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Title: | Effect of injury-curing cataplasma on expression of AQP3 in skeletal muscles of rats by regulating cAMP-PKA signal pathway |
Authors: | Wang, Weiqi Wu, Ruikai Ru, Xuan Liang Sun, Yali |
Keywords: | Curing-injury Cataplasma AQP-3 PGE2 cAMP PKA |
Issue Date: | 20-Sep-2017 |
Publisher: | Karachi:Pakistan Journal of Pharmaceutical Sciences, university of Karachi. |
Citation: | Wang, W., Wu, R., Ru, X. L., & Sun, Y. (2017). Effect of injury-curing cataplasma on expression of AQP3 in skeletal muscles of rats by regulating cAMP-PKA signal pathway. Pakistan Journal of Pharmaceutical Sciences, 30. |
Abstract: | Curing-injury Cataplasma to promote regulatory mechanism of acute closed soft tissue injury swelling of rats may be related to inhibit PGE2, regulating the cAMP - PKA signaling pathways, high expression of AQP - 3. SD rats. 48 rats randomly divided into three groups, each group of 16. Blank group: only hair removal treatment, marking the scope, not building; Control group: marking the depilation area shall be made within the scope of acute closed soft tissue injury model of rats, don't give medication; Experimental group: building local injury Papua gels, a fixed tape. Building after 1 d, 3 d, 7 d, 14 d four phase randomly put to death in the rat 4, only partial muscle tissue specimens after using Western Blot to detect AQP - 3 protein expression level, enzyme-linked immunoassay detection PGE2, cAMP, the expression of PKA, parallel correlation analysis. In 3 d, 7 d, 14 d three time points, AQP-3 and PKA of Experimental group on the expression is higher than the Control group (P<0.01), the expression of PGE2 and cAMP is lower than the Control group (P<0.01); And Experimental group, Control group and Blank group differences were statistically significant (P<0.05). Acute closed soft tissue Curing-injury Cataplasma to promote a swelling, may be related to inhibit PGE2, regulating the cAMP - PKA signaling pathways, high expression of AQP - 3. |
URI: | http://142.54.178.187:9060/xmlui/handle/123456789/14050 |
ISSN: | 1011-601X |
Appears in Collections: | No.5(Special), September, 2017 |
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