 238.22g/ml, 29.17g/ml and 22.92g/ml respectively. The activities were found to be comparable with the reference drugs. Different groups of animals (Wistar albino rats) were administered with paracetamol (500 mg/kg, p.o., once in a day for 7 days). EBM at the dose of 300 mg/kg/day and silymarin at 25 mg/kg/day were administered to the paracetamol treated rats for seven days. The effects of EBM and silymarin on serum transaminases (SGOT, SGPT), alkaline phosphatase (ALP), bilirubin (Direct and Total), cholesterol (HDL and Total) and total protein were measured in the paracetamol-induced hepatotoxic rats. Further, the effects of the extract on lipid peroxidation (LPO), glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) were estimated. EBM and silymarin produced significant (p<0.05) hepatoprotective effect by decreasing the activity of serum enzymes, bilirubin, total cholesterol and in vivo lipid peroxidation and significantly (p<0.05) increasing the levels of GSH, SOD, CAT and HDL cholesterol. EBM also showed antioxidant effects on FeCl2-ascorbate-induced lipid peroxidation in rat liver homogenate. From these results, it was suggested that EBM could protect the liver cells from paracetamol-induced liver damage perhaps, by its antioxidative effect on hepatocytes, hence eliminating the deleterious effects of toxic metabolites of paracetamol.

The scientific evaluation of medicinal plants used in the preparation of folk remedies has provided modern medicine with effective pharmaceuticals for the treatment of diseases. The methanol extract of Berberis tinctoria Lesch (Berberidaceae) leaves was investigated for its hepatoprotective and antioxidant effects on paracetamol (750 mg/kg) induced acute liver damage in Wistar albino rats. Hepatoprotection activity was measured by using biochemical parameters such as serum glutamate oxalate transaminase and se-rum Glutamate Pyruvate Transaminase (SGOT and SGPT), alkaline phosphatase (ALP), bilirubin and total protein. The methanol extract of Berberis tinctoria (MEBT) at the doses of (150 mg/kg and 300 mg/Kg) produced significant hepatoprotective effect by decreasing the activity of serum enzymes, bilirubin and lipid peroxidation while it significantly increased the levels of glutathione (GSH), catalyse (CAT) and super oxide dismutase (SOD) in a dose dependant manner. The effects of MEBT were comparable to that of standard drug silymarin. These results suggest that MEBT may have potential therapeutic value in the treatment of some liver disorders, probably by its antioxidative effect on hepatocytes.

Objective: In the present study, the hepatoprotective effects of Bmyrcene (MYR) on acetaminophen-induced hepatotoxicity were investigated. Materials and Methods: A total of 40 Balb/c mice were randomly divided into five groups as follows: 1) Normal control group which received only carboxymethylcellulose (CMC), the vehicle used to dissolve acetaminophen (N-acetyl-paminophenol, APAP, paracetamol) and MYR,2) APAP group which received a single dose of acetaminophen (250 mg/kg) orally on day 7,3) Silymarin group which received 200 mg/kg/day of silymarin,and 4 and 5) pretreatment groups in which, mice were treated with 100 or 200 mg/kg/day of MYR. Liver and blood samples were collected to analyze serum aminotransferases, inflammatory response, oxidative stress markers, and histopathological insults. Results: Our results showed that MYR pretreatment attenuated liver damage and restored liver cells function and integrity as it decreased the leakage of serum aminotransferases (alanine and aspartate aminotransferases (ALT and AST, respectively)) into the blood (p<0. 01). MYR treatment also reduced levels of myeloperoxidase (MPO) activity and nitric oxide (NO) (p<0. 001). In addition, MYR pretreatment demonstrated significant antioxidant activity by decreasing malondialdehyde (MDA), reactive oxygen species (ROS), and reduced glutathione (GSH) levels (p<0. 001). Furthermore, it restored the hepatic level of superoxide dismutase (SOD), catalase (CAT), and oxidized glutathione (GSSG) (p<0. 001). Conclusion: For the first time, our results showed that MYR treatment significantly improved liver function by reducing oxidative stress and the inflammatory response induced by APAP.

The liver and kidney are the most important organs in the body, and they both act as target structures for druginduced injury as a consequence of their functions in metabolisms, detoxifications, storage, elimination of medications, and their metabolites. The present study aimed to examine the role of the natural and free radical scavenger "CoQ10" against diclofenac-induced hepatic and renal tissue injury. In total, 36 adult Wistar rats were randomly divided into three equal groups (n=12). The animals in the control group did not receive any medication or treatments, and the second group included animals that received intramuscular (IM) injection of Diclofenac (DF) (at a dose of 10 mg/kg once daily for 14 days). Moreover, the third group was given the IM injection of DF (at a dose of 10 mg/kg once daily for 14 days) +CoQ10. After 14 days, DF prompted signified hepatic and renal injury indicated by elevated biochemical parameters, such as total serum bilirubin, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, blood urea nitrogen, creatinine, and uric acid, compared to the control and the third group. However, the group that received Diclofenac+CoQ10 had significantly lower hepatic and renal dysfunctions, compared to the second treated group. DF toxic effects could be the consequences of mitochondrial dysfunction and free radical effects. Remarkably, therapeutic supplementation of CoQ10 diminished the DF-induced toxic oxidative injury and apoptotic cell death. The protective effects of CoQ10 were attributed to its antioxidants and free radical scavenger activity.