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机构地区:[1]新乡医学院第一附属医院急诊科 [2]新乡医学院第三附属医院神经内科 [3]新乡医学院第一附属医院小儿外科,卫辉453100
出 处:《天然产物研究与开发》2014年第9期1483-1487,共5页Natural Product Research and Development
摘 要:本研究探讨百里醌对胶原诱导大鼠关节炎(RA)模型的抗氧化和抗炎机理。实验采用60只Wistar大鼠随机分为6组,分别为正常对照组、模型对照组、阳性对照组、百里醌低、中和高剂量组,每组10只。除正常对照组外,采用II型胶原(CIA)诱导大鼠RA模型。阳性对照组灌胃给予8 mg/kg吲哚美辛,百里醌各剂量组分别给予低(10 mg/kg)、中(25 mg/kg)和高(50 mg/kg)三种剂量的百里醌灌胃,其余各组给予等体积的生理盐水,连续21日。足趾容积法测定大鼠关节继发性肿胀程度。测定机体关节组织中氧化损伤与抗氧化指标髓过氧化物酶(MPO)、丙二醛(MDA)、超氧化物歧化酶(SOD)和一氧化氮(NO)。ELISA法测定血清炎症因子白介素-1β(IL-1β)、肿瘤坏死因子α(TNF-α)和IL-6的水平。结果发现25 mg/kg和50 mg/kg的百里醌有效缓解II型胶原引起的足趾肿胀,降低RA发病中MPO、MDA和NO的含量,升高组织中SOD的水平,与模型对照组相比,差异具有显著性(P<0.05)。此外,百里醌可以显著降低RA大鼠血清IL-1β和TNF-α的含量,促进IL-10表达(P<0.05)。综上,百里醌可以有效缓解RA的症状,其机制与维持机体氧化-抗氧化体系的平衡和对抗前炎症因子导致的组织破坏相关。This study aimed to evaluate mechanisms concerning the antioxidant and antiarthritic effects of thymoquinone on collagen-induced rat arthritis (RA) model. Sixty Wistar rats were randomly divided into a normal control group, a model control group, a pasitive control group, a low-dose, a medium-dose and a high-dose thymoquinone group (n = 10). RA model,except for the normal control group,was established by being induced by type II collagen. For 21 continuous days,the three thymoquinone groups were intragastrically administered with low-dose (10 mg/kg),medium-dose (25 mg/kg) and high-dose (50 mg/kg) thymoqninone,the positive control group was intragastrically administered with 8 mg/kg indometacin,and other groups were intragastrically administered with same volume of normal saline. Secondary joint swelling of the rats was determined by a paw volume method. Biochemical indices for oxidative damage, including levels of myeloperoxidase ( MPO ), malondialdehyde ( MDA ), superoxide dismntase (SOD) and nitric oxide (NO), were detected. ELISA assay was used to measure the levels of serum intlarmnatory cytokine interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and IL-10. The results showed that 25 mg/kg and 50 mg/kg of thymoquinone remarkably re- lieved type II collagen-induced articular swelling, decreased the levels of MPO, MDA and NO, and increased the SOD ac- tivity, being significantly different from those of the model control group (P 〈 0.05). In addition, thymoqninone signifi- cantly lowered the contents of IL-1β and TNF-α in serum and promoted the expression of IL-10 (P 〈0.05). In conclu- sion, thymoquinone managed to effectively mitigate RA with the mechanism related to the maintained balance between oxidation and antioxidation as well as the suppressed tissue lesions caused by proinflammatory eytokines.
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