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Effect of PNS on expression of apoptosis-relating mRNA and protein in impaired CNC caused by hypoxia/re-oxygenation
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DOI   10.11656/j.issn.1673-9043.2010.01.09
Key Words   PNS apoptosis;Bax;Bcl-2;caspase-3;mRNA;protein
Author NameAffiliation
KANG Li-yuan Tianjin University of Traditional Chinese Medicine, Tianjin300193, China 
ZHOU Zhi-huan Tianjin University of Traditional Chinese Medicine, Tianjin300193, China 
ZHANG Meng Tianjin University of Traditional Chinese Medicine, Tianjin300193, China 
柴丽娟 Tianjin University of Traditional Chinese Medicine, Tianjin300193, China 
高秀梅 Tianjin University of Traditional Chinese Medicine, Tianjin300193, China 
王怡 Tianjin University of Traditional Chinese Medicine, Tianjin300193, China 
郭红 Tianjin University of Traditional Chinese Medicine, Tianjin300193, China 
闫晨 Tianjin University of Traditional Chinese Medicine, Tianjin300193, China 
Abstract
    [Objective] In order to research the protective effect of PNS against apoptosis, we observed the effects of PNS on the mRNA expression of Bcl-2, Bax, caspase-3 and caspase-3 activity in impaired CNC model caused by hypoxia/re-oxygenation.[Methods] We cultured cortical neuronal cell (CNC) of rat in vitro and established an impaired cell model by hypoxia/re-oxygenation (H/R). We treated the impaired cells with three dosages, 50 mg/L, 10 mg/L, 2 mg/L of PNS, and studied the mRNA expression of Bcl-2, Bax, caspase-3 by the method of real time RT-PCR. We studied the protein activity of caspase-3 by the method of Lowrry.[Results] 50 mg/L, 10 mg/L of PNS decreased the expression of Bax significantly compared with H/R group. 50 mg/L of PNS increased the expression of Bcl-2 significantly compared with H/R group. H/R group had a tendency of up-regulating and PNS group had a tendency of down-regulating the expression of caspase-3. These three dosages of PNS inhibited the protein activity of caspase-3 with a tendency of dose -dependent manner.[Conclusion] The possible protective mechanism of PNS against apoptosis may be by decreasing the expression of Bax, increasing the expression of Bcl-2 and inhibiting the protein activity of caspase-3.

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