Liu Mei, Li Shu-Jie, Xin Yong-Ning, Ji Shu-Sheng, Xie Rui-Jin, Xuan Shi-Ying
Medical College, Qingdao UniversityQingdao, China; Department of Gastroenterology, Jining First People's HospitalJining, Shandong Province, China.
Department of Rheumatology, Jining First People's Hospital Jining, Shandong Province, China.
Int J Clin Exp Med. 2015 Oct 15;8(10):18074-81. eCollection 2015.
Reactive oxidative species (ROS)-induced apoptosis of human hepatic stellate (HSC) is one of the treatments for liver fibrosis. However, how ROS (reactive oxygen species) affect HSC apoptosis and liver fibrosis is still unknown. In our study, ROS in human HSC cell line LX-2 was induced by ferric nitrilotriacetate (Fe-NTA) and assessed by superoxide dismutase (SOD) activity and methane dicarboxylic aldehyde (MDA) level. We found that in LX2 cells Fe-NTA induced notable ROS, which played a protective role in HSCs cells apoptosis by inhibiting Caspase-3 activation. Fe-NTA-induced ROS increased mRNA and protein level of anti-apoptosis Bcl-2 and decreased mRNA protein level of pro-apoptosis gene Bax, As a result, maintaining mitochondrial membrane potential of HSCs. Fe-NTA-induced ROS play a protective role in human HSCs by regulating Bcl-2 family proteins and mitochondrial membrane potential.
活性氧（ROS）诱导人肝星状细胞（HSC）凋亡是肝纤维化的治疗方法之一。然而，ROS（活性氧）如何影响HSC凋亡和肝纤维化仍不清楚。在我们的研究中，用次氮基三乙酸铁（Fe-NTA）诱导人HSC细胞系LX-2中的ROS，并通过超氧化物歧化酶（SOD）活性和丙二醛（MDA）水平进行评估。我们发现，在LX2细胞中，Fe-NTA诱导产生显著的ROS，其通过抑制半胱天冬酶-3激活在HSCs细胞凋亡中发挥保护作用。Fe-NTA诱导的ROS增加了抗凋亡蛋白Bcl-2的mRNA和蛋白水平，降低了促凋亡基因Bax的mRNA和蛋白水平，从而维持了HSCs的线粒体膜电位。Fe-NTA诱导的ROS通过调节Bcl-2家族蛋白和线粒体膜电位在人HSCs中发挥保护作用。
