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AIM: To evaluate human pancreatic carcinoma cell line(PANC-1) cells apoptosis and Bcl-2 and Bax expression induced by Yin Chen Hao Decoction(YCHD).METHODS: The cell growth inhibitory rate was determined by MTT assay. Apoptosis of PANC-1 cells before and after treatment with YCHD was determined by TUNEL staining. Expression of the apoptosisassociated genes, Bcl-2 and Bax, was detected by immunohistochemical staining and reverse transcription-PCR.RESULTS: YCHD inhibited the growth of PANC-1 cells. Following treatment with YCHD for 24-96 h, the apoptotic rate of PANC-1 cells increased with time. In addition, the positive rate of Bcl-2 protein expression decreased in a time-dependent manner, whereas the positive rate of Bax protein expression increased in a time-dependent manner. Following treatment of with YCHD for 24-96 h, expression of BAX m RNA increased gradually and BCL-2 m RNA reduced gradually with time.CONCLUSION: YCHD induces apoptosis of PANC-1 cells mediated in part via up-regulation of BAX and down-regulation of BCL-2.
AIM: To evaluate human pancreatic carcinoma cell line (PANC-1) cells apoptosis and Bcl-2 and Bax expression induced by Yin Chen Hao Decoction (YCHD) .METHODS: The cell growth inhibitory rate was determined by MTT assay. Apoptosis of PANC- 1 cells before and after treatment with YCHD was determined by TUNEL staining. Expression of the apoptosisassociated genes, Bcl-2 and Bax, was detected by immunohistochemical staining and reverse transcription-PCR.RESULTS: YCHD inhibited the growth of PANC-1 cells. Following treatment with YCHD for 24-96 h, the apoptotic rate of PANC-1 cells increased with time. In addition, the positive rate of Bcl-2 protein expression decreased in a time-dependent manner, and the positive rate of Bax protein expression increased following treatment of with YCHD for 24-96 h, expression of BAX m RNA increased gradually and BCL-2 m RNA reduced gradually with time. CONCLUSION: YCHD induces apoptosis of PANC-1 cells mediated in part via up-regu lation of BAX and down-regulation of BCL-2.