Corylin inhibits Ang Ⅱ-induced cardiomyocyte hypertrophy by modulating SIRT1-/NF-κB-dependent signaling pathway
- VernacularTitle:补骨脂异黄酮调控SIRT1/NF-κB依赖的信号通路抑制AngⅡ诱导的心肌肥大
- Author:
Min TAN
1
;
Li-duan HUANG
;
Yan-hong HOU
;
Xiang-yue HU
;
Jing CHEN
;
Xian-qing WANG
;
Shan HUANG
;
Yi CAI
Author Information
- Publication Type:Journal Article
- Keywords: corylin; cardiomyocyte hypertrophy; SIRT1; NF-κB; angiotensin Ⅱ; histone deacetylation
- From: Chinese Pharmacological Bulletin 2025;41(6):1142-1148
- CountryChina
- Language:Chinese
- Abstract: Aim To investigate the role of corylin in angiotensin Ⅱ(Ang Ⅱ)-induced cardiomyocyte hy-pertrophy and its underlying mechanisms.Methods An Ang Ⅱ-induced cardiomyocyte hypertrophy model was established and treated with corylin.Real-time PCR was employed to assess hypertrophic gene mRNA expression,and immunofluorescence was used to meas-ure cardiomyocyte surface area.Western blot and en-zyme activity assay kits were used to evaluate SIRT1 expression and activity.Results Corylin markedly mitigated Ang Ⅱ-induced hypertrophic gene expression and cardiomyocyte surface area enlargement.Moreo-ver,it prevented the Ang Ⅱ-mediated decline in SIRT1 protein levels and deacetylase activity.Further investi-gation indicated that corylin inhibited Ang Ⅱ-driven NF-κB transcriptional activity and the expression of its downstream target genes,such as TNF-α,IL-6,and IL-1β.Notably,SIRT1 silencing abolished the protective effects of corylin against cardiomyocyte hypertrophy,as well as its regulation of the SIRT1/NF-κB signaling pathway.Conclusion Corylin suppresses cardiomyo-cyte hypertrophy by modulating the SIRT1-dependent NF-κB signaling pathway.
