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英文作者:Bao Jiewei1 Shi Fengfei2 Qiu Quanhe1 Xiao Weiping1 Yang Wenlong1 Liu Xiang1
单位:1江西中医药大学附属医院脊柱二科,南昌330006;2江西中医药大学附属医院康复科,南昌330006
英文单位:1The Second Department of Spine the Affiliated Hospital of Jiangxi University of Chinese Medicine Nanchang 330006 China; 2Department of Rehabilitation the Affiliated Hospital of Jiangxi University of Chinese Medicine Nanchang 330006 China
关键词:腰椎间盘退变;电针;炎症因子
英文关键词:Lumbardiscdegeneration;Electroacupuncture;Inflammatoryfactor
目的 探讨电针委中穴、夹脊穴对大鼠腰椎间盘退变(LDD)模型椎间盘组织中炎症因子表达的影响。方法 采用随机数字表法将30只清洁级健康雄性SD大鼠分为对照组、模型组和电针组,各10只,采用纤维环穿刺法将模型组、电针组大鼠建立LDD模型。电针组从造模后第4周开始电针委中穴、夹脊穴治疗,连续14 d,对照组和模型组不做任何干预。治疗结束后取出腰椎间盘组织,检测白细胞介素1β(IL-1β)、肿瘤坏死因子α(TNF-α)表达水平及基质金属蛋白酶3(MMP-3)、基质金属蛋白酶抑制因子1(TIMP-1)的mRNA和蛋白表达水平。结果 模型组的髓核细胞大小随着细胞核聚集而变小,并被蛋白多糖基质的密集区域隔开;电针组干预后髓核细胞大小趋于正常,核细胞簇现象减少,蛋白多糖基质的密集区域减轻。模型组IL-1β、TNF-α表达水平均高于对照组[(0.457±0.006)μg/L比(0.231±0.001)μg/L、(0.147±0.001)μg/L比(0.119±0.004)μg/L],而电针组[(0.347±0.007)μg/L、(0.138±0.001)μg/L]均低于模型组(均P<0.05)。模型组MMP-3 mRNA和蛋白表达水平高于对照组,而电针组均低于模型组;模型组TIMP-1 mRNA和蛋白表达水平低于对照组,而电针组均高于模型组(均P<0.05)。结论 电针可下调椎间盘组织炎症因子IL-1β、TNF-α、MMP-3表达水平,上调 TIMP-1的水平,缓解LDD。
Objective To observe the effect of electroacupuncture(EA)at Weizhong (BL40) and Jiaji (EX-B2) on the expression of inflammation factors in the rat model of lumbar disc degeneration (LDD). Methods A total of 30 clean healthy male SD rats were randomly divided into control group, model group and EA group, with 10 rats in each group. Rats in model group and EA group were established the LDD model by puncturing the annulus. Four weeks after modeling, EA group was treated with EA stimulation to Weizhong (BL40) and Jiaji (EX-B2) for 14 d, and the control group and model group were not given intervention. After the treatment, intervertebral disc tissue was isolated to detect expression levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), mRNA and proteins of matrix metalloproteinase-3 (MMP-3) and tissue inhibitor of metalloproteinase-1 (TIMP-1). Results The size of the nucleus pulposus (NP) cells decreased with nucleus clustering, and NP cells were separated by dense areas of proteoglycan matrix in the model group; after intervention, the size of NP cells tended to be normal, the phenomenon of nucleus clusters reduced, and the dense area of proteoglycan matrix became smaller in EA group. The expression levels of IL-1β and TNF-α in model group were higher than those in the control group [(0.457±0.006)μg/L vs (0.231±0.001)μg/L,(0.147±0.001)μg/L vs (0.119±0.004)μg/L], while the levels in the EA group [(0.347±0.007)μg/L,(0.138±0.001)μg/L] were lower than those in the model group (all P<0.05). The expression levels of MMP-3 mRNA and protein in the model group were higher than those in the control group, and the levels in the EA group were lower than those in the model group; the expression levels of TIMP-1 mRNA and protein in the model group were lower than those in the control group, and the levels in the EA group were higher than those in the model group (all P<0.05). Conclusion EA can down-regulate the expression levels of inflammatory factors of IL-1β, TNF-α and MMP-3, up-regulat the level of TIMP-1 and relieve LDD.
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