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目的:观察姬松茸多糖对地塞米松(dexamethasone,DEX)诱发大鼠胸腺细胞凋亡和线粒体膜电位的影响。方法:Wistar大鼠随机分为4组:正常组,模型组,姬松茸多糖低、高剂量组,每组10只。正常组和模型组灌胃(ig)生理盐水,姬松茸多糖低、高剂量组ig姬松茸多糖溶液(60,120 mg.kg-1),1次/d,连续7 d。模型组和姬松茸多糖低、高剂量于第7日腹腔注射DEX(0.02 g.kg-1)。3 h后处死各组动物,迅速无菌取胸腺,采用显微观察、流式细胞技术观察胸腺细胞形态学改变,胸腺细胞凋亡、脱氧核糖核酸(DNA)断裂百分率及线粒体膜电位变化,胸腺组织超氧化物歧化酶(SOD)、丙二醛(MDA)的变化。结果:与模型组比较,姬松茸多糖组大鼠胸腺细胞线粒体嵴肿胀明显减轻;姬松茸多糖组大鼠胸腺细胞凋亡率[低、高剂量(5.96±1.14)%,(5.07±1.02)%],DNA断裂率[低、高剂量(3.67±0.49)%,(3.24±0.45)%]及胸腺组织MDA含量[低、高剂量(1.87±0.25),(1.72±0.23)μg.mg-1]均明显低于模型组[(7.14±1.62)%,(4.25±0.86)%,(2.16±0.38)μg.mg-1];姬松茸多糖组大鼠胸腺细胞线粒体膜电位(荧光指数:低剂量38.57±6.29,高剂量41.36±7.18)及胸腺组织SOD活性量[低、高剂量(25.78±3.94),(27.36±4.21)U.mg-1]明显高于模型组(32.76±5.48)荧光指数,(21.45±3.52)μg.mg-1。结论:姬松茸多糖可阻断胸腺细胞DNA断裂和线粒体膜电位的下降,有效抑制DEX诱导的胸腺细胞凋亡,其作用机制与姬松茸多糖提高胸腺组织抗氧化功能有关。
Objective: To observe the effect of Agaricus Blazei polysaccharide on dexamethasone (DEX) -induced thymocyte apoptosis and mitochondrial membrane potential in rats. Methods: Wistar rats were randomly divided into 4 groups: normal group, model group, Agaricus blazei polysaccharide low and high dose group, 10 rats in each group. The normal group and model group were given ig (ig) physiological saline, Agaricus blazei polysaccharide low and high dose group (60,120 mg.kg-1) once daily for 7 days. The model group and Agaricus blazei polysaccharide low and high dose on the 7th day of intraperitoneal injection of DEX (0.02 g.kg-1). After 3 h, all the animals were sacrificed and thymus was rapidly aseptically removed. Morphological changes of thymocytes, apoptosis of thymus cells, percentage of DNA cleavage and mitochondrial membrane potential were observed by microscopic observation and flow cytometry. Thymus The changes of superoxide dismutase (SOD) and malondialdehyde (MDA) were observed. Results: Compared with the model group, the mitochondrial cristae swelling of the thymus cells in the Agaricus blazei polysaccharide group was significantly reduced. The apoptosis rate of the thymus cells in the Agaricus blazei polysaccharide group [5.96 ± 1.14%, (5.07 ± 1.02)%, ], The rate of DNA breakage [low, high dose (3.67 ± 0.49)%, (3.24 ± 0.45)%] and thymus MDA content [low and high dose (1.87 ± 0.25) and (1.72 ± 0.23) μg.mg-1 ] Were significantly lower than those in model group [(7.14 ± 1.62)%, (4.25 ± 0.86)%, (2.16 ± 0.38) μg.mg-1], respectively. The mitochondrial membrane potential Dose of 38.57 ± 6.29, high dose of 41.36 ± 7.18) and thymic activity of SOD [low dose (25.78 ± 3.94), (27.36 ± 4.21) U.mg-1] were significantly higher than those in model group (32.76 ± 5.48) Index, (21.45 ± 3.52) μg.mg-1. Conclusion: Agaricus blazei polysaccharides can block DNA damage of thymus and decrease of mitochondrial membrane potential, and effectively inhibit the apoptosis of thymocytes induced by DEX. The mechanism of action is related to the anti-oxidation function of Agaricus Blazei polysaccharide in thymus tissue.