5(A–E). Histopathological studies provided supportive evidence for the biochemical analysis. The photomicrograph of the liver of G-I animals showed normal architecture Screening Library of hepatic cells with clear cytoplasm and slightly dilated central veins, normal kupffer cells and all cells had normal large nuclei (Fig. 5A). The liver tissue showed distorted architecture with extensive area of necrosis and hemorrhage in PCM only

treated group (Fig. 5B). G-III and G-IV animals treated with the plant extracts (100 and 200 mg/kg), showed the more of normal architecture of the liver tissue with minimum inflammation (Fig. 5C, D). The induction of hepatotoxicity by PCM and hepatoprotective effect of MEMV is also supported by histological Tariquidar purchase observations as is evident from the levels of blood and tissue biochemical parameters. The silymarin treated group (G-V) also showed less inflammation and no necrosis in liver cells (Fig. 5E). The

present study was undertaken to establish the hepatoprotective effect of methanolic extract of M. vulgare (MEMV) against paracetamol induced liver injury. Paracetamol a well-known hepatotoxin is widely employed in the experimental cell or tissue model of hepatic injury; it is normally eliminated as sulfate and glucuronide conjugate. The increase in enzyme levels such as AST, ALT, ALP, bilirubin, albumin and triglycerides along with the oxidative stress markers like catalase, LPO and GSH have

been directly correlated with the severity of hepatic injury. 21 ALT catalyses the conversion of alanine to pyruvate and glutamate and is released in a similar manner. Therefore, ALT is more specific to the liver, and is thus a better parameter for detecting liver injury. Serum ALP and bilirubin level on other hand are related to the function of hepatic cell. Increase in serum level of ALP is due to increased synthesis, in presence of increasing biliary pressure. 22 Administration of paracetamol significantly (P < 0.01) increased the levels of AST, ALT, ALP, bilirubin and triglycerides in serum which Ergoloid is attributed to the liver damage as these enzymes are located in cytoplasm which are leaked to blood as a result of cell damage indicating development of hepatotoxicity 23 when compared to control. Treatment of MEMV (100 and 200 mg/kg) caused significant (P < 0.01) restoration of these markers in dose dependent manner. Similar observations were recorded with the treatment of silymarin (200 mg/kg). The reversal of increased serum enzymes in PCM induced liver injury by MEMV may be due to stabilization of the membranes thereby preventing the leakage of intracellular enzymes. This is in agreement with the commonly accepted view that serum levels of transaminases return to normal with the healing of hepatic parenchyma and the regeneration of hepatocytes.