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Objective : To investigate the yellow inducing protection Aβ 25-35 -induced PC12 cell damage and its role in the regulation of apoptosis gene . Methods : PC12 cells in vitro culture divided into six groups : blank control group , model control group the , VitE control group , Dihuangyinzi low dose group , Dihuangyinzi middle dose group , Dihuangyinzi high dose group . To absorb the culture medium until the cells enter logarithmic growth phase , blank culture medium were added to 10% , normal CSF 10% of VitE cerebrospinal fluid of 10% , 5% of the low dose of Chinese medicine cerebrospinal fluid , in doses of 10 % , 20% of the high dose . Canadian culture medium to make up to the same amount , 37 ℃ incubated for 2h . Then the blank group outside group joined by the aging treatment Aβ 25-35 ( final concentration of 10 μmol / L ) , to establish a cellular model of AD . The blank group, an equal volume of culture solution, incubation was continued 24h . And then to collect the culture medium, the cells were centrifuged . MTT assay and LDH detection cell viability was culture medium ; centrifugal resulting cells extracted total RNA , and the application of the two-step RT-PCR and agarose gel electrophoresis methods of Bax , Bcl -2 and Caspase-3 gene expression . Results: Dihuangyinzi elevated MTT metabolic rate , lower LDH release cut of Bax , caspase -3 gene expression , raised the Bcl-2 gene expression . Conclusion: one aging Aβ 25-35 -induced AD cell model , cultured 24h , MTT metabolism decreased LDH release in the culture medium increased cell survival activity was reduced . Second, Dihuangyinzi enhanced MTT metabolism , reduce LDH release , thus improving Aβ 25-35 injury PC12 cell survival of the state , to improve the vitality of cell survival . Third , RT-PCR results showed that , of Dihuangyinzi upregulated Bcl-2 and Bax ratio , reducing Caspase-3 mRNA expression may play the role of prevention and treatment of AD, through the regulation of apoptosis gene expression .
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