Study on inhibitory effect and mechanism of hydrogen sulfide on the proliferation of cardiac fibroblasts
- VernacularTitle:硫化氢对心肌成纤维细胞增殖的抑制作用及机制研究
- Author:
Lulu LIU
1
,
2
;
Yan QIN
1
,
2
;
Guoliang MENG
2
;
Jinhua GU
1
,
2
;
Lin ZHANG
1
;
Xiaoyan BAO
3
Author Information
1. Dept. of Pharmacy，the Affiliated Maternity & Child Health Care Hospital of Nantong University/Nantong Children’s Hospital，Jiangsu Nantong 226007，China
2. School of Pharmacy，Nantong University，Jiangsu Nantong 226001，China
3. Electrocardiographic Room，the Affiliated Maternity & Child Health Care Hospital of Nantong University/ Nantong Children’s Hospital，Jiangsu Nantong 226007，China
- Publication Type:Journal Article
- Keywords:
hydrogen sulfide;
cardiac fibroblasts;
angiotensin Ⅱ;
sirtuin 3
- From:
China Pharmacy
2023;34(4):438-443
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To investigate the inhibitory effect and the possible mechanism of hydrogen sulfide （H2S） on the proliferation of cardiac fibroblasts. METHODS The heart of neonatal SD rats was collected， and cardiac fibroblasts were separated with differential centrifugation. Using sodium hydrosulfide as the donor of H2S， the effects of H2S on the proliferation of cardiac fibroblasts induced by angiotensin Ⅱ （Ang Ⅱ）， hydroxyproline content and the expression of sirtuin 3 （SIRT3） protein were detected. After SIRT3 knockdown with siRNA technology， the effects of H2S on the proliferation of cardiac fibroblasts induced by Ang Ⅱ， hydroxyproline content， the expressions of collagen Ⅰ （Col Ⅰ）， collagen Ⅲ （Col Ⅲ ） and optic atrophy protein 1 （OPA1） were detected. RESULTS H2S could inhibit the proliferation of Ang Ⅱ-induced cardiac fibroblasts， reduce the content of hydroxyproline and increase the expression of SIRT3 （P＜0.05）. After down-regulating the expression of SIRT3 with siRNA technology， the inhibition of H2S on the proliferation of Ang Ⅱ-induced cardiac fibroblasts and the reduction of hydroxyproline content were both inhibited， and the effect of H2S on reducing the expression of Col Ⅰ and Col Ⅲ and enhancing the expression of OPA1 was also significantly weakened. CONCLUSIONS H2S inhibits the proliferation of Ang Ⅱ -induced cardiac fibroblasts through increasing the expression of SIRT3.
