Yang Jia-Yu, Zhong Yu-Te, Hao Wei-Nan, Liu Xiang-Xiang, Shen Qiong, Li Yan-Fei, Ren Shen, Wang Zi, Li Wei, Zhao Li-Chun
College of Chinese Medicinal Materials, Jilin Agricultural University Changchun 130118 China
College of Pharmacy, Guangxi University of Chinese Medicine Nanning 530200 China
RSC Adv. 2020 May 12;10(31):18044-18053. doi: 10.1039/d0ra00020e. eCollection 2020 May 10.
Acetaminophen (APAP)-induced acute liver injury (ALI) is a health issue that has gradually attracted attention, and is often regarded as a model of drug-induced hepatotoxicity. The leaves of Rehd. (named as "sweet tea", ST) usually serve as tea drink and folk medicine for healthcare in the southwest part of China. In previous reports, it has been proven to protect various animal models, except for APAP-induced liver injury model. Therefore, this study initially explored the protective effect of ST leaf extract (STL-E) on hepatotoxicity induced by APAP in ICR mice. STL-E of 50 and 100 mg kg were given to each group for 7 days. ALI was intraperitoneally induced by APAP treatment (i.p. 250 mg per kg body weight). Biochemical markers, levels of inflammatory factors, histopathological staining and western blotting were used to analyze the inflammation and apoptosis of liver tissues. Interestingly, the treatment with STL-E significantly attenuated APAP-induced liver injury ( < 0.05). Moreover, STL-E partially mitigated APAP-induced liver injury by effectively activating the PI3K/Akt pathway and inhibiting the NF-κB pathway. In a word, STL-E protected liver against APAP-induced hepatotoxicity by inhibiting the PI3K/Akt-mediated apoptosis signal pathway and inhibiting the NF-κB-mediated signaling pathway.
对乙酰氨基酚（APAP）诱导的急性肝损伤（ALI）是一个逐渐受到关注的健康问题，常被视为药物性肝毒性的模型。川鄂甜茶（Rehd.，名为“甜茶”，ST）的叶子通常用作茶饮和中国西南部地区的保健民间药物。在先前的报道中，已证明它对各种动物模型具有保护作用，但APAP诱导的肝损伤模型除外。因此，本研究初步探讨了甜茶叶提取物（STL-E）对APAP诱导的ICR小鼠肝毒性的保护作用。每组给予50和100 mg/kg的STL-E，持续7天。通过APAP处理（腹腔注射，每千克体重250 mg）诱导ALI。使用生化标志物、炎症因子水平、组织病理学染色和蛋白质印迹法分析肝组织的炎症和凋亡情况。有趣的是，STL-E处理显著减轻了APAP诱导的肝损伤（P<0.05）。此外，STL-E通过有效激活PI3K/Akt途径和抑制NF-κB途径部分减轻了APAP诱导的肝损伤。总之，STL-E通过抑制PI3K/Akt介导的凋亡信号途径和抑制NF-κB介导的信号途径保护肝脏免受APAP诱导的肝毒性。
