Planta Med 2017; 83(01/02): 78-86
DOI: 10.1055/s-0042-109069
Biological and Pharmacological Activity
Original Papers
Georg Thieme Verlag KG Stuttgart · New York

Protective Effects of α-Boswellic Acids in a Pulmonary Arterial Hypertensive Rat Model

Binhuan Xiao
Hypertension Research Institute, Central South University, China
,
Guogang Zhang
Hypertension Research Institute, Central South University, China
,
Md Sayed Ali Sheikh
Hypertension Research Institute, Central South University, China
,
Ruizheng Shi
Hypertension Research Institute, Central South University, China
› Author Affiliations
Further Information

Publication History

received 26 November 2015
revised 07 May 2016

accepted 16 May 2016

Publication Date:
01 July 2016 (online)

Abstract

The purpose of this study was to observe the protective effects of α-boswellic acids on hypoxia-induced pulmonary vascular structural remodeling in pulmonary arterial smooth muscle cells in a hypertensive rat model. Pulmonary arterial smooth muscle cells were cultured and then randomly divided into four groups: normoxia, hypoxia (3 % O2; 24 h), hypoxia plus α-boswellic acids, and hypoxia plus DMSO (as a positive control), according to the different concentrations of α-boswellic acids (21.90 µM, 43.79 µM, and 87.58 µM). Apoptosis and proliferation of pulmonary arterial smooth muscle cells significantly decreased in the hypoxia plus α-boswellic acids group compared with the hypoxia and hypoxia plus DMSO groups (n = 8, p < 0.05). The mRNA and protein phosphorylation levels of c-Jun N-terminal kinase 1 and extracellular regulated protein kinase 1 were significantly elevated in hypoxic cells compared with normal cells. However, the mRNA and protein phosphorylation levels of c-Jun N-terminal kinase 1 and extracellular regulated protein kinase 1 markedly decreased in the hypoxia plus α-boswellic acids group compared with the hypoxia plus DMSO group (n = 8, p < 0.05; n = 13, p < 0.05, respectively). Our findings suggest that α-boswellic acids can inhibit inappropriate apoptosis and excessive proliferation of pulmonary arterial smooth muscle cells and pulmonary vascular remodeling by repressing the expression of c-Jun N-terminal kinase 1 and extracellular regulated protein kinase 1 under hypoxic conditions.

Supporting Information

 
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