Affiliation:
1. Department of Cardiothoracic Surgery, Cangzhou Central Hospital, Cangzhou, 061000, Hebei Province, China
Abstract
This study assesses the effect of dihydroartemisinin on pyroptosis and ferroptosis. Rat H9C2 cardiomyocytes were intervened with 35 mmol/L high glucose through assigned blank control, dihydro artemisinin, and dihydroartemisinin+Sirt1 groups. Confocal microscopy was used to observe the
ROS levels, while proliferation ability was detected by CCK-8 method, and apoptosis was assessed by flow cytometry, and migration ability by Transwell transfer method. Moreover, analysis of pyroptosis-related factors expression and content of lipid peroxide were done using laser confocal microscopy.
The average fluorescence intensity of dihydro artemisinin group and dihydroartemisinin+SIRT 1 group decreased significantly (P <0.05), among which the dihydroartemisinin+SIRT 1 group had lowest average fluorescence intensity (P <0.05). SIRT 1 level in the dihydroartemisinin
and dihydroartemisinin+SIRT 1 groups was higher than blank control (P <0.05), with highest level in the dihydroartemisinin+SIRT 1 group (P <0.05). Cell proliferation in the dihydroartemisinin and dihydroartemisinin+SIRT 1 group was reduced (P <0.05), with lowest
proliferation in combination group (P < 0.05). Cell migration in the dihydroartemisinin and dihydroartemisinin+SIRT 1 groups was reduced (P <0.05), with lowest number of migratory cells in the dihydroartemisinin+SIRT 1 group (P <0.05). Cell apoptosis in the dihydroartemisinin
and dihydroartemisinin+SIRT 1 groups was increased (P <0.05), with lowest apoptosis in the dihydroartemisinin+SIRT 1 group (P <0.05). There was upregulation of SIRT 1 and PGC-1α mRNA expression in the dihydroartemisinin and dihydroartemisinin+SIRT 1 groups
was elevated (P <0.05). The expression of NLRP3, GSDMD, and Caspase-1 were all decreased (P <0.05), while that of GPX4 was increased (P <0.05). Dihydroartemisinin inhibits the function of H9C2 cardiomyocytes, pyroptosis and ferroptosis, playing a positive role
in ameliorating Diabetic cardiomyopathy (DCM).
Publisher
American Scientific Publishers
Subject
General Materials Science