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艾灸预处理对大鼠应激性胃黏膜损伤的保护作用 被引量:22

Protective effect of moxibustion preconditioning on stress-induced gastric mucosal lesion in rats
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摘要 目的:探讨艾灸预处理对大鼠应激性胃黏膜损伤保护作用及抗炎症损伤机制。方法:将48只健康SD大鼠随机分为4组,即空白组、模型组、艾灸穴位组、艾灸非穴组。束缚冷应激法制作应激性胃黏膜损伤大鼠模型,按Guth法计算胃黏膜损伤指数(UI),光镜下观察大鼠胃黏膜组织学改变,放射免疫法测定血清IL-1β,TNF-α和IL-10的含量。结果:与艾灸非穴组比较,艾灸足三里、中脘等穴位可使应激性胃黏膜损伤大鼠UI明显下降(P<0.01)、血清IL-1β含量降低(P<0.05)、TNF-α含量降低(P<0.01)、IL-10含量升高(P<0.05)。结论:艾灸足三里、中脘等穴位预处理可促进束缚水浸应激所造成大鼠胃黏膜损伤的修复、减轻急性炎症反应,该保护作用可能是通过抑制细胞炎症反应的免疫促炎因子IL-1β、TNF-α和促进抗炎因子IL-10而达到其抗胃黏膜损伤作用。 Objective: To explore the protective effect of moxibustion preconditioning on the stress-induced gastric mucosal lesion in rats.Methods: 48 SD rats were randomly allocated to blank,model,acupoints moxibustion and non-acupoints moxibustion groups.After 8 days of pretreatment,the rats except those in blank group,received water restraint stress(WRS) to induce stress-induced gastric mucosal lesion.The ulcer index(UI) was evaluated by Guth method,histomorphologic changes in gastric mucosa were observed by light microscopy and serum contents of IL-1β,TNF-α and IL-10 was measured by radioimmunoassay.Results: Gastric mucosal ulcer index and serum contents of IL-1β and TNF-α decreased markedly(P0.05,P0.01) while IL-10 increased markedly(P0.05) in the acupoints moxibustion group compared with the model group and the non-acupoints moxibustion group.Conclusion: Moxibustion preconditioning at Zusanli,Zhongwan,and so on can repair gastric mucosal injury caused by WRS,alleviate acute inflammatory reaction and prevent gastric mucosa from inflammatory injury,which is closely related to its actions in suppressing proinflammatory factors(IL-1β,TNF-α) and promoting anti-inflammatory IL-10.
出处 《中华中医药杂志》 CAS CSCD 北大核心 2012年第1期58-62,共5页 China Journal of Traditional Chinese Medicine and Pharmacy
基金 国家重点基础研究发展计划(973计划)(No.2009CB522904) 国家自然科学基金项目(No.30973802 No.81173326) 湖南省研究生科研创新项目(No.CX2009B172)~~
关键词 艾灸预处理 应激性胃黏膜损伤 白细胞介素1Β 肿瘤坏死因子-Α 白细胞介素10 Moxibustion preconditioning Stress-induced gastric mucosal lesion Interleukin 1β Tumor necrosis factor-α Interleukin 10
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