QUAN Bo-wen, WU Tong, LIU Qing, GAO Chen, ZHOU Hong-bing, BAI Ying-chun, SHI Song-li. Protective Effect of Different Polar Parts of Amygdalus mongolica on Pulmonary Fibrosis Rat Models Induced by Bleomycin[J]. Science and Technology of Food Industry, 2020, 41(22): 305-309. DOI: 10.13386/j.issn1002-0306.2020050143
Citation: QUAN Bo-wen, WU Tong, LIU Qing, GAO Chen, ZHOU Hong-bing, BAI Ying-chun, SHI Song-li. Protective Effect of Different Polar Parts of Amygdalus mongolica on Pulmonary Fibrosis Rat Models Induced by Bleomycin[J]. Science and Technology of Food Industry, 2020, 41(22): 305-309. DOI: 10.13386/j.issn1002-0306.2020050143

Protective Effect of Different Polar Parts of Amygdalus mongolica on Pulmonary Fibrosis Rat Models Induced by Bleomycin

  • Objective:This study aimed to investigate the effect of different polarities of Amygdalus mongolica on pulmonary fibrosis induced by bleomycin in rats. Methods:The rat model of pulmonary fibrosis was established by intratracheal injection of bleomycin. Then the rat was treated with Amygdalus mongolica. The pathological changes of lung tissues were detected by using HE stain and Masson's trichrome stain, and the contents of superoxide dismutase (SOD) and malondialdehyde (MDA) in lung tissues were measured. In addition, the expression of TGF-β1, Smad3 and α-SMA protein in lung tissue was detected to observe the effect of different polarities of Amygdalus mongolica on pulmonary fibrosis induced by bleomycin in rats. Results:Compared with the model group, extracts from petroleum ether and n-butanol of Amygdalus mongolica significantly decreased the indexes of pulmonary fibrosis (P<0.05), significantly increased the activity of SOD in lung tissue (P<0.05), reduced the alveolar inflammation and pulmonary fibrosis (P<0.05), and significantly decreased the expression of MDA, TGF-β1, Smad3 and α-SMA mRNA in lung tissue (P<0.05). Conclusion:Of the four active components of Amygdalus mongolica, the extracts of petroleum ether and n-butanol produce a good protective effect on pulmonary fibrosis induced by bleomycin in rats. The mechanism is that Smad3 downregulated and TGF-β1 and α-SMA are inhibited by scavenging reactive oxygen species against lipid peroxidation, so as to produce effect against pulmonary fibrosis.
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