Inhibitory effect of coenzyme Q10 on apoptosis of human coronary endothelial cells induced by high glucose and its mechanism / 吉林大学学报(医学版)

ABSTRACT

Objective: To investigate the inhibitory effect of coenzyme Q10 (Co-QlO) on the apoptosis of human coronary endothelial cells (HCAECs) induced by high glucose, and to elucidate its possible mechanism. Methods: The HCAECs were divided into control group, high glucose group and high glucose combined with 5, 10, and 20 μmol · L-1 Co-QlO treatment groups; the HCAECs in control group were cultured for 24 h using a routine culture method. The cells in high glucose group were treated with 30 mmol · L-1 glucose for 24 h; the cells in high glucose combined with 5, 10, and 20 μmol · L-1 Co-QlO treatment groups were treated with 5, 10, and 20 jumol · L-1 Co-QlO combined with 30 mmol · L-1 glucose for 24 h, respectively. The cell viabilities of HCAECs in various groups were measured by CCK-8 assay. The apoptotic rates of HCAECs in high glucose group and high glucose combined with 10 μmol · L-1 Co-QlO treatment group were detected by Hoechst-PI double staining. The cell mitochondrial membrane potentials of HCAECs in high glucose group and high glucose combined with 10 μmol · L-1 Co-QlO treatment group were determined by Mito-tracker staining. The mitochondrial reative oxygen species (mtROS) levels in the HCAECs in high glucose group and high glucose combined with 10 jumol · L-1 Co-QlO treatment group were measured by MitoSox staining. The protein expression levels of B cell lymphoma/leukemia 2 protein (Bcl-2), Bel-2 assaciated X protein (Bax), Bel-2 assaciated death promoter (Bad) and X-linked inhibitor of apoptosis protein (x-IAP) in the HCAECs in high glucose group and high glucose combined with 10 μmol · L-1 Co-QlO treatment group were detected by Western blotting method. Results: Compared with control group, the cell viability of HCAECs in high glucose group was significantly reduced (P<0. 01); compared with high glucose group, the cell viabilities of HCAECs in high glucose combined with 5, 10, and 20 μmol · L-1 Co-QlO treatment groups were significantly increased (P<0. 05 or P<0. 01), especially in high glucose combined with 10 jumol · L-1 Co-QlO treatment group (P<0. 01). Compared with high glucose group, the apoptotic rate, the mitochondrial membrane potential and the mtROS level of HCAECs in high glucose combined with 10 μmol · L-1 Co-QlO treatment group were significantly decreased (P<0. 01). The Western blotting results showed that compared with high glucose group, the expression levels of Bax and Bad proteins in the HCAECs in high glucose combined with 10 μmol · L-1 Co-QlO treatment group were decreased significantly (P<0. 01), and the expression levels of Bcl-2 and x-IAP proteins were increased significantly (P<0.01). Conclusion: Co-QlO may reduce the apoptosis of HCAECs induced by high glucose through inhibiting the mitochondrial apoptosis-related pathway to ptotect the cells.