Cryptotanshinone attenuates isoproterenol-induced myocardial hypertro-phy in rats through JAK2/STAT3 signaling pathway
10.3969/j.issn.1000-4718.2025.05.008
- VernacularTitle:隐丹参酮通过JAK2/STAT3信号通路抑制异丙肾上腺素诱导的大鼠心肌肥厚
- Author:
Lina LIU
1
;
Chunxiang LI
;
Changzhi GUO
;
Qun WANG
;
Yan ZHAO
;
Hongye ZHAO
;
Fengchun DENG
Author Information
1. 齐齐哈尔医学院附属第一医院输血科,黑龙江 齐齐哈尔 161041;齐齐哈尔医学院基础医学院,黑龙江 齐齐哈尔 161003
- Publication Type:Journal Article
- Keywords:
cryptotanshinone;
isoprenaline;
myocardial hypertrophy;
myocardial remodeling;
JAK2/STAT3 signaling pathway
- From:
Chinese Journal of Pathophysiology
2025;41(5):902-908
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effect of cryptotanshinone(CPT)on myocardial hypertrophy induced by isoprenaline(ISO)in rats and explore its potential mechanism.METHODS:The experimental design consisted of two parts.The first aimed to investigate the effects of CPT on cardiac function,pathological manifestations,and the Janus ki-nase 2(JAK2)/signal transducer and activator of transcription 3(STAT3)signaling pathway in rats with myocardial hyper-trophy.The rats were divided into six groups,namely the control,CPT control,and model groups and low-(15 mg·kg-1·d-1),medium-(30 mg·kg-1·d-1),and high-dose(60 mg·kg-1·d-1)CPT treatment groups,with six rats per group.The sec-ond part aimed to validate the role of the JAK2/STAT3 signaling pathway in the CPT-mediated myocardial hypertrophy treatment.Rats were divided into four groups,namely the control,model,high-dose CPT treatment,and coumermycin A1(CA1,a JAK2/STAT3 agonist)intervention(rats received ISO injection followed by 60 mg·kg-1·d-1 of high-dose CPT and 1 mg·kg-1·d-1 of CA1 for 15 d)groups,with five rats per group.Myocardial hypertrophy was induced in rats via intra-peritoneal injection of ISO(5 mg/kg),and CPT intervention lasted for 15 days.Cardiac function-related parameters were assessed using echocardiography,and pathological changes were evaluated through hematoxylin-eosin,Masson,and wheat germ agglutinin staining.Protein expression levels of atrial natriuretic peptide(ANP),brain natriuretic peptide(BNP),β-myosin heavy chain(β-MHC),and JAK2/STAT3 signaling pathway-related proteins were detected by Western blot analysis.RESULTS:Compared with the model group,CPT administration improved cardiac dysfunction-related ul-trasound markers and significantly reduced ISO-induced cardiomyocyte hypertrophy and myocardial fibrosis in rats with hy-pertrophy in a dose-dependent manner(P<0.05).Additionally,CPT decreased the levels of ANP,BNP,and β-MHC in-duced by ISO modeling(P<0.05),and inhibiting the phosphorylation of JAK2 and STAT3(P<0.05).Furthermore,a partial reversal of the therapeutic effect on myocardial hypertrophy induced by ISO modeling was observed when CA1 was administered(P<0.05).CONCLUSION:The CPT exhibits potential as a therapeutic agent for cardiac hypertrophy by effectively attenuating ISO-induced cardiac hypertrophy in rats through JAK2/STAT3 signaling inhibition.
