人参皂苷 Rg1 通过钙蛋白酶-1/STAT3 信号通路缓解缺氧诱导的肺动脉高压小鼠的血管重塑

IF 6.8 2区 医学 Q1 CHEMISTRY, MEDICINAL
Chenyang Ran , Meili Lu , Fang Zhao , Yi Hao , Xinyu Guo , Yunhan Li , Yuhong Su , Hongxin Wang
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引用次数: 0

摘要

缺氧性肺动脉高压(HPH)是血管重塑的主要病理变化,是由缺氧引起的一种复杂的心肺疾病。一些研究结果表明,人参皂苷Rg1(Rg1)可以改善血管重塑,但Rg1对缺氧诱发的肺动脉高压的作用和机制尚不清楚。本研究旨在探讨 Rg1 对肺动脉高压的潜在作用机制。将 C57BL/6 小鼠、钙蛋白酶-1 基因敲除小鼠和肺动脉平滑肌细胞(PASMCs)暴露在低氧环境中,并进行或不进行不同的处理。在动物和细胞水平测定了 Rg1 和钙蛋白酶-1 沉默对炎症、纤维化、增殖以及钙蛋白酶-1、STAT3 和 p-STAT3 蛋白表达水平的影响。在小鼠和细胞水平上,缺氧会促进炎症、纤维化和细胞增殖,钙蛋白酶-1和p-STAT3的表达也会增加。服用人参皂苷 Rg1 和敲除钙蛋白酶-1、MDL-28170 和 HY-13818 对缺氧诱导的炎症、纤维化和细胞增殖有保护作用,这可能与下调小鼠和细胞中钙蛋白酶-1 和 p-STAT3 的表达有关。此外,过表达钙蛋白酶 1 会增加 p-STAT3 的表达,加速缺氧 PASMCs 的炎症、纤维化和细胞增殖。人参皂苷 Rg1 可通过抑制钙蛋白酶 1/STAT3 信号通路,改善缺氧引起的肺血管重塑。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Ginsenoside Rg1 alleviates vascular remodeling in hypoxia-induced pulmonary hypertension mice through the calpain-1/STAT3 signaling pathway

Ginsenoside Rg1 alleviates vascular remodeling in hypoxia-induced pulmonary hypertension mice through the calpain-1/STAT3 signaling pathway

Background

Hypoxic pulmonary hypertension (HPH) is the main pathological change in vascular remodeling, a complex cardiopulmonary disease caused by hypoxia. Some research results have shown that ginsenoside Rg1 (Rg1) can improve vascular remodeling, but the effect and mechanism of Rg1 on hypoxia-induced pulmonary hypertension are not clear. The purpose of this study was to discuss the potential mechanism of action of Rg1 on HPH.

Methods

C57BL/6 mice, calpain-1 knockout mice and Pulmonary artery smooth muscle cells (PASMCs) were exposed to a low oxygen environment with or without different treatments. The effect of Rg1 and calpain-1 silencing on inflammation, fibrosis, proliferation and the protein expression levels of calpain-1, STAT3 and p-STAT3 were determined at the animal and cellular levels.

Results

At the mouse and cellular levels, hypoxia promotes inflammation, fibrosis, and cell proliferation, and the expression of calpain-1 and p-STAT3 is also increased. Ginsenoside Rg1 administration and calpain-1 knockdown, MDL-28170, and HY-13818 treatment showed protective effects on hypoxia-induced inflammation, fibrosis, and cell proliferation, which may be associated with the downregulation of calpain-1 and p-STAT3 expression in mice and cells. In addition, overexpression of calpain 1 increased p-STAT3 expression, accelerating the onset of inflammation, fibrosis and cell proliferation in hypoxic PASMCs.

Conclusion

Ginsenoside Rg1 may ameliorate hypoxia-induced pulmonary vascular remodeling by suppressing the calpain-1/STAT3 signaling pathway.

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来源期刊
Journal of Ginseng Research
Journal of Ginseng Research CHEMISTRY, MEDICINAL-INTEGRATIVE & COMPLEMENTARY MEDICINE
CiteScore
11.40
自引率
9.50%
发文量
111
审稿时长
6-12 weeks
期刊介绍: Journal of Ginseng Research (JGR) is an official, open access journal of the Korean Society of Ginseng and is the only international journal publishing scholarly reports on ginseng research in the world. The journal is a bimonthly peer-reviewed publication featuring high-quality studies related to basic, pre-clinical, and clinical researches on ginseng to reflect recent progresses in ginseng research. JGR publishes papers, either experimental or theoretical, that advance our understanding of ginseng science, including plant sciences, biology, chemistry, pharmacology, toxicology, pharmacokinetics, veterinary medicine, biochemistry, manufacture, and clinical study of ginseng since 1976. It also includes the new paradigm of integrative research, covering alternative medicinal approaches. Article types considered for publication include review articles, original research articles, and brief reports. JGR helps researchers to understand mechanisms for traditional efficacy of ginseng and to put their clinical evidence together. It provides balanced information on basic science and clinical applications to researchers, manufacturers, practitioners, teachers, scholars, and medical doctors.
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