Objective To explore the function of CISD1 on pulmonary fibrosis and ferroptosis and its mechanism related to oxidative stress.Methods A549 cells were divided into five groups:the control group,the TGF-β1 group,the erastin group,the TGF-β1+erastin group and the TGF-β1+NL-1 group.QRT-PCR and Western Blot techniques were used to investigate the impact and mechanism of CDGSH iron sulfur domain 1(CISD1)gene inhibiting on pulmonary fibrosis and ferroptosis,and to im-prove the understanding of the relationship between pulmonary fibrosis and ferroptosis.Results Both TGF-β1 and erastin treat-ments reduced the expression levels of E-cadherin(E-Ca)and CISD1 in A549 cells,and increased the contents of Fe2+,mito-chondrial ROS(mitoROS),4-Hydroxynonenal(4-HNE)and α-smooth muscle actin(α-SMA)expression.NL-1 treatments in-hibited the expression levels of CISD1,and increased the levels of Fe2+,mitoROS,4-HNE and α-SMA expression,while de-creased the expression levels of E-Ca.Conclusion CISD1 can inhibit pulmonary fibrosis and ferroptosis through reducing Fe2+levels,reducing oxidative stress and lipid peroxidation.
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