Carthamus tinctorius L.-derived nanovesicles alleviate cardiomyocyte hypertrophy by inhibiting the NF-κB signaling pathway
10.19405/j.cnki.issn1000-1492.2026.08.011
- VernacularTitle:红花来源外泌体样纳米囊泡通过抑制NF-κB信号通路缓解心肌细胞肥大
- Author:
Guojun ZHANG
1
;
Zhongpeng DU
2
;
Lu WANG
2
;
Junyu CHEN
2
;
Huanjun RUAN
2
;
Ye LUO
3
;
Weili DUAN
2
;
Shiyu CHEN
2
;
Teng LI
2
;
Xiao KE
2
Author Information
1. Department of Clinical Nutrition， Southern University of Science and Technology Hospital， Shenzhen 518055
2. Department of Cardiology， Fuwai Shenzhen Hospital， Chinese Academy of Medical Sciences， Shenzhen 518000
3. Department of Cardiology， Shenzhen Hospital of Peking University， Shenzhen 518036
- Publication Type:Journal Article
- Keywords:
Carthamus tinctorius L.-derived nanovesicles;
NF-κB signaling pathway;
cardiomyocyte;
cell hypertrophy;
angiotensin Ⅱ
- From:
Acta Universitatis Medicinalis Anhui
2026;61(8):1416-1423
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate whether Carthamus tinctorius L.-derived nanovesicles （CDNVs） can alleviate angiotensin Ⅱ （ANGⅡ）-induced cardiomyocyte （H9C2） hypertrophy by inhibiting the NF-κB signaling pathway and to elucidate the underlying molecular mechanisms. MethodsCDNVs were isolated and purified by ultracentrifugation combined with sucrose density gradient centrifugation， and their morphology and particle size distribution were identified by transmission electron microscopy and nanoparticle tracking analysis. Rat H9C2 cardiomyocytes were cultured in vitro and randomly divided into the normal control group （NC）， ANGⅡ （1.0 μmol/L） group， ANGⅡ+CDNVs group， and ANGⅡ+CDNVs+NF-κB activator 1 group. After 24 h of intervention， cell viability was detected by the CCK-8 assay， the expression of myocardial hypertrophy-related genes （ANP， BNP） was determined by qPCR， the relative cell area was measured by phalloidin staining， the expression of hypertrophy marker proteins and NF-κB pathway proteins （P-p65/p65， P-IκBα/IκBα） was examined by Western blot， and nuclear translocation of p65 was observed by immunofluorescence. Subsequently， NF-κB signaling pathway agonist activator 1 was added， and the expression of myocardial hypertrophy marker proteins and NF-κB pathway proteins was detected. ResultsCDNVs exhibited a typical round-like vesicle structure with an average particle size of 140.4 nm， which was consistent with the morphological characteristics of exosomes. ANGⅡ at concentrations of 0.1-1.0 μmol/L had no significant effect on cardiomyocyte viability. Compared with the NC group， ANGⅡ significantly upregulated the gene expression of ANP and BNP， increased the relative surface area of cardiomyocytes， elevated the levels of myocardial hypertrophy marker proteins and NF‑κB pathway proteins， and promoted the nuclear translocation of p65 （P<0.05）. Following treatment with CDNVs， all the above indicators were markedly reduced in comparison with the ANGⅡ group （all P<0.05）. However， all these experimental results were reversed after the addition of an NF‑κB agonist. ConclusionCDNVs alleviate ANGⅡ-induced H9C2 cell hypertrophy by inhibiting the NF-κB signaling pathway.
