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Chinese Journal of Biochemical Pharmaceutics ; (6): 45-48, 2016.
Article in Chinese | WPRIM | ID: wpr-496331


Objective To investigate the effect of ginsenoside Rg1 on the apoptosis of spermatogenic cell in rats with experimentally induced varicocele.Methods A total of 32 adolescent male Wistar rats were included and randomly divided into 4 groups, including sham operation, left varicocele induced, left varicocele induced and low-dose ginsenoside Rg1(5 mg/kg), left varicocele induced and high-dose ginsenoside Rg1 (10 mg/kg), 8 rats in each group.The experimentally induced varicocele was established by Turner method.4 weeks after modeling, the two treatment groups received ginsenoside Rg1 of different dosages by gavage and sham operation and left varicocele induced group received the same volume of NS by gavage, once daily.4 weeks after gavaging, the rats were sacrificed then tissue from left testicle were taken, and the spermatogenic cell apoptosis was detected by TUNEL and Bcl-2 and caspase-3 expressions were detected by immunohistochemistry.Results The protein level of Bcl-2 in ginsenoside Rg1 intervention group was significantly higher than varicocele group, and it was obviously higher in high-dose ginsenoside Rg1 group than low-dose ginsenoside Rg1 group (P<0.05).However, the expression of caspase-3 in ginsenoside Rg1 intervention group was significantly lower than varicocele group, but was higher than sham operation, the expression of caspase-3 in high dose ginsenoside Rg1 group was obviously lower than low dose ginsenoside Rg1 group (P<0.05).The apoptotic index was lowest in sham operation, and which was significantly lower in ginsenoside Rg1 intervention group than varicocele group, and the apoptotic index in high-dose ginsenoside Rg1 group was obviously lower than low-dose ginsenoside Rg1 group ( P<0.05 ) . Conclusion Ginsenoside Rg1 could significantly reduce the testicular sperm cells apoptosis in experimental varicocele rats, raise the Bcl-2 gene expression and inhibiting the expression of caspase-3.

Journal of Jilin University(Medicine Edition) ; (6): 967-971, 2014.
Article in Chinese | WPRIM | ID: wpr-485414


Objective To observe the influence of sirtinol,a silent information regulator 1(SIRT1)inhibitor,in the cell proliferation, cell cycle progression and the expression levels of positive regulator proteins of the cell cycle including Cyclin D1,CDK4 and pRb in prostate cancer DU145 cells,and to explore the possible mechanism of SIRT1 in occurrence of prostagte cancer.Methods The DU145 cells at logarithmic growth phase were cultured in vitro and divided into control group(DMSO)and different doses (10,25,50μmol·L-1 )of sirtinol groups.The inhibitory rate of growth of DU145 cells was detected with MTT method,the SIRT1 mRNA and protein expression levels were determined by RT-PCR and Western blotting method, and the cell cycle was measured by flow cytometry.The Cyclin D1,CDK4 and pRb protein expression levels were examined by Western blotting method. Results Compared with control group, the inhibitory rates of growth of the DU145 cells in different doses of sirtinol groups were increased markedly in a dose-dependent manner(P0.05).Conclusion SIRT1 inhibition by sirtinol can inhibit the cell growth of prostate cancer DU145 cells in a dose-dependent manner and arrest the cell cycle progression,and its mechanism may be related to decreasing the CyclinD1 and pRb protein expressions.