Zhao Yuling, Li Hailing, Gao Zhonghong, Gong Yuefa, Xu Huibi
Department of Chemistry, Huazhong University of Science and Technology, Wuhan, 430074, PR China.
Eur J Pharmacol. 2006 Apr 24;536(1-2):192-9. doi: 10.1016/j.ejphar.2006.02.045. Epub 2006 Mar 3.
Hemin-nitrite-H2O2 system may play a role in liver oxidative injury in some pathological events. In this paper, the effects of the three active components of the root of Scutellaria baicalensis Georgi, i.e. baicalin, baicalein and wogonin, on hemin-nitrite-H2O2 induced liver injury were studied in liver homogenate, liver microsome and human hepatoblastoma cell line HepG2 cells. It was found that hemin-nitrite-H2O2 could induce liver homogenate protein nitration, lipid peroxidation and liver microsome protein oxidation; it also caused a decrease of HepG2 cells viability. Baicalein, baicalin and wogonin could inhibit protein nitration and lipid peroxidation in liver homogenate as well as in HepG2 cells in a dose-dependent manner, the inhibition order was baicalein>baicalin>>wogonin. These three flavonoids also inhibited the oxidation of protein in liver microsome, the decrease of cell viability and the content of GSH in HepG2 cells, among which baicalin represented the most inhibitory effect. Besides, hemin-H2O2 induced cell injury could be augmented with the existence of nitrite, indicating protein nitration involved in hemin-nitrite-H2O2 induced liver injury. These results demonstrated hemin-nitrite-H2O2 could induce liver injury through oxidizing or nitrating different biomolecules. Baicalein, baicalin and wogonin could inhibit hemin-nitrite-H2O2 induced liver injury in dose-dependent manners by inhibiting oxidation and nitration.
高铁血红素-亚硝酸盐-H2O2系统可能在某些病理事件中参与肝脏氧化损伤。本文在肝匀浆、肝微粒体及人肝癌细胞系HepG2细胞中研究了黄芩根的三种活性成分黄芩苷、黄芩素和汉黄芩素对高铁血红素-亚硝酸盐-H2O2诱导的肝损伤的影响。结果发现，高铁血红素-亚硝酸盐-H2O2可诱导肝匀浆蛋白硝化、脂质过氧化及肝微粒体蛋白氧化，还可导致HepG2细胞活力下降。黄芩素、黄芩苷和汉黄芩素可剂量依赖性地抑制肝匀浆及HepG2细胞中的蛋白硝化和脂质过氧化，抑制顺序为黄芩素>黄芩苷>>汉黄芩素。这三种黄酮类化合物还可抑制肝微粒体中蛋白的氧化、HepG2细胞活力的下降及谷胱甘肽含量的降低，其中黄芩苷的抑制作用最为明显。此外，高铁血红素-H2O2诱导的细胞损伤在有亚硝酸盐存在时会增强，表明蛋白硝化参与了高铁血红素-亚硝酸盐-H2O2诱导的肝损伤。这些结果表明，高铁血红素-亚硝酸盐-H2O2可通过氧化或硝化不同生物分子诱导肝损伤。黄芩素、黄芩苷和汉黄芩素可通过抑制氧化和硝化以剂量依赖性方式抑制高铁血红素-亚硝酸盐-H2O2诱导的肝损伤。
