The protective effect of naringin on cardiac injury in diabetic rats via activating Maxi K
10.3969/j.issn.1001-1978.2022.01.009
- Author:
Wen-Jing XIAO
1
;
Kai-Wen DENG
1
;
Yong-He HU
1
;
Jim HOU
1
;
Ting-Ting WANG
2
Author Information
1. General Hospital of Western Theater Command of Pla, Dept of Pharmacy
2. College of Medicine, Southwest Jiaotong University
- Publication Type:Journal Article
- Keywords:
diabetic cardiomyopathy;
Ion channel activator;
myocardial fibrosis;
myocardial remodelling;
naringin;
the large conduction Ca2 + activated K+ channels
- From:
Chinese Pharmacological Bulletin
2022;38(1):38-42
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the protective effect of naringin ( NA) on diabetic cardiomyopathy by activating the large conduction Ca2+ activated K4 channels (Maxi K ).Methods SD rats were fed with high-fat diet combined with intraperitoneal injection of strepto- zotocin (STZ) to establish a diabetic rat model.Then the rats were randomly divided into model group ( DCM) , naringin group ( NA) and naringin + Maxi K-specific inhibitor group ( NA + PAX) , with 8 rats in each group.Hats in treatment group received administration for 12 weeks and blood glucose was monitored regularly during experiments.The changes of cardiac function, morphology and fibrosis were detected after the treatment.The changes of cx and (3 subunits of Maxi K in heart were detected.Results Cardiac ultrasound results showed that NA could partially restore the cardiac function of rats.However, the cardiac protec tive function of NA was significantly reduced in diabetic rats after Maxi K was specifically blocked.Fibrosis analysis showed that the expression of collagen and fi- bronectin in rats could be decreased after NA treatment, which could be partially reversed by PAX.Western blot results showed that the expression of Maxi K a and p-subunit decreased in DCM group, but there was no significant change after NA treatment.Conclusions NA has a cardioprotective effect on diabetic rats by promoting the opening of the Maxi K channel on the membrane surface rather than increasing its expression.
