title: Protective Effects of α-Boswellic Acids in a Pulmonary Arterial Hypertensive Rat Model.
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.
authors.affiliation: Hypertension Research Institute, Central South University, China.
authors.forename: Binhuan
authors.initials: B
authors.lastname: Xiao
authors.affiliation: Hypertension Research Institute, Central South University, China.
authors.forename: Guogang
authors.initials: G
authors.lastname: Zhang
authors.affiliation: Hypertension Research Institute, Central South University, China.
authors.forename: Md Sayed
authors.initials: MS
authors.lastname: Ali Sheikh
authors.affiliation: Hypertension Research Institute, Central South University, China.
authors.forename: Ruizheng
authors.initials: R
authors.lastname: Shi
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D015687:Cell Hypoxia; D049109:Cell Proliferation / Q000187:drug effects; D006973:Hypertension / Q000188:drug therapy* / Q000503:physiopathology; D000860:Hypoxia; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000503:physiopathology; D032389:Myocytes, Smooth Muscle / Q000187:drug effects; D010766:Phosphorylation / Q000187:drug effects; D011651:Pulmonary Artery / Q000187:drug effects / Q000503:physiopathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D014315:Triterpenes / Q000494:pharmacology*; D066253:Vascular Remodeling / Q000187:drug effects
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D014315:Triterpenes; C054625:boswellic acid