To study the mechanism of curcumin-attenuated inflammation and liver pathology in early stage of alcoholic liver disease, female Sprague-Dawley rats were divided into four groups and treated with ethanol or curcumin via an intragastric tube for 4 weeks. A control group treated with distilled water, and an ethanol group was treated with ethanol (7.5 g/kg bw). Treatment groups were fed with ethanol supplemented with curcumin (400 or 1 200 mg/kg bw). The liver histopathology in ethanol group revealed mild-to-moderate steatosis and mild necroinflammation. Hepatic MDA, hepatocyte apoptosis, and NF-κB activation increased significantly in ethanol-treated group when compared with control. Curcumin treatments resulted in improving of liver pathology, decreasing the elevation of hepatic MDA, and inhibition of NF-κB activation. The 400 mg/kg bw of curcumin treatment revealed only a trend of decreased hepatocyte apoptosis. However, the results of SOD activity, PPARγ protein expression showed no difference among the groups. In conclusion, curcumin improved liver histopathology in early stage of ethanol-induced liver injury by reduction of oxidative stress and inhibition of NF-κB activation.

AIM:To evaluate attenuating properties of N-acetylcysteine (NAC) on oxidative stress and liver pathology in rats with non-alcoholic steatohepatitis (NASH). METHODS:Male Sprague-Dawley rats were randomly divided into three groups. Group 1 (control, n = 8) was free accessed to regular dry rat chow (RC) for 6 wk.Group 2 (NASH, n = 8) was fed with 100% fat diet for 6 wk. Group 3 (NASH + NAC20, n = 9) was fed with 100% fat diet plus 20 mg/kg per day of NAC orally for 6 wk. All rats were sacrificed to collect blood and liver samples at the end of the study. RESULTS:The levels of total glutathione (GSH) and hepatic malondialdehyde (MDA) were increased significantly in the NASH group as compared with the control group (GSH; 2066.7 ± 93.2 vs 1337.5 ± 31.5 µmol/L and MDA; 209.9± 43.9 vs 3.8 ±1.7 µmol/g protein, respectively, P < 0.05). Liver histopathology from group 2 showed moderate to severe macrovesicular steatosis, hepatocyte ballooning, and necroinflammation. NAC treatment improved the level of GSH (1394.8 ± 81.2 µmol/L, P < 0.05), it did not affect MDA (150.1 ± 27.0 µmol/g protein), but led to a decrease in fat deposition and necroinflammation.CONCLUSION: NAC treatment could attenuate oxidative stress and improve liver histology in rats with NASH.

The effect of Aloe vera gel on paracetamol induced liver injury in rats was studied using male Wistar rats divided into four groups. Group 1 (control) received 50% sucrose orally twice daily for 2 days. Group 2 (paracetamol) received a single dose (2.5 g/kg BW) of paracetamol dissolved in 50% sucrose. Groups 3 and 4 (A. vera 100 mg and 300 mg, respectively) received a single dose (2.5 g/kg BW) of paracetamol dissolved in 50% sucrose followed by 100 or 300 mg/kg BW of A. vera gel twice daily for 2 days. Blood was collected to determine alanine aminotransferase (ALT) and aspartate aminotransferase (AST) enzymatic activities. Liver tissue samples were collected for hepatic glutathione, hepatic malondialdehyde (MDA), and histopathology. The results showed that the serum levels of ALT, AST, and hepatic MDA increased significantly in the paracetamol group compared to that of the control group. The liver histopathology in the paracetamol group revealed vacuolization, cell swelling, and mild infiltration of inflammatory cells around the central vein. Necrosis was observed predominantly around the centrilobular and midzonal regions. There were no differences in hepatic glutathione levels between groups and no difference in hepatic MDA levels between the paracetamol group and A. vera gel treated groups. This study concluded that neither 100 nor 300 mg/kg BW of A. vera protected rats from the liver damage induced by a high dose of paracetamol.

Benjakul, a traditional Thai formulation, has been used as a carminative and adaptogenic drug. It consists of five plants, Piper chaba Hunter, Piper sarmentosum Roxb., Piper interruptum Opiz., Plumbago indica Linn., and Zingiber officinale Roscoe, in equal ratios. Some individual herbs present in Benjakul were reported to modulate cytochrome P450 (CYP) enzymes. This study aimed to investigate the effects of Benjakul extract on the activities and mRNA expression levels of hepatic CYP2C11 and CYP3A1 in rats. Adult male rats were orally administered 200, 400, or 600 mg/kg BW Benjakul extract for 28 days. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN) and creatinine levels were assayed. CYP2C11 and CYP3A1 activities were analyzed using cytochrome P450 assay kits. The mRNA expression of CYP2C11 and CYP3A1 was measured using a quantitative real-time PCR assay. Benjakul treatment significantly increased the serum ALT and BUN levels. At doses of 200, 400, and 600 mg/kg BW, Benjakul treatment increased hepatic CYP3A1 activity and CYP3A1 mRNA expression. CYP2C1 1 mRNA expression was unchanged by treatment with Benjakul extract; however, treatment with the high and middle doses of Benjakul extract increased CYP2C11 activity. Treament with Benjakul extract induced CYP2C11 and CYP3A1 activity in rats. Concurrent use of Benjakul with conventional drugs should be considered to potentially induce herb-drug interactions.