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| Baicalin inhibits hypoxia-induced pulmonary hypertension via the LncRNA-MALAT1/miR-361-3p/TGF-β pathway |
| WU Peiliang, CHEN Mayun, WANG Liangxing, HUANG Xiaoying |
| Department of Pulmonary and Critical Care Medicine, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China |
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| Cite this article: |
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WU Peiliang,CHEN Mayun,WANG Liangxing, et al. Baicalin inhibits hypoxia-induced pulmonary hypertension via the LncRNA-MALAT1/miR-361-3p/TGF-β pathway[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2022, 52(1): 1-8.
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Abstract Objective: To explore the therapeutic effect of baicalin on hypoxic pulmonary hypertension and its potential mechanism. Methods: A total of eighteen male C57BL/6 mice were randomly divided into three groups: the normoxia group, hypoxia-saline group and hypoxia-baicalin group (n=6 in each group). After 21 days, right ventricular pressure (RVSP) and mean carotid artery pressure (mCAP) were detected by cardiac catheter. Hematoxylin-eosin (HE) staining was applied to visualize pulmonary artery remodeling and immunohistochemistry was used to detect the expression of TGF-β signaling pathway. Murine pulmonary artery smooth muscle cells (MPASMCs) were cultured for 48 h under hypoxic and normoxic conditions. CCK-8 assay was used to detect MPASMCs viability. The migration ability of MPASMCs was determined by wound healing assay and transwell assay. TGF-β pathway proteins expression was measured with Western blot analysis.Bioanalysis and dual luciferase reporter gene detection verify the regulatory relationship of LncRNA-MALAT1/miR-361-3p/TGF-β axis. Results: Compared with the hypoxia group, the baicalin group has significantly decreased proliferation and migration ability of MPASMCs (P<0.05), RVSP of mice was significantly decreased (P<0.05), and the pulmonary vascular remodeling was improved. Compared to the normoxic group, the hypoxiagroup had significantly increased expression of TGF-β signaling pathway related proteins TGF-β, p-smad2 and p-smad3, while the TGF-β signaling pathway was significantly inhibited after baicalin treatment. Mechanism exploration suggests that baicalin regulates the expression of TGF-β by regulating the LncRNA-MALAT1/miR-361-3p axis. Conclusion: Baicalin may regulate the expression of TGF-β by regulating the LncRNA-MALAT1/miR-361-3p axis, which can improve the abnormal proliferation and migration of hypoxic MPASMCs and attenuates pulmonary vascular remodeling in hypoxic pulmonary hypertension mice, thereby decreasing pulmonary arterial pressure.
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Received: 11 August 2021
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