论文部分内容阅读
以100μmol·L~(-1)亚硫酸氢钠对H9C2心肌细胞染毒不同时间(3,6,12,24 h),采用Wistar大鼠作为模型进行整体动物染毒,SO_2组动式吸入SO_2(7 mg·m~(-3))28 d,每天4 h;SO~(2+)NALC(N-乙酰半胱氨酸)组吸入同样条件的SO_2,且自SO_2染毒之日起隔天腹腔注射50 mg·kg-1(b.w.)NALC,对照组吸入新鲜空气并注射生理盐水.测定大鼠心脏组织和H9C2细胞内ROS含量;采用荧光定量PCR和Western blot分析I型胶原(Col1a1)和III型胶原(Col3a1)的mRNA转录和蛋白表达水平.结果显示SO_2及其衍生物引起的氧化应激显著增加了活性氧(ROS)的产生;SO_2及其衍生物不能诱导大鼠心脏组织和H9C2细胞中Col1a1和Col3a1 mRNA转录水平的显著改变,但Col1a1和Col3a1的蛋白表达水平显著升高;同时NALC可减少心脏组织中ROS的产生,有效抑制SO_2吸入后Col1a1和Col3a1蛋白表达的上升.提示SO_2吸入后可能通过产生ROS最终导致胶原蛋白表达的增加.
The H9C2 cardiomyocytes were exposed to 100 μmol·L -1 sodium bisulfite for different times (3, 6, 12 and 24 hours), and Wistar rats were used as the model to inoculate whole animals. SO 2 group was inhaled SO 2 (7 mg · m -3) for 28 days daily for 4 h. SO 2 NACC inhaled SO 2 in the same condition, The rats were injected intraperitoneally with 50 mg · kg-1 (bw) NALC intraperitoneally and the control group was infused with fresh air and injected with normal saline. The content of ROS in rat heart tissue and H9C2 cells was measured. The expression of type I collagen (Col1a1) And collagen type III (Col3a1) mRNA and protein expression levels were analyzed.The results showed that the oxidative stress induced by SO2 and its derivatives significantly increased the production of reactive oxygen species (ROS); SO2 and its derivatives can not induce cardiac tissue and H9C2 cells Col1a1 and Col3a1 mRNA levels were significantly changed, but Col1a1 and Col3a1 protein expression levels were significantly increased; the same time, NALC can reduce ROS production in the heart tissue, effectively inhibit SO2 inhalation Col1a1 and Col3a1 protein expression. Inhalation of SO2 may eventually lead to increased collagen expression through the production of ROS.