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Study Of Molecular Mechanisms Underlying Anti-tumor Effect Of Ganoderma Polysaccharides

Posted on:2008-11-22Degree:MasterType:Thesis
Country:ChinaCandidate:L H QinFull Text:PDF
GTID:2144360218958584Subject:Crop biotechnology
Abstract/Summary:PDF Full Text Request
Objective: To study the effect of Ganoderma lucidum polysaccharide(GLP)anticancer in vivo or in vitro, and that on the expression of bax protein, P53 protein inLewis lung carcinoma -bearing mice.Method: 40 C57 mice were devided into 4 groups randomly (n=10 each), 0.2mLLewis lung cancer cell (St 1.5×10~6/mL) were implanted into each of the twogroups(the first and the second) by subcutaneous injection. After 48h, the second andthe third groups were given 0.2mL GLP (20mg/ml) respectively, once a day. The drugwas given continuously for 7 days. The mice were killed by decapitation 7 day afterstopping being given the drug. And then, calculated the carcinoma inhibition rate, thethymus index number and the rate of life prolonging, and observed the expression ofBax, P53 protein by SABC immunohistochemistry method.In addition MTT colorimetry was used for the assay of cell proliferation, andphagocytosis of chicken erythrocytes by mouse peritoneal macrophages wasinvestigatedResult: 1. The group with drug had effect on inhibiting Lewis lung carcinoma invivo (p<0.05), but not in vitro.2. Anti-oncogene Bax and P53 mutation protein werestained in cytoplasm and nucleus respectively with brown color, Anti-oncogene Baxprotein expression increase after given DLP, whereas anti-oncogene P53 mutationprotein expression reduced.Conclusion: 1.GLP can not inhibit the growth of Lewis lung carcinoma cell invitro. 2. GLP can inhibit the growth of Lewis lung carcinoma cell in vivo. 3. GLP canregulate anti-oncogene Bax protein and P53 protein expression—anti-oncogene Baxprotein expression increase after given DLP, but anti-oncogene P53 mutation proteinexpression reduced.
Keywords/Search Tags:Ganoderma lucidum polysaccharide, Lewis lung carcinoma, protein Bax, protein P53
PDF Full Text Request
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