Guoyin Zheng, Hao Peng, Min Li, Wei Gu, Zhe Chen, Changquan Ling
Department of Traditional Chinese Medicine, Changhai Hospital, Second Military Medical University, Shanghai, China.
Evid Based Complement Alternat Med. 2017;2017:8231358. doi: 10.1155/2017/8231358. Epub 2017 Jun 4.
The purpose of the present study was to evaluate the pharmacological effects of L. (Purslane) (PL) on N-nitrosodiethylamine- (NDEA-) induced hepatocellular carcinomas (HCC) and explore its potential mechanism. Mice were randomly assigned to four groups: control group, NDEA group, NDEA + Purslane (100 mg/kg) group, and NDEA + Purslane (200 mg/kg) group. The animal of each group was given NDEA (100 ppm) in drinking water. 1 h later, Purslane dissolved in PBS was intragastrically administered for continuous seven days. The results showed that Purslane reduced the activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in liver and serum. Purslane also reduced the contents of interleukin-6 (IL-6), IL-1, tumor necrosis factor- (TNF-), and methane dicarboxylic aldehyde (MDA) and restored the activity of superoxygen dehydrogenises (SOD) in serum. Purslane could obviously attenuate the hepatic pathological alteration. Furthermore, treatment with Purslane effectively inhibited the phosphorylations of phosphatidylinositol 3 kinase (PI3K), protein kinase B (Akt), mammalian target of rapamycin (mTOR), nuclear factor-kappa B (NF-B), and inhibitor of NF-B (IB) and upregulated the expressions of NF-E2-related factor 2 (Nrf2) and heme oxygenase- (HO-) 1. In conclusion, our research suggested that Purslane exhibited protective effects on NDEA-induced hepatocellular carcinomas by anti-inflammatory and antioxidative properties via the PI3K/Akt/mTOR and Nrf2/HO-1/NF-B pathway.
本研究旨在评估马齿苋（Portulaca oleracea L.，PL）对N-亚硝基二乙胺（NDEA）诱导的肝细胞癌（HCC）的药理作用，并探讨其潜在机制。将小鼠随机分为四组：对照组、NDEA组、NDEA + 马齿苋（100 mg/kg）组和NDEA + 马齿苋（200 mg/kg）组。每组动物饮用含NDEA（100 ppm）的水。1小时后，将溶于PBS的马齿苋灌胃给药，持续7天。结果表明，马齿苋降低了肝脏和血清中丙氨酸转氨酶（ALT）和天冬氨酸转氨酶（AST）的活性。马齿苋还降低了血清中白细胞介素-6（IL-6）、IL-1、肿瘤坏死因子-α（TNF-α）和丙二醛（MDA）的含量，并恢复了超氧化物歧化酶（SOD）的活性。马齿苋可明显减轻肝脏病理改变。此外，马齿苋治疗有效抑制了磷脂酰肌醇3激酶（PI3K）、蛋白激酶B（Akt）、雷帕霉素靶蛋白（mTOR）、核因子-κB（NF-κB）和NF-κB抑制剂（IκB）的磷酸化，并上调了核因子E2相关因子2（Nrf2）和血红素加氧酶-1（HO-1）的表达。总之，我们的研究表明，马齿苋通过PI3K/Akt/mTOR和Nrf2/HO-1/NF-κB途径的抗炎和抗氧化特性，对NDEA诱导的肝细胞癌具有保护作用。
