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Effects of puerarin on pulmonary vascular remodeling and protein kinase C-alpha in chronic cigarette smoke exposure smoke-exposed rats / 华中科技大学学报(医学)(英德文版)
Article in English | WPRIM (Western Pacific) | ID: wpr-634576
Responsible library: WPRO
ABSTRACT
In order to investigate the effects of puerarin on pulmonary vascular remodeling and protein kinase C-alpha (PKC-alpha) in chronic exposure smoke rats, 54 male Wistar rats were randomly divided into 7 groups control group (C group), smoke exposure groups (S(4w) group, S(8w) group), puerarin groups (P(4w) group, P(8w) group), propylene glycol control groups (PC(4w) group, PC(8w) group). Rats were exposed to cigarette smoke or air for 4 to 8 weeks. Rats in puerarin groups also received puerarin. To evaluate vascular remodeling, alpha-smooth muscle actin (alpha-SM-actin) staining was used to count the percentage of completely muscularised vessels to intraacinar pulmonary arteries (CMA/IAPA) which was determined by morphometric analysis of histological sections. Pulmonary artery smooth muscle cell (PASMC) apoptosis was detected by in situ end labeling technique (TUNEL), and proliferation by proliferating cell nuclear antigen (PCNA) staining. Reverse transcription-polymerase chain reaction (RT-PCR), immunofluorescence staining and Western blot analysis were done to detect the PKC-alpha mRNA and protein expression in pulmonary arteries. The results showed that in cigarette smoke-exposed rats the percentage of CMA/IAPA and alpha-SM-actin expression were increased greatly, PASMC apoptosis was increased and proliferation was markedly increased; Apoptosis indices (AI) and proliferation indices (PI) were higher than in C group; AI and PI were correlated with vascular remodeling indices; The expression of PKC-alpha mRNA and protein in pulmonary arteries was significantly higher than in C group. In rats treated with puerarin, the percentage of CMA/IAPA and cell proliferation was reduced, whereas PASMC apoptosis was increased; The expression levels of PKC-alpha mRNA and protein were lower than in smoke exposure rats. There was no difference among all these data between S groups and PC groups. These findings suggested that cigarette smoke-induced pulmonary vascular remodeling was most likely an effect of the imbalance of PASMC proliferation and apoptosis. Puerarin appears to be able to reduce cell proliferation and vascular remodeling possibly through PKC signaling transduction pathway.
Subject(s)
Full text: Available Health context: SDG3 - Target 3A Strengthen the implementation of the WHO Framework Convention on Tobacco Control / SDG3 - Health and Well-Being Health problem: Protection from Exposure / Target 3.9: Reduce the amount of deaths produced by dangerous chemicals and the pollution of the air, water and soil Database: WPRIM (Western Pacific) Main subject: Pulmonary Artery / Tobacco Smoke Pollution / Vasodilator Agents / Endothelium, Vascular / Smoking / Rats, Wistar / Apoptosis / Myocytes, Smooth Muscle / Cell Proliferation / Protein Kinase C-alpha Language: English Journal: Journal of Huazhong University of Science and Technology (Medical Sciences) Year: 2008 Document type: Article
Full text: Available Health context: SDG3 - Target 3A Strengthen the implementation of the WHO Framework Convention on Tobacco Control / SDG3 - Health and Well-Being Health problem: Protection from Exposure / Target 3.9: Reduce the amount of deaths produced by dangerous chemicals and the pollution of the air, water and soil Database: WPRIM (Western Pacific) Main subject: Pulmonary Artery / Tobacco Smoke Pollution / Vasodilator Agents / Endothelium, Vascular / Smoking / Rats, Wistar / Apoptosis / Myocytes, Smooth Muscle / Cell Proliferation / Protein Kinase C-alpha Language: English Journal: Journal of Huazhong University of Science and Technology (Medical Sciences) Year: 2008 Document type: Article
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