铁皮石斛多糖对MPP+诱导的PC12细胞损伤的抑制作用

摘要

Objective To investigate the inhibitory effect of polysaccharides from candidum dendrobium on the inju-ry induced by 1-methyl-4-phenylpyridinium ( MPP+) in PC12 cells. Methods The PC12 cells were divided into con-trol,injury model and polysaccharides from candidum dendrobium (50,100,200 and 400μg/mL) group. The cells were in-cubated with 10μmol/L MPP+ for 24 h to induce the injury in injury model group. After the cells were pretreated with poly-saccharides from candidum dendrobium (50,100,200 and 400 μg/mL) for 2 hours,cells were incubated with 10 μmol/L MPP+ for 24 h in polysaccharides from candidum dendrobium group. The cells were incubated with the same volume of sa-line in control group. MTT assay was used to detect the survival rate of cells. The level of lactate dehydrogenase ( LDH) in the medium,the level of malondialdehyde ( MDA) in the cells and the activity of superoxide dismutase ( SOD) in the cells were measured. Results Compared with the control group,the survival rate of cells was singificantly decreased,the level of LDH in the medium and MDA in the cells were singificantly increased,the activity of SOD in the cells was singificantly decreased in the injury model group. Compared with the injury model group,the survival rate of cells was singificantly in-creased,the level of LDH in the medium and MDA in the cells were singificantly decreased,the activity of SOD in the cells was singificantly increased in the polysaccharides from candidum dendrobium (200 and 400 μg/mL) group. Conclusion Polysaccharides from candidum dendrobium inhibits the injury induced by MPP+ in PC12 cells,of which the mechanism may be related to the inhibition of oxidative stress induced by polysaccharides from candidum dendrobium.%目的：观察铁皮石斛多糖对1-甲基-4-苯基吡啶离子( MPP+)所致PC12细胞损伤的抑制作用及可能机制。方法实验分为对照组、MPP+损伤模型组、铁皮石斛多糖组(50、100、200和400μg/mL)。 MPP+损伤模型组细胞用含10μmol/L MPP+的培养基处理细胞24 h；铁皮石斛多糖组细胞用含50、100、200和400μg/mL铁皮石斛多糖的培养基预处理2 h后,再加入MPP+(10μmol/L)处理细胞24 h；对照组细胞给予等量生理盐水处理。 MTT比色法检测细胞存活率,检测细胞内丙二醛( MDA)含量和超氧化物歧化酶( SOD)的活性。结果与对照组比较,MPP+处理显著降低了PC12细胞的存活率,显著升高了细胞培养液中LDH的水平和细胞中MDA的含量,显著降低了细胞中SOD的活性(均P<0.05)；与损伤模型组比较,200和400μg/mL铁皮石斛多糖组PC12细胞的存活率显著升高,细胞培养液中LDH的活性和细胞中MDA的含量显著升高,细胞中SOD的活性显著降低(均P<0.05)。结论铁皮石斛多糖抑制了MPP+诱导的PC12细胞损伤,其机制可能与铁皮石斛多糖抑制氧化应激有关。