PPARβ-related signal pathway involves in the effect of polydatin on high glucose-and insulin-induced cardiomyocyte hypertrophy
10.3969/j.issn.1001-1978.2015.09.017
- VernacularTitle:PPARβ在虎杖苷抗高糖高胰岛素诱导心肌肥大中的作用
- Author:
Bo HUANG
;
Fen JIANG
;
Lai XUE
;
Yang WU
;
Weimin DU
;
Hongmei QIU
;
Qingsong JIANG
- Publication Type:Journal Article
- Keywords:
polydatin;
cardiomyocyte hypertrophy;
high glucose and insulin;
PPARβ;
NF-κB;
NO;
dia-betes mellitus
- From:
Chinese Pharmacological Bulletin
2015;(9):1264-1269
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect of polydatin on cardiomyocyte hypertrophy induced by high glucose (25.5 mmol·L -1 )and insulin (0.1 μmol ·L -1 ) (HGI)and its possible influence on peroxisome prolif-erator-activated receptor-β (PPARβ)/nuclear tran-scription factor-κB (NF-κB)/nitric oxide (NO)signa-ling pathway.Methods The cardiomyocyte hypertro-phy was characterized in rat primary cardiomyocytes by measuring the cell surface area,protein content,and atrial natriuretic factor (ANF)mRNA expression.The mRNA and protein expressions were measured by qRT-PCR and Western blotting,respectively.The activity of NO synthase (NOS)and NO content were measured by reagent kit through ultraviolet spectroscopy.Results HGI significantly induced cardiomyocyte hypertrophy which increased the cell surface area,protein content and ANF mRNA expression (P <0.01 ).Meanwhile, the expressions of PPARβmRNA and protein reduced while the NF-κB p65 and iNOS expressions increased significantly which occurred in parallel with rising NOS activity and NO concentration (P <0.01 ).Polydatin (0.1,1,10 μmol·L -1 )inhibited the cardiomyocyte hypertrophy induced by HGI (P <0.01 ),and re-versed the mRNA and protein expressions of PPARβ, NF-κB p65 and iNOS,and NOS activity,as well as NO content.These effects of polydatin were abolished by GSK0660 (1 μmol·L -1 ),a selective PPARβan-tagonist (P <0.05 ).Conclusion Polydatin resists HGI-induced cardiomyocyte hypertrophy,which may be mediated by PPARβup-regulation,and then NF-κB-iNOS-NO pathway inactivation.
