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

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.