The Model Of Vascular Smooth Muscle Cells Cultured In Vitro Damaged By Aβ And Protective Effect Of Rifampicin

Part One The Model of Vascular Smooth Muscle Cells Cultured in Vitro Damaged by AβObjective: To establish an effective model of vascular smooth muscle cells cultured in vitro damaged by Aβ1-40. Methods: The cultured smooth muscle cells of the rat's carotid artery were observed in these present experiments. Matrigel was used to mimic the basement membrane of the blood vessels.The cells were divided into control group and experimental group,in the experimental groups the Aβ1-40 was deposited into the dishes before the experiment. Under the microscope we observed the morphologic changes of the cells. The viability of the VSMCs was evaluated by MTT assay and the growth curve. LDH efflux was used to show damage degree of the membrane. Results: Compared with the controlled group,The viability at various stages of the groups under Aβ1-40 treatment decreased,because the morphous of the cells changed worse,the LDH release rate increased and the living cells rate decreased . Conclusions: The model of vascular smooth muscle cells cultured in the analogic basement membrane in Vitro damaged by Aβ1-40 succeeded. Part Two The Protective Effect of Rifampicin on Vascular Smooth Muscle Cells and it's Relation with InflammationObjective: To observe the protective effect of Rifampicin on the vascular smooth muscle cells cultured in vitro damaged by Aβ1-40 and the relation with inflammation Methods: The cultured smooth muscle cells were divided into control group (no Aβ1-40) and Rifampicin treating group (with Aβ1-40) ,both group was was divided into 5 groups ( for the final concentrations of Rifampicin were 0,1,5,10 and 20 mg/mL). Under the microscope we observed their morphologic changes .The viability of the VSMC was evaluated by MTT assay. LDH efflux was used to show damage degree of the membrane. The levels of IL-6 and TNF-αin the cell culture supernatants were detected. Results: Compared with the controlled group,The viability of the groups treated by Rifampicin increased, for the morphous of the cells became better,the rate of dead cells and LDH release decreased. At the same time, the levels of IL-6 and TNF-αin the groups treated by Rifampicin were much fewer than the control group. Conclusions: Rifampicin can protect the vascular smooth muscle cells cultured in Vitro damaged by Aβ1-40 and this effect results from its capability of reduce the inflammatory reaction.