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The Influence Of The Abnormal Savda Munziq And Munshil On H2O2-induced Lymphocyte Apoptosis And Bcl-2, NF Kappa B Expression

Posted on:2006-01-18Degree:MasterType:Thesis
Country:ChinaCandidate:Y ChenFull Text:PDF
GTID:2144360182960071Subject:Biochemistry and molecular biology
Abstract/Summary:PDF Full Text Request
Objective: To investigate the effect of the Abnormal Savda Munziq and Mushil on the expression of Bcl-2 and Nuclear Factor (NF) κB induced by Hydrogen Peroxide (H2O2) in human peripheral blood lymphocytes, and both of them how to influence lymphocyte's apoptosis. Methods: Human lymphocytes were cultured in vitro, detecting apoptosis index (AI) by Hoechst 33258 dying method to apoptosis cells, morphological analysis of apoptosis lymphocytes by electron microscopy, DNA fragment analyzing by electrophoresis, then the mode of apoptosis was established. To observe the influence upon lymphocyte's apoptosis by detecting apoptosis index, Western blot was used to determine the expression of Bcl-2 and NF-κB subunit p65 in apoptosis lymphocytes, while treated with Abnormal Savda Munziq and Mushil in the mentioned mode. Results: The Abnormal Savda Munziq can decrease AI obviously, and shows an obvious up-regulation upon Bcl-2 protein expression in apoptosis lymphocytes, while can inhibit the expression of p65 protein. Contrast to the Abnormal Savda Munziq, no changes in AI was measured between the Abnormal Savda Munshil and H2O2 control, but can inhibit Bcl-2 protein expression. At the same time, it can inhibit the expression of p65 protein, too. Conclusion: In the process of apoptosis, the Uighur medicine Abnormal Savda Munziq shows protecting human lymphocytesfrom apoptosis. Furthermore, the Abnormal Savda Munziq and Mushil play different role in Bcl-2 protein expression, even contrary each other. and both of them could inhibit the expression of NF-kB in human peripheral blood lymphocytes induced by H2O2.
Keywords/Search Tags:Abnormal Savda Munziq and Mushil, apoptosis, H2O2, Bcl-2, Nuclear Factor-κB
PDF Full Text Request
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