Salidroside inhibits phenotypic transformation of rat pulmonary artery smooth muscle cells induced by hypoxia.
10.19540/j.cnki.cjcmm.20211103.706
- Author:
Jia-Qi MAO
1
;
Chuan-Chuan LIU
2
;
Yu-Wei ZHANG
3
;
Qing-Qing ZHANG
4
;
Hong LIU
3
;
Lan MA
3
Author Information
1. Qinghai University Xining 810001, China Research Center for High Altitude Medicine, Medical School, Qinghai University Xining 810001, China Qinghai Provincial Key Laboratory of Traditional Chinese Medicine Research for Glucolipid Metabolic Diseases Xining 810001, China.
2. Qinghai University Xining 810001, China Research Center for High Altitude Medicine, Medical School, Qinghai University Xining 810001, China the Echinococcosis Key Laboratory of Qinghai University Xining 810001, China.
3. Qinghai University Xining 810001, China Research Center for High Altitude Medicine, Medical School, Qinghai University Xining 810001, China.
4. Qinghai University Xining 810001, China Research Center for High Altitude Medicine, Medical School, Qinghai University Xining 810001, China Department of Respiratory, Affiliated Hospital of Qinghai University Xining 810001, China.
- Publication Type:Journal Article
- Keywords:
hypoxia;
phenotypic transformation;
pulmonary artery smooth muscle cells;
salidroside
- MeSH:
Animals;
Cell Proliferation;
Cells, Cultured;
Glucosides;
Hypoxia;
Myocytes, Smooth Muscle;
Phenols;
Pulmonary Artery;
Rats
- From:
China Journal of Chinese Materia Medica
2022;47(4):1024-1030
- CountryChina
- Language:Chinese
-
Abstract:
This study investigated the effect of salidroside on phenotypic transformation of rat pulmonary artery smooth muscle cells(PASMCs) induced by hypoxia. Rat pulmonary arteries were isolated by tissue digestion and PASMCs were cultured. The OD values of cells treated with salidroside at different concentrations for 48 hours were measured by cell counting kit-8(CCK-8) to determine the appropriate concentration range of salidroside. The cells were divided into a normal(normoxia) group, a model(hypoxia) group, and three hypoxia + salidroside groups(40, 60, and 80 μg·mL~(-1)). Quantitative real-time PCR(qRT-PCR) was used to detect the mRNA expression of cell contractile markers in each group, such as α-smooth muscle actin(α-SMA), smooth muscle 22(SM22), and calcium-binding protein(calponin), and synthetic marker vimentin. The expression levels of cell phenotypic markers and proliferating cell nuclear antigen(PCNA) were detected by Western blot. The proliferation of cells in each group was detected by the 5-ethynyl-2'-deoxyuridine(EdU) assay. Cell migration was measured by Transwell assay. As revealed by results, compared with the normal group, the model group showed decreased mRNA and protein expression of contractile phenotypic markers of PASMCs and increased mRNA and protein expression of synthetic markers. Compared with the conditions in the model group, salidroside could down-regulate the mRNA and protein expression of synthetic markers in PASMCs and up-regulated the mRNA and protein expression of contractile phenotypic markers. Compared with the normal group, the model group showed potentiated proliferation and migration. Compared with the model group, the hypoxia + salidroside groups showed blunted proliferation and migration of cells after phenotypic transformation. The results suggest that salidroside can inhibit the expression of synthetic markers in PASMCs and promote the expression of contractile markers to inhibit the hypoxia-induced phenotypic transformation of PASMCs. The mechanism of salidroside in inhibiting the proliferation and migration of PASMCs is related to the inhibition of the phenotypic transformation of PASMCs.
