Chen Wei-Ting, Yang Chieh-Ling, Yin Mei-Chin
Department of Nutrition, China Medical University, 91, Hsueh-shih Rd, Taichung, Taiwan.
Biomedicine (Taipei). 2014;4(1):5. doi: 10.7603/s40681-014-0005-2. Epub 2014 Aug 27.
Protective effects of aqueous extract (HCAE) against acetaminophen-induced hepatotoxicity in Balb/cA mice were examined.
HCAE, at 1 or 2 g/L, was added into the drinking water for 4 weeks. Acute liver injury was induced by acetaminophen treatment intraperitoneally (350 mg/kg body weight).
Acetaminophen treatment significantly depleted hepatic glutathione (GSH) content, increased hepatic malonyldialdehyde (MDA), reactive oxygen species (ROS) and oxidized glutathione (GSSG) levels, and decreased hepatic activity of glutathione peroxidase (GPX), catalase and superoxide dismutase (SOD) (<0.05). The pre-intake of HCAE alleviated acetaminophen-induced oxidative stress by retaining GSH content, decreasing MDA, ROS and GSSG production, and maintaining activity of GPX, catalase and SOD in liver (<0.05). The pre-intake of HCAE also significantly lowered acetaminophen-induced increase in cytochrome P450 2E1 activity (<0.05). Acetaminophen treatment increased hepatic release of interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-alpha and monocyte chemoattractant protein-1 (<0.05). HCAE intake significantly diminished acetaminophen-induced elevation of these cytokines (<0.05).
These results support that HCAE could provide hepato-protection.
研究了水提取物（HCAE）对乙酰氨基酚诱导的Balb/cA小鼠肝毒性的保护作用。
将1或2 g/L的HCAE添加到饮用水中，持续4周。通过腹腔注射乙酰氨基酚（350 mg/kg体重）诱导急性肝损伤。
乙酰氨基酚处理显著降低了肝脏谷胱甘肽（GSH）含量，增加了肝脏丙二醛（MDA）、活性氧（ROS）和氧化型谷胱甘肽（GSSG）水平，并降低了肝脏谷胱甘肽过氧化物酶（GPX）、过氧化氢酶和超氧化物歧化酶（SOD）的活性（<0.05）。预先摄入HCAE通过保留GSH含量、减少MDA、ROS和GSSG的产生以及维持肝脏中GPX、过氧化氢酶和SOD的活性来减轻乙酰氨基酚诱导的氧化应激（<0.05）。预先摄入HCAE还显著降低了乙酰氨基酚诱导的细胞色素P450 2E1活性增加（<0.05）。乙酰氨基酚处理增加了肝脏白细胞介素（IL）-6、IL-10、肿瘤坏死因子（TNF）-α和单核细胞趋化蛋白-1的释放（<0.05）。摄入HCAE显著降低了乙酰氨基酚诱导的这些细胞因子的升高（<0.05）。
这些结果支持HCAE可以提供肝脏保护作用。
