Protective Effect Of Chlorogenic Acid On Differentiated Chondrogenic MSCs Apoptosis Induced By Hypoxia

Backround and ObjectiveCartilage cells constitutes the basis of articular cartilage, because of its highly differentiated proliferative capacity caused regeneration ability of cartilage low after injury, make poor to natural repair cartilage. Stem cells and its origin chondrocyte transplantation therapy solves the problem of cartilage cells low proliferation force, has become clinically effective method of treatment of cartilage injury. In vitro oxygen environment study found the cultivation of articular cavity cell transplantation into similar oxygen in environment decreased activity and survival after, Wakitani transplanted cells that low survival rate of stem cells to differentiate the cartilage of making the thickness and mechanical strength, so all not as good as normal cartilage cell transplantation low survival was restricted factors of this method. Chlorogenic acid (chlorogenic acid, CGA outlets) for styrene-acrylic element class polar organic acid, strong antioxidant capacity inhibits oxidation emergency cause apoptosis. Chlorogenic acid inside cells to anoxic environment caused by ros change the role of apoptosis, is unclear. This experiment in vitro induced to bone marrow stromal cells for chondroid cells,0.1%O2 anoxic environment simulation of oxygen environment within articular cavity model, to observe the acid green anoxic environment for chondroid cells role, to investigate the influence of cartilage cells and the possible mechanism.Contents and methods of researchTo investigate the effect of chlorogenic acid on the injury of chondrocytes differentiated from rats marrow stromal cells induced by hypoxia in vitro and to explore its underlying mechanism. The chondrocytes differentiated from rats marrow stromal cells (5weeks'Rats) by 0.2mg·L-1 BMP-2 for 12days.This study was conducted as follows:(A)normal control group, (B)chlorogenic acid group,(C) hypoxia injury group,(D)chlorogenic acid and hypoxia injury group. Cell apoptosis were observed by Hoechst33258; Detection of reactive oxygen species; chondrocytes Bcl-2 gene and Caspase-3 changes were detected by RT-PCR. Results:Comparied with normal control group, hypoxia induced damage of differentiated Chondrogenic MSCs (P<0.05), Chlorogenic acid can disturb the damage of Differentiated Chondrogenic MSCs induced by hypoxia, It shows a reduction in the rate of apoptosis (P<0.05), decrease in reactive oxygen species, inhibit the gene expression of Caspase-3,increase the gene expression of Bcl-2.Conclusion:Chlorogenic acid can inhibit the apoptosis of chondrocytes differentiated from rats marrow stromal cells induced by hypoxia, and its mechanism may be related to protect mitochondrial membrance potential, increase the gene expression of Bcl-2 and inhibit the gene expression of Caspase-3.