State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macao, China.
Food Funct. 2015 May;6(5):1510-7. doi: 10.1039/c5fo00098j.
The aim of the present study was to evaluate the effects of Penthorum chinense Pursh (PCP), a health food and folk medicine, against acute alcohol-induced liver injury and further to elucidate its probable mechanisms. Male C57BL/6 mice were treated with an aqueous extract of PCP (5.2 and 10.3 g per kg BW) once daily for 7 consecutive days prior to ethanol gavage (4.7 g kg(-1)) every 12 h for a total of three doses. Pretreatment with PCP significantly decreased the elevations of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and hepatic triglyceride after the last ethanol administration. PCP suppressed the elevation of the malondialdehyde (MDA) level, restored the glutathione (GSH) level and enhanced the activities of superoxide dismutase (SOD) and catalase (CAT) in both the serum and liver, which were associated with the inhibition of hepatic cytochrome P450 2E1 (CYP2E1). In addition, alcohol exposure markedly induced the lipolysis of white adipose tissue (WAT) through up-regulating protein expressions of adipose triglyceride lipase (ATGL) and phosphorylation of hormone-sensitive lipase (p-HSL), and enhancing the fatty acid uptake capacity in the liver by elevated hepatic CD36 expression, which were attenuated by PCP treatment. These data demonstrated that pre-treatment with PCP protected against acute ethanol-induced liver injury, possibly by reducing CYP2E1-dependent oxidative stress and ameliorating dysfunctional WAT derived-fatty acid influx to the liver. Our findings suggest that PCP might be a promising agent for the prevention of acute alcohol-induced liver injury.
本研究旨在评价贯叶连翘（PCP）作为一种保健品和民间药物对急性酒精性肝损伤的作用，并进一步阐明其可能的机制。雄性 C57BL/6 小鼠在乙醇灌胃（4.7 g/kg BW）前 7 天每天用 PCP 水提物（5.2 和 10.3 g/kg BW）处理一次，每 12 小时一次，共 3 次。PCP 预处理可显著降低末次乙醇给药后丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）和肝甘油三酯的升高。PCP 抑制丙二醛（MDA）水平升高，恢复谷胱甘肽（GSH）水平，增强血清和肝脏中超氧化物歧化酶（SOD）和过氧化氢酶（CAT）的活性，这与肝细胞色素 P450 2E1（CYP2E1）的抑制有关。此外，酒精暴露通过上调脂肪甘油三酯脂肪酶（ATGL）的蛋白表达和激素敏感脂肪酶（p-HSL）的磷酸化，以及通过升高肝 CD36 表达增强肝脏脂肪酸摄取能力，显著诱导白色脂肪组织（WAT）的脂解作用，这一作用被 PCP 处理所减弱。这些数据表明，PCP 预处理可预防急性乙醇性肝损伤，可能通过减少 CYP2E1 依赖性氧化应激和改善功能失调的 WAT 衍生脂肪酸向肝脏的流入。我们的研究结果表明，PCP 可能是预防急性酒精性肝损伤的一种有前途的药物。
