Azithromycin inhibited oxidative stress and apoptosis of high glucose‐induced podocytes by inhibiting STAT1 pathway

다국어 초록 (Multilingual Abstract)

Azithromycin (AZM) has a therapeutic effect on diabetes, but there is no report on whether AZM has a therapeutic effect on diabetic nephropathy (DN) and its specific mechanism. Cell survival was detected by CCK‐8. The expression of the inflammatory factors TNF‐α, IL‐1β, and IL‐6 was determined by ELISA. The expression of inflammatory proteins MCP‐1, NLPR3, and ASC was detected by western blot. The expression of MDA, LDH, and SOD was detected by the appropriate kit. Apoptosis was detected by flow cytometry and apoptosis‐related proteins Bcl‐2, Bax, Caspase‐3, 6, 9, and Cleaved caspase‐3, 6, 9 were detected by western blot. In addition, the expression of STAT1 was detected by western blot. AZM can increase the activity of high glucose‐induced podocytes (p < .05). After high glucose induction, the expression of TNF‐α, IL‐1β, and IL‐6 was increased and the expression of MCP‐1, NLPR3, and ASC proteins was also increased (p < .001). When AZM was added, the expression of all the above‐mentioned proteins was decreased (p < .001). In addition, MDA, LDH, and SOD were increased after high glucose induction, while decreased after AZM treatment (p < .001). AZM can inhibit apoptosis and the expression of Bax and Cleaved caspase‐3, 6, 9, and promote the expression of Bcl‐2 (p < .001). Furthermore, the expression of STAT1 was increased after high glucose induction, while the expression of STAT1 was decreased after AZM action (p < .01). By adding a STAT1 agonist IFN‐γ, the effects of AZM on inflammation, oxidative stress, and apoptosis of high glucose‐induced podocytes were inhibited (p < .05). AZM inhibited inflammation, oxidative stress, and apoptosis of high glucose‐induced podocytes by inhibiting STAT1 pathway.