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作 者:陈孜[1] 胡剑卓[2] 邱细敏[3] 程梦婕[1]
机构地区:[1]湖南中医药大学,湖南长沙410208 [2]湖南中医药大学第二附属医院,湖南长沙410005 [3]湖南师范大学医学院,湖南长沙410006
出 处:《湖南中医杂志》2017年第12期134-136,共3页Hunan Journal of Traditional Chinese Medicine
基 金:湖南省发改委项目(湘发改高技[2012]1493号);湖南省中医药管理局科研项目(编号:2013146);湖南省科技厅科研专项项目(编号:2014SK4040);湖南省长沙市科技管理局项目(编号:K1401010-31)
摘 要:目的:研究人工虫草多糖对环磷酰胺(CTX)所诱导的免疫抑制小鼠的免疫调节作用。方法:将50只昆明小鼠分为空白组、模型组和人工虫草多糖高、中、低剂量组。采取腹腔注射环磷酰胺诱导造模方式,连续灌胃给药20d。观察各组体质量等一般情况的变化,末次给药后检测脾脏组织中乳酸脱氢酶(LDH)和酸性磷酸酶(ACP)的活性、腹腔巨噬细胞吞噬功能、胸腺及脾脏指数、血清溶血素及小鼠血清细胞因子IL-2、TNF-α含量的变化。结果:与模型组比较,人工虫草多糖各剂量组一般情况均有不同程度的改善,中、高剂量组LDH和ACP活性提高,腹腔巨噬细胞的吞噬指数及胸腺、脾脏指数提升(P<0.01),血清溶血素水平及血清IL-2、TNF-α含量均有所提高(P<0.05)。结论:人工虫草多糖能够拮抗环磷酰胺的免疫抑制作用,进而有效提高机体免疫功能。Objective:To investigate the immunoregulatory effect of polysaccharides from cultured Cordyceps sinensison mice with immunosuppression induced by cyclophosphamide(CTX).Methods:A total of 50 Kunming mice were divided into blank group,model group,and high-,medium-,and low-dose polysaccharide groups.The model was established by intraperitoneal injection of CTX,and the drug was given by gavage for 20 consecutive days.The changes in general conditions including body weight were observed,and the activities of lactate dehydrogenase(LDH) and acid phosphatase(ACP) in the liver tissue were measured after the last administration,as well as the changes in phagocytosis of abdominal macrophages,thymus and spleen indices,and serum levels of hemolysin,interleukin-2(IL-2),and tumor necrosis factor-α(TNF-α).Results:Compared with the model group,the high-,medium-,and low-dose polysaccharide groups had varying degrees of improvements in general conditions;the medium-and high-dose polysaccharide groups had significant increases in the activities of LDH and ACP,phagocytic index of abdominal macrophages,and thymus and spleen indices(P0.01),as well as significant increases in the serum levels of hemolysin,IL-2,and TNF-α(P0.05).Conclusion:Polysaccharides from cultured Cordyceps sinensis have an antagonistic effect on immunosuppression induced by CTX and thus effectively improve immune function.
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