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作 者:张乃哲[1] 陈兴[2] 张敬一[1] 赵会军[1] 付琳杰[1]
机构地区:[1]河北省医学科学院实验医学研究所,石家庄050021 [2]白求恩国际和平医院检验科
出 处:《中国实验动物学报》2000年第4期203-206,共4页Acta Laboratorium Animalis Scientia Sinica
摘 要:目的探讨大鼠实验性肝癌发病中刺五加对肌体免疫功能和抗氧化酶活性的影响。方法46只SD雄性大鼠被随机分成对照组(喂普通饲料)、3-甲基4-双甲氨基偶氮苯(3-Me-DAB)组(喂含0.06%3Me-DAB饲料 10周)和刺五加组(饲喂同 3-Me-DAB外、另加入刺五加 4.5g/kg饲料,用常规方法检测全血谷光甘肽过氧化物酶(GSH-PX)、血清超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量,用微量化学发光造检测吞噬细胞活性(PMN-CL)。结果1.PMN-CL检测峰值、积分值和吞噬细胞指数,3-MeDAB组较正常组和刺五加组均有显著升高(P<0.05和P<0.01)2.全血GSH-PX活性、SOD活性,刺五加组较3-MeDAB组均有显著升高(P<0.05)。MDA含量刺五加组和3-MeDAB组均较正常组升高(均P<0.05)。结论刺五加在大鼠实验性肝癌诱发过程中有提高抗氧化酶活性和对抗致癌剂引起的机体中性粒细胞吞噬功能代偿性增高的作用。Objective To study the effect of Acanthopanax Senticosus (APS) on the immune function and the activity of glutathione peroxidase (GSH-PX) and superoxide dismutase (SOD) during 3-MeDAB hepatocarcinogenesis of rats. Methods 46 male SD rats were divided into three groups randomly: control group received the basal diet, 3-MeDAB group received 0.06% 3-MeDAB in the diet for 10 consecutive weeks, then changed to basal diet, APS group received 0.06% 3-MeDAB along with APS (4.5 g/kg diet) daily in food for 10 weeks, then changed to basal diet along with the same dose of APS till the end of experiment. Phagocytic function of leucocyte was detected by chemiluminescence and the activity of GSH-PX and SOD by method of DTNB and xanthine oxidase. Results Peak/103 PMN and integral (CL 60 min) of 3-MeDAB group were higher than that of control group (P<0.05) and APS group (p<0.01). Phagocytic index/109 WBC of 3-MeDAB group was higher than that of APS group (P<0.05). GSH-PX activity in blood of APS group was higher than that of 3-MeDAB group (P<0.05) and was similar to control group. SOD activity in serum of APS group was higher than both control group (p<0.01) and 3-MeDAB group (P<0.05). MDA content in serum of control was lower than both APS group and 3-MeDAB group. Conclusions The effect of APS against cancer and its immunoregulatory function are evidenced through improving the activity of GSH-PX and SOD and depressing the lipid peroxidation and resisting the compensable increase of phagocytic function of leucocyte duing the hepatocarcinogenesis of rats.
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