Feng-Hua Li

Alcoholic liver disease (ALD) is a liver disease caused by long-term alcohol consumption. ROS-mediated oxidative stress is the leading cause of ALD. Pien-Tze-Huang (PZH), a traditional formula, is famous in China. This study was designed to evaluate the effects and explore the potential mechanisms of PZH in ALD. Forty mice were randomly divided into five groups: control group (normal diet + vehicle), model group (ethanol diet + vehicle), PZH-L group (ethanol diet + PZH (0.125 g/kg)), PZH-M group (ethanol diet + PZH (0.25 g/kg)), and PZH-H group (ethanol diet + PZH (0.5 g/kg)). The mice were sacrificed, and their liver and blood samples were preserved. Liver steatosis, triglyceride (TG), total cholesterol, serum alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were assayed. Malondialdehyde (MDA), glutathione peroxidase (GSH-PX), and total superoxide dismutase were identified using commercial kits. Oxylipins were profiled, and the data were analyzed. The AMPK/ACC/CPT1A pathway was identified using real-time polymerase chain reaction and western blotting. The PZH-H intervention significantly alleviated hepatic steatosis and injury and reduced the levels of liver TG and serum ALT and AST. In addition, MDA levels were markedly reduced, and GSH-PX activity significantly increased after PZH-H intervention. Finally, PZH-H increased the levels of 17-HETE, 15-HEPE, 9-HOTrE, 13-HOTrE, and 5,6-dihydroxy-8Z,11Z,14Z,17Z-eicosatetraenoic acid, and reduced PGE2 levels. PZH-H intervention also promoted the phosphorylation of AMPK and ACC, and the expression of CPT1A. In conclusion, PZH reduced oxidative stress and alleviated hepatic steatosis and injury. The mechanism was correlated with the oxylipin metabolites/AMPK/ACC/CPT1A axis.

Huangqi decoction was first described in Prescriptions of the Bureau of Taiping People's Welfare Pharmacy in Song Dynasty (AD 1078), and it is an effective recipe that is usually used to treat consumptive disease, anorexia, and chronic liver diseases. Transforming growth factor beta 1 (TGFβ1) plays a key role in the progression of liver fibrosis, and Huangqi decoction and its ingredients (IHQD) markedly ameliorated hepatic fibrotic lesions induced by ligation of the common bile duct (BDL). However, the mechanism of IHQD on hepatic fibrotic lesions is not yet clear. The purpose of the present study is to elucidate the roles of TGFβ1 activation, Smad-signaling pathway, and extracellular signal-regulated kinase (ERK) in the pathogenesis of biliary fibrosis progression and the antifibrotic mechanism of IHQD.

To study the mechanism of Corydyceps polysaccharide (CP) actions against liver fibrosis. SD rats were randomly divided into normal control group, DMN-induced liver fibrosis model group and CP treated group. Model group and CP group were injected intraperitonealy with 0. 5% dimethylnitrosamine (DMN) at dose of 2 mL x kg(-1) for 4 weeks to induce liver fibrosis. Then the later group was orally taken CP for 4 weeks. Liver tissue hydroxyproline (Hyp) content was determined by Jamall's method. The liver serum of ALT and AST activities, level of albumin and total bilirubin were analyzed The liver collagen deposition and were observed with Masson' collagen stains. In addition,the tissue inhibitor of metallprteinase-2 (TIMMP-2) level, metalloproteinade-2 (MMP-2) activity, type IV collagen content were observed. Liver samples were also analyzed malondiadehyde (MDA)level and superoxide dismutase (SOD) activity. Compare with model group, CP improved the hepatic function (ALT, AST, Alb and Tbil). There were significant decreased of MDA content in CP group, SOD of CP group were markedly increased. Compared to those of normal control group, Hyp content, IV collagen content, TIMMP-2 level in liver tissue of model group increase significantly, and MMP-2 activity decreased, while CP decrees these pathological increase at different degrees. CP exerts rather good action against liver fibrosis, and with the mechanism relating to improve degradation of the deposited collagens and anti-lipid peroxiation.