Vildagliptin Protects Palmitic Acid-induced Myocardial Inflammatory Damage in Diabetes Mellitus
10.13748/j.cnki.issn1007-7693.20233257
- VernacularTitle:维格列汀对棕榈酸诱导糖尿病心肌炎性损伤的保护作用
- Author:
Ruinan YANG
1
;
Ying YU
2
;
Kan QIN
1
Author Information
1. School of Pharmacy, Anhui Medical University, Hefei 230061, China；Department of Pharmacy, The Third Affiliated Hospital of Anhui Medical University, Hefei 230061, China
2. Department of Pharmacy, The Third Affiliated Hospital of Anhui Medical University, Hefei 230061, China
- Publication Type:Journal Article
- Keywords:
dipeptidyl peptidase-4；vildagliptin； diabetic cardiomyopathy；palmitic acid ； NF-κB
- From:
Chinese Journal of Modern Applied Pharmacy
2024;41(11):1484-1490
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the mechanism of vildagliptin, a dipeptidyl peptidase 4 inhibitor(DPP-4i), in improving the inflammatory damage of cardiomyocytes induced by diabetes mellitus.
METHODS
The AC16 cardiomyocytes cultured in vitro were randomly divided into blank group, palmitic acid(PA) group, 0.1, 1, 10 μmol·L−1 vildagliptin group, and sitagliptin group (positive control group). The cell viability was detected by CCK-8 kit. The expressions of DPP-4, p-NF-κB and IκB were detected by Western blotting. The expression level of inflammatory cytokines TNF-α and IL-6 were detected by ELISA kit. TUNEL kit was used to detect cell apoptosis.
RESULTS
After PA treatment, the cell morphology of AC16 human cardiomyocytes changed, CCK-8 results showed a decrease in cell survival rate, Western blotting results showed increased phosphorylation of NF-κB and increased expression of DPP-4 protein, and ELISA results showed increased expression level of inflammatory factors TNF-α and IL-6. The increase of TUNEL positive ratio promoted apoptosis of cardiomyocytes. After administration of DPP-4i vildagliptin, it could effectively inhibit the abnormal expression of DPP-4 protein induced by PA, improve the morphology of cardiomyocytes, and down-regulate the level of NF-κB phosphorylation. ELISA results showed that vildagliptin could improve the expression level of PA-induced inflammatory factors TNF-α and IL-6, and reduce the proportion of TUNEL positive(P<0.05).
CONCLUSION
Vildagliptin can effectively antagonize PA-induced inflammatory injury of cardiomyocytes, antagonize myocardial injury induced by diabetic cardiomyopathy by inhibiting the phosphorylation level of NF-κB, reducing the expression level of intracellular inflammatory factors and inhibiting apoptosis.
