| Citation: |
ZHU Yaqian, HU Gaochao, QU Xingguang. Expression of serum inflammatory cytokines in patients with diabetic cardiomyopathy and their effects on mitochondrial function of cardiomyocytes[J]. Journal of Clinical Medicine in Practice, 2022, 26(24): 57-60, 85. DOI: 10.7619/jcmp.20222221
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To investigate the expression levels of inflammatory cytokines interleukin (IL)-1β and IL-18 in diabetic cardiomyopathy (DCM) and their effects on mitochondrial function of cardiomyocytes.
The peripheral blood serum of 104 DCM patients (DCM group) and 90 healthy volunteers (healthy control group) were collected, and the serum levels of IL-1β and IL-18 in the two groups were detected. Human myocardial cell line AC16 was cultured and divided into control group, IL-1β group (adding 10 ng/mL recombinant human IL-1β) and IL-18 group (adding 10 ng/mL recombinant human IL-18). Cell proliferation activity was detected by CCK-8 assay; mitochondrial membrane potential and permeability were detected by JC-1 staining and calcein staining, respectively; the expression levels of apoptosis-related proteins Bax, Bcl-2 and Cleaved Caspase-3 (C-Casp3) were detected by western blot.
Compared with the healthy control group, serum IL-1β and IL-18 concentrations in the DCM group were increased, and the difference was statistically significant (P < 0.05). Compared with the control group, the proliferating activity of AC16 cells was significantly decreased after incubation with IL-1β or IL-18 for 48 and 72 h (P < 0.05); compared with the control group, the percentage of cells with decreased mitochondrial membrane potential in the IL-1β and IL-18 groups was significantly increased (P < 0.001); the average fluorescence intensity of calcein in the IL-1β group and IL-18 group was significantly higher than that in the control group (P < 0.001). Compared with the control group, the Bax/Bcl-2 and C-Casp3/GAPDH in the IL-1β and IL-18 groups were significantly increased (P < 0.01 or P < 0.001).
The expression levels of IL-1β and IL-18 in peripheral blood of DCM patients are increased, and the function of cardiomyocytes is affected by inhibiting mitochondrial activity.
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