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Chinese Journal of Pathophysiology ; (12): 302-306, 2016.
Article in Chinese | WPRIM | ID: wpr-487121


AIM:To investigate the effect of heat shock protein 75 ( Hsp75 ) over-expression on Aβ-induced neurotoxicity in the neural stem cells and to explore its mechanism.METHODS:An adenovirus-mediated Hsp75 over-ex-pression vector was used in vitro.The mouse neural stem cell C17.2 was cultured in vitro and divided into control group, Aβgroup, negative adenovirus vector transfection group and Hsp75 over-expression adenovirus vector transfection group. The transfection and cellular immune identification were detected by fluorescence microscopy.The cell morphology was ob-served under inverted phase-contrast microscope.The cell viability and apoptosis were detected by MTT assay and flow cy-tometry, respectively.Hsp75 over-expression and cleaved caspase-3 protein level were measured by Western blot.RE-SULTS:Observation by fluorescence microscopy indicated that C17.2 cells were successfully transfected and Hsp75 gene was effectively expressed in the neural stem cells after transfection.In addition, the morphology and viability of the cells did not change and these cells did not differentiate after transfection.As compared with control group, the cell viability in Aβgroup and negative adenovirus vector transfection group was significantly decreased (P<0.05), and the cell apoptotic rate and cleaved caspase-3 level (P<0.05) were increased.As compared with Aβgroup and negative adenovirus vector transfection group, Hsp75 over-expression significantly increased the cell viability, and decreased the cell apoptosis and cleaved caspase-3 level ( P<0.05 ) .CONCLUSION: Hsp75 over-expression protects the neural stem cells against Aβ-induced injury.The mechanism may be related to inhibiting caspase-3 pathway-dependent apoptosis.

Basic & Clinical Medicine ; (12): 1303-1307, 2015.
Article in Chinese | WPRIM | ID: wpr-481333


Objective_To investigate the effects of hypoxia-inducible factor-1 alpha ( HIF-1α) inhibitor YC-1 on hy-poxia induced human pulmonary artery smooth muscle cells ( HPASMCs) proliferation, apoptosis and the expression of P53, and to explore the molecular mechanism in the processes.Methods_HPASMCs were cultured in DMEM me-dium supplemented with 10%FBS in vitro.Then divided them into four groups:normoxia, hypoxia and hypoxia+YC-1(0.01 and 0.05 mmol/L).Cell proliferation was measured by CCK-8 and apoptosis was detected by flow cytom-etry.The expressions of HIF-1αand P53 were tested by Western blot, and the mRNA expression of P53 was tested by RT-PCR.Results_Hypoxia can promote the proliferation of HPASMCs.Treatment of HPASMCs with different concentrations of YC-1 intervention for 24h obviously dropped proliferation rate (P<0.05), and the apoptosis rate increased significantly (P<0.05).YC-1 can also down-regulate the expression of HIF-1αand up-regulate the ex-pression of P53 significantly ( P<0.05 ) .Conclusions_YC-1 can inhibit hypoxia-induced HPASMCs proliferation and promote apoptosis, the mechanism is potentially related to the up-regulation of P53 expression.