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作 者:李晨光[1] 周泉[1] 唐占英[1] 施杞[1] 王拥军[1]
机构地区:[1]上海中医药大学附属龙华医院上海中医药大学脊柱病研究所,200032
出 处:《中国药物与临床》2008年第9期689-692,共4页Chinese Remedies & Clinics
基 金:国家自然科学基金资助重点项目(30330700);国家杰出青年科学基金资助项目(30625043);上海市中医药研究重点项目(03DZ19511);上海市医学重点学科建设项目(05Ⅲ027);上海市重点学科建设项目(T0303)
摘 要:目的探讨复方芪灵片对腰椎间盘突出症动物模型的抗炎镇痛作用及其机理。方法利用硅胶片模拟椎间盘突出,通过压迫腰5神经根,建立大鼠腰椎间盘突出症动物模型,并运用酶联免疫吸附试验(ELISA)研究复方芪灵片的抗炎镇痛作用。结果与正常对照组比较,模型组大鼠表现为运动功能障碍,功能不良评分升高(P<0.01);压迫区神经根组织内磷脂酶(PL)A2、前列腺素(PG)E2、血栓素(TX)B2含量增高(P<0.01),TXB2/6-K-PGFIα比例失衡性增高(P<0.01)。复方芪灵片治疗组与模型组相比,大鼠左下肢运动功能分级和站立姿势与跛行步态明显改善(P<0.01)。神经根压迫区炎性介质PLA2、PGE2、TXB2的含量降低(P<0.01),TXB2/6-K-PGFIα比例下降(P<0.01)。结论单纯的机械性卡压可以刺激压迫区神经根组织内产生大量的致炎因子PLA2、PGE2、TXB2,6-K-PGFIα活性降低。复方芪灵片可以有效减少神经根压迫区炎性介质PLA2、PGE2和TXB2的含量,维持TXB2/6-K-PIα的平衡,调节两者的比例,保护血管内皮细胞功能。Objective To explore the anti-inflammatory and analgesic mechanism of Composite Qi-ling Tablets (developed from the "Yi-Qi Hua-Yu Bu-Shen Remedy") in established animal model of lumbar disc herniation. Methods The animal model was. established using silica gel to simulate the intervertebral disc herniation and thereby causing artificial compression of L5 roots. The anti-inflammatory and analgesic mechanism of Composite Qi-ling Tablets was assessed with ELISA. Results Compared with normal controls, rats with lumbar intervertebral disc protrusion presented with locomotive disorders and elevated malfunction scores (P〈0.01). Increased levels of PLA2, PGE2 and TXB2, and imbalanced TXB2/6-K-P were found in compressed nerve tissues (both P〈0.01). Compared with the untreated model group, locomotive dysfunction was significantly improved with Composite Qi-ling Tablets in terms of standing posture, claudication and function score of the left lower llmb. The decreased contents of PLA2, PGE2 and TXB2 (P〈0.01) and imbalance of TXB2/6-K-P resumed to normal (P〈0.01). Conclusion Silica gel compression of the L5 nerve root can lead to massive release of inflammatory mediators, such as PLA2, PGE2, TXB2 and imbalance of TXB2/6-K-P. Yi-Qi Hua-Yu Bu-Shen Remedy appeared to relieve the locomotive dysfunction among animal models of lumbar intervertebral disc protrusion through effective reduction of inflammatory mediators and regulation of TXB2/ 6-K-P balance.
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