SGLT1 knockdown prevents glucose fluctuation-induced apoptosis of cardiomyocytes through attenuating oxidative stress and mitochondrial dysfunction.

SGLT1 knockdown prevents glucose fluctuation-induced apoptosis of cardiomyocytes through attenuating oxidative stress and mitochondrial dysfunction. Biochem Cell Biol. 2020 Dec 01;: Authors: Chai Q, Miao J, Liu M, Zhang Z, Meng Z, Wu W Abstract Blood glucose fluctuation has been validated to be more detrimental than constant high glucose in the development of cardiovascular complications of diabetes mellitus (DM). Sodium‑glucose cotransporter 2 (SGLT2) inhibitors have been developed as antidiabetic drugs with cardiovascular benefits. However, whether inhibition of SGLT1 protects the diabetic heart remains to be elucidated. The present study investigated the role of SGLT1 in rat H9c2 cardiomyocytes subjected to glucose fluctuation and the underlying mechanisms. The results indicated that SGLT1 knockdown was able to restore cell proliferation and suppress cytotoxicity induced by glucose fluctuation. Glucose fluctuation induced oxidative stress in H9c2 cells, while these changes were reversed effectively by SGLT1 knockdown, as manifested by reduction of intracellular reactive oxygen species and increased antioxidase activity. Further study demonstrated that SGLT1 knockdown attenuated mitochondrial dysfunction in H9c2 cells exposed to glucose fluctuation, including restoration of mitochondrial membrane potential and promotion of mitochondrial fusion. In addition, SGLT1 knockdown downregulated Bax expression, upregulated Bcl-2 expressio...
Source: Biochemistry and Cell Biology - Category: Biochemistry Authors: Tags: Biochem Cell Biol Source Type: research