Huanglian Jiedu Decoction Improves Hypertensive Cardiac Hypertrophy in Rats Through the Notch1/NF-κB Signaling Pathway
10.11969/j.issn.1673-548X.2025.02.020
- VernacularTitle:黄连解毒汤通过Notch1/NF-κB信号通路改善大鼠高血压性心肌肥厚
- Author:
Ziyu LU
1
;
Jianying LI
1
;
Bihui JIANG
1
Author Information
1. 010059 呼和浩特,内蒙古医科大学基础医学院
- Publication Type:Journal Article
- Keywords:
Huanglian jiedu decoction;
Hypertensive cardiac hypertrophy;
Notch1signaling pathway;
NF-κB signaling pathway
- From:
Journal of Medical Research
2025;54(2):123-131
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective mechanisms of huanglian jiedu decoction(HLJDD)against hypertensive cardiac hypertrophy(HCH)in rats.Methods The HCH model was constructed in SD rats through abdominal aortic constriction(AAC).Rats were randomly divided into the sham operation(Sham)group,model(Mod)group,Mod+HLJDD high,medium and low-dose(Mod+H,Mod+M,Mod+L)groups,and Mod+Captopril(Cap)group using a simple random sampling method.Blood pressure,echocardiography,hematoxylin-eosin staining,and Masson staining were performed to assess the impact of HLJDD on HCH.Based on the results of part one,rats were further randomly divided into Sham group,Mod group,Mod+Notch1 inhibitor(DAPT)group,Mod+Notch1 agonist(Jagged-1)group,Mod+HLJDD high-dose(HLJDD)group,Mod+HLJDD high-dose+Notch1 inhibitor(DAPT+H)group,and Mod+HLJDD high-dose+Notch1 agonist(Jagged-1+H)group using a simple random sampling method.Hematoxylin-eosin staining and Masson staining were observed.Real-time fluorescence quantitative polymerase chain reaction(RT-qPCR)and Western blot were used to detect the expression levels of related inflammatory factors,to further explore the mechanisms of HLJDD.Results Compared with the Mod group,rats in the Mod+H group exhibited reduced blood pressure(P＜0.05),improved cardiac func-tion(P＜0.05),relieved myocardial injury and decreased myocardial fibrosis(P＜0.05).Compared with the Mod group,the DAPT group displayed aggravated myocardial injury and fibrosis,decreased expression levels of Notch1 and Hes1(P＜0.05),and increased ex-pression levels of inflammatory factors and NF-κB p65(P＜0.05).The Jagged-1 group and HLJDD group showed opposite results.Compared with HLJDD group,the DAPT+H group displayed aggravated myocardial injury and fibrosis,decreased expression levels of Notch1 and Hes1(P＜0.05,P＜0.01),and increased expression levels of inflammatory factors and NF-κB p65(P＜0.05).The Jag-ged-1+H group showed opposite results,indicating that HLJDD can partially activate the Notch1signaling pathway while inhibiting the NF-κB signaling pathway and the release of inflammatory factors.Conclusion HLJDD can alleviate AAC-induced HCC in rats,and its mechanism may be achieved through the modulation of the Notch1/NF-κB signaling pathway.Additionally,a certain negative feed-back regulatory relationship exists between the Notch1 signaling pathway and the NF-κB signaling pathway.
