ABSTRACT
【Objective】 To investigate the effect and mechanism of arctigenin (ARG) on hypoxia-reoxygenation (H/R) induced pyroptosis of cardiomyocytes. 【Methods】 H9C2 cells were cultured in vitro, and underwent hypoxia for 2 hours and reoxygenation for 4 hours to establish H/R cell injury model. The cells were divided into control group (Control), model group (H/R), ARG group, miR-21 simulation group (miR-21 mimic), and ARG+miR-21 inhibitor group (ARG+miR-21 inhibitor). TUNEL staining was used to detect the pyroptosis index of H9C2 cells; the lactate dehydrogenase (LDH) kit was used to detect the release of LDH in each group of cells; the enzyme-linked immunosorbent assay (ELISA) was used to detect the content of interleukin-1β (IL-1β) and interleukin-18 (IL-18). Western blotting was used to detect the expressions of pyroptosis-related proteins (Caspase-1, GSDMD, IL-1β and IL-18) in each group. 【Results】 Compared with those in the control group, the pyroptosis index, the release of LDH, IL-1β and IL-18, and the protein expressions of Caspase-1p20, GSDMD-N, IL-1β and IL-18 in the H/R group were significantly increased (P<0.01). Compared with H/R group, ARG group and miR-21 mimic group had significantly reduced pyroptosis index, LDH, IL-1β and IL-18 release, and protein expressions of Caspase-1 p20, GSDMD-N, IL-1β and IL-18 (P<0.01), and the above-mentioned index changes could be reversed after treatment with +miR-21 inhibitor. 【Conclusion】 ARG can inhibit H/R-induced pyroptosis of cardiomyocytes, and its mechanism is related to the promotion of miR-21 expression.