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Please use this identifier to cite or link to this item: http://142.54.178.187:9060/xmlui/handle/123456789/16132
Title: The effects of taurochenodeoxycholic acid in preventing pulmonary fibrosis in mice Chuan Zhou1 , Youfei Shi1
Authors: Zhou, Chuan
Shi, Youfei
Li, Jinlian
Zhang, Wen
Fu, Changqi
Wang, Yanmin
Liu, Yan
Liu, Jianzhu
Keywords: Taurochenodeoxycholic acid
preventing
pulmonary fibrosis
mice
Issue Date: 17-Jul-2013
Publisher: Karachi: Faculty of Pharmacy & Pharmaceutical Sciences University of Karachi
Citation: Zhou, C., Shi, Y., Li, J., Zhang, W., Fu, C., Wang, Y., ... & Liu, J. (2013). The effects of taurochenodeoxycholic acid in preventing pulmonary fibrosis in mice. Pakistan Journal of Pharmaceutical Sciences, 26(4), 761-766.
Abstract: The present study prepared the pulmonary fibrosis model in mice by using Bleomycin and carry out the investigations on the effects of taurochenodeoxycholic acid (TCDCA) in preventing pulmonary fibrosis in mice. Expression profiles of the bile acid receptors in the lung of mice FXRα and TGR5 were examined, and pulmonary coefficient, pathohistology as well as expression of TNF-α, MMP-2, MMP-9 and TIMP-2 in pulmonary fibrosis mice. The results showed that FXRα and TGR5 simultaneously expressed in the lung of the mice; TCDCA in dosages of 0.05 and 0.1g/kg can extremely significantly decrease the pulmonary coefficient in the model mice (P<0.01), TCDCA in a dosage of 0.2g/kg significantly decreased the pulmonary coefficient in the model mice (P<0.05); TCDCA in dosages of 0.05 and 0.1g/kg significantly reduce the pathological damages on their lungs; TCDCA can extremely significantly decrease the expression levels of TNF-α and TIMP-2 in pulmonary tissues in the pulmonary fibrosis mice (P<0.01), the expression level of MMP-9 extremely significantly increased (P<0.01), while it has no significant effects on MMP2. The results as mentioned above indicated that TCDCA had antagonistic actions on pulmonary fibrosis in mice.
URI: http://142.54.178.187:9060/xmlui/handle/123456789/16132
ISSN: 1011-601X
Appears in Collections:Issue 04

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