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出 处:《安徽医科大学学报》2017年第10期1504-1507,1512,共5页Acta Universitatis Medicinalis Anhui
基 金:安徽省自然科学基金(编号:06043095);安徽省科技攻关计划项目(编号:07010300179)
摘 要:目的观察尿酸盐结晶(MSU)诱导家兔急性尿酸性关节炎(UA)与环氧化酶-2(COX-2)关系及鸡矢藤提取物(EPS)的干预作用。方法采用注射无菌MSU液诱导制备家兔急性UA模型,检测指标:家兔膝关节肿胀度;关节灌洗液中性粒细胞数量及关节腔灌洗液前列腺素E2(PGE2)含量;关节滑膜组织病理组织学;RT-PCR法检测滑膜组织COX-2 mRNA表达。EPS采用灌胃给药,连续1周,观察药物的干预作用。结果 UA模型家兔关节明显肿胀,滑膜组织内可见大量炎性细胞浸润,伴有增生样改变,关节灌洗液内PGE2含量升高,滑膜组织COX-2 mRNA表达上调(P<0.01);EPS能显著有效地改善UA家兔关节的炎性肿胀程度,降低组织炎性细胞浸润,改善滑膜增生样改变,降低关节灌洗液中PGE2的生成,下调滑膜组织COX-2 mRNA的表达(P<0.01,P<0.05)。结论 MSU可激活COX-2表达,引发PGE2含量升高与组织炎症,促进家兔急性UA模型形成;EPS可抑制滑膜细胞COX-2 mRNA表达,减少滑膜液PGE2生成,减轻炎性细胞浸润,显示对家兔急性UA干预作用良好。Objective To study the role of cyclooxygenase (COX) -2 on monosodium urate induced acute urate ar- thritis (UA) in rabbits and the intervention effect of extracts of paederia scandens(EPS). Methods UA model was prepared by injecting monosodium urate crystals(MSU) into rabbit's joint. Joint sizes were measured with ver- nier caliper at different time, leukocyte infiltration in synovial fluids were analyzed. HEstaining was used to study the histopathology of articular synovial tissue, prostaglandin E2 ( PGE2 ) level was measured by ultraviolet spectro- photometry, COX-2 mRNA levels were monitored by RT-PCR. Treatment groups received different doses of EPS daily for 7 days. Results Joints of UA rabbit showed significant swelling, synovial membrane tissue presented in- flammatory cell infiltration, hyperplasia like change, PGE2 content in the joint effusion increased and the mRNA ex- pression of COX-2 up-regulated( P 〈 0.01 ). Intervention of EPS significantly inhibited joint swelling of rabbits, improved the histopathologic changes, reduced the content of PGE2 in synovial fluid, and suppressed the COX-2 mRNA expression in synovium of UA rabbits (P 〈 0.01, P 〈 O. 05 ). Conclusion MSU could activate the expres- sion of COX-2 mRNA, increase the content of PGE= and inflammation, and promote the formation of acute UA mod- el in rabbits. EPS possess anti-uarthritis effects, its mechanism may be related to the inhibition of leukocyte infiltra- tion, reducing the content of PGE2, down-regulating the mRNA expression for COX-2 in UA joints, thus reducing COX-2-mediated inflammatory injury.
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