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1.南通大学附属妇幼保健院/南通市儿童医院药学部,江苏 南通 226007
2.南通大学药学院,江苏 南通 226001
3.南通大学附属妇幼保健院/南通市儿童医院心电图室,江苏 南通 226007
Published:28 February 2023,
Received:07 September 2022,
Revised:19 December 2022,
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刘露露,秦燕,孟国梁等.硫化氢对心肌成纤维细胞增殖的抑制作用及机制研究 Δ[J].中国药房,2023,34(04):438-443.
LIU Lulu,QIN Yan,MENG Guoliang,et al.Study on inhibitory effect and mechanism of hydrogen sulfide on the proliferation of cardiac fibroblasts[J].ZHONGGUO YAOFANG,2023,34(04):438-443.
刘露露,秦燕,孟国梁等.硫化氢对心肌成纤维细胞增殖的抑制作用及机制研究 Δ[J].中国药房,2023,34(04):438-443. DOI: 10.6039/j.issn.1001-0408.2023.04.11.
LIU Lulu,QIN Yan,MENG Guoliang,et al.Study on inhibitory effect and mechanism of hydrogen sulfide on the proliferation of cardiac fibroblasts[J].ZHONGGUO YAOFANG,2023,34(04):438-443. DOI: 10.6039/j.issn.1001-0408.2023.04.11.
目的
2
研究硫化氢(H
2
S)对心肌成纤维细胞增殖的抑制作用及机制。
方法
2
取新生SD雄性大鼠心脏,采用差速离心法分离心肌成纤维细胞。以硫氢化钠作为H
2
S的供体,检测H
2
S对血管紧张素Ⅱ(Ang Ⅱ)诱导心肌成纤维细胞增殖、羟脯氨酸含量以及去乙酰化酶3(SIRT3)蛋白表达的影响。用干扰RNA技术下调SIRT3表达后,观察H
2
S对Ang Ⅱ诱导的心肌成纤维细胞增殖、羟脯氨酸的含量以及Ⅰ型胶原(Col Ⅰ)、Ⅲ型胶原(Col Ⅲ)和视神经萎缩蛋白1(OPA1)表达的影响。
结果
2
H
2
S可抑制Ang Ⅱ诱导的心肌成纤维细胞增殖,降低羟脯氨酸含量,增强SIRT3蛋白表达(
P
<0.05)。用干扰RNA技术下调SIRT3表达后,H
2
S对Ang Ⅱ诱导的心肌成纤维细胞增殖抑制作用、羟脯氨酸含量降低作用均被抑制,且H
2
S降低Col Ⅰ、Col Ⅲ表达的作用和增强OPA1表达的作用也明显减弱。
结论
2
H
2
S依赖增加SIRT3表达来抑制Ang Ⅱ诱导的心肌成纤维细胞增殖。
OBJECTIVE
2
To investigate the inhibitory effect and the possible mechanism of hydrogen sulfide (H
2
S) on the proliferation of cardiac fibroblasts.
METHODS
2
The heart of neonatal SD rats was collected, and cardiac fibroblasts were separated with differential centrifugation. Using sodium hydrosulfide as the donor of H
2
S, the effects of H
2
S 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 H
2
S 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
2
H
2
S 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 H
2
S on the proliferation of Ang Ⅱ-induced cardiac fibroblasts and the reduction of hydroxyproline content were both inhibited, and the effect of H
2
S on reducing the expression of Col Ⅰ and Col Ⅲ and enhancing the expression of OPA1 was also significantly weakened.
CONCLUSIONS
2
H
2
S inhibits the proliferation of Ang Ⅱ-induced cardiac fibroblasts through increasing the expression of SIRT3.
硫化氢心肌成纤维细胞血管紧张素Ⅱ去乙酰化酶3
cardiac fibroblastsangiotensin Ⅱsirtuin 3
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