安徽医药
安徽醫藥
안휘의약
ANHUI MEDICAL AND PHARMACEUTICAL JOURNAL
2015年
5期
850-854,855
,共6页
类风湿性关节炎%三氧化二砷%细胞因子%细胞凋亡
類風濕性關節炎%三氧化二砷%細胞因子%細胞凋亡
류풍습성관절염%삼양화이신%세포인자%세포조망
rheumatoid arthritis%arsenic trioxide%cytokine%apoptosis
目的:探讨三氧化二砷对鸡卵蛋白诱导日本大耳白兔致类风湿关节炎模型的滑膜组织核因子NF-κB(p65)表达活性及血清中白细胞介素-1(IL-1)、肿瘤坏死因子-α(TNF-α)水平的影响。方法48只日本大耳白兔随机分为模型组、正常对照组、三氧化二砷低剂量组(1.0 mg·kg-1·d-1)、三氧化二砷中剂量组(2.0 mg·kg-1·d-1)、三氧化二砷高剂量组(4.0 mg ·kg-1·d-1)、醋酸泼尼松龙组(10 mg·d-1),每组8只。成功建立卵蛋白诱导关节炎模型后,分别给药2周;采用酶联免疫吸附法(ELISA)检测兔外周血中的 IL-1、TNF-α,免疫组化实验方法检测核因子(NF-κB)(p65)在各组动物模型中的表达情况。结果卵蛋白诱导法可以成功诱导兔的关节炎,模型组外周血中的 IL-1、TNF-α含量较正常对照组升高(P<0.05);三氧化二砷各剂量组兔的关节炎症状有不同程度改善,IL-1、TNF-α含量较模型组降低(P<0.05);免疫组化结果显示,模型组关节滑膜的NF-κB(p65)表达较正常组增强(P<0.05),而三氧化二砷各剂量组关节滑膜的NF-κB(p65)表达随砷剂剂量的增加表达减弱,但仍然强于正常对照组(P<0.05)。结论三氧化二砷对实验性类风湿关节炎日本大耳白兔模型有治疗作用。其机制可能与抑制了滑膜细胞中NF-κB(p65)活性和表达,降低了炎性因子IL-1、TNF-α的水平有关。
目的:探討三氧化二砷對鷄卵蛋白誘導日本大耳白兔緻類風濕關節炎模型的滑膜組織覈因子NF-κB(p65)錶達活性及血清中白細胞介素-1(IL-1)、腫瘤壞死因子-α(TNF-α)水平的影響。方法48隻日本大耳白兔隨機分為模型組、正常對照組、三氧化二砷低劑量組(1.0 mg·kg-1·d-1)、三氧化二砷中劑量組(2.0 mg·kg-1·d-1)、三氧化二砷高劑量組(4.0 mg ·kg-1·d-1)、醋痠潑尼鬆龍組(10 mg·d-1),每組8隻。成功建立卵蛋白誘導關節炎模型後,分彆給藥2週;採用酶聯免疫吸附法(ELISA)檢測兔外週血中的 IL-1、TNF-α,免疫組化實驗方法檢測覈因子(NF-κB)(p65)在各組動物模型中的錶達情況。結果卵蛋白誘導法可以成功誘導兔的關節炎,模型組外週血中的 IL-1、TNF-α含量較正常對照組升高(P<0.05);三氧化二砷各劑量組兔的關節炎癥狀有不同程度改善,IL-1、TNF-α含量較模型組降低(P<0.05);免疫組化結果顯示,模型組關節滑膜的NF-κB(p65)錶達較正常組增彊(P<0.05),而三氧化二砷各劑量組關節滑膜的NF-κB(p65)錶達隨砷劑劑量的增加錶達減弱,但仍然彊于正常對照組(P<0.05)。結論三氧化二砷對實驗性類風濕關節炎日本大耳白兔模型有治療作用。其機製可能與抑製瞭滑膜細胞中NF-κB(p65)活性和錶達,降低瞭炎性因子IL-1、TNF-α的水平有關。
목적:탐토삼양화이신대계란단백유도일본대이백토치류풍습관절염모형적활막조직핵인자NF-κB(p65)표체활성급혈청중백세포개소-1(IL-1)、종류배사인자-α(TNF-α)수평적영향。방법48지일본대이백토수궤분위모형조、정상대조조、삼양화이신저제량조(1.0 mg·kg-1·d-1)、삼양화이신중제량조(2.0 mg·kg-1·d-1)、삼양화이신고제량조(4.0 mg ·kg-1·d-1)、작산발니송룡조(10 mg·d-1),매조8지。성공건립란단백유도관절염모형후,분별급약2주;채용매련면역흡부법(ELISA)검측토외주혈중적 IL-1、TNF-α,면역조화실험방법검측핵인자(NF-κB)(p65)재각조동물모형중적표체정황。결과란단백유도법가이성공유도토적관절염,모형조외주혈중적 IL-1、TNF-α함량교정상대조조승고(P<0.05);삼양화이신각제량조토적관절염증상유불동정도개선,IL-1、TNF-α함량교모형조강저(P<0.05);면역조화결과현시,모형조관절활막적NF-κB(p65)표체교정상조증강(P<0.05),이삼양화이신각제량조관절활막적NF-κB(p65)표체수신제제량적증가표체감약,단잉연강우정상대조조(P<0.05)。결론삼양화이신대실험성류풍습관절염일본대이백토모형유치료작용。기궤제가능여억제료활막세포중NF-κB(p65)활성화표체,강저료염성인자IL-1、TNF-α적수평유관。
Objective To observe the difference of transcription factor NF-κB (p65 )in the rabbit with rheumatoid arthritis(RA)mod-el induced by chicken ovalbumin as well as the level of IL-1 and TNF-αin the serum,and to explore the possible mechanism of treating RA with arsenic trioxide (ATO).Methods Forty-eight Japanese big-ear rabbits (JBRs)were randomized into 6 groups after the mod-els had been injected with ovalbumin successfully,which included the control group (group A,n=8),the model group (group B,n=8),low-dose ATO group (group C,1.0 mg·kg-1·d-1,n=8),medium-dose ATO group (group D,2.0 mg·kg-1·d-1,n=8), high-dose ATO group (group E,4.0 mg·kg-1 ·d-1 ,n=8)and prednisolone acetate group (group F,10 mg·d-1 ,n=8).Drugs were given for 2 weeks after the successful establishment of the rheumatoid arthritis model induced by chicken ovalbumin.ELISA and immunohistochemical experimental method were adopted to test the level of IL-1 and TNF-αin peripheral blood and the expressions of NF-κB(p65 )in various groups.Results Chicken ovalbumin could induce the arthritis in rabbits.Compared with the control group, the levels of IL-1 and TNF-αin peripheral blood in the model group increased(P<0.05).Symptoms of arthritis in different ATO groups were decreased and their levels of IL-1 and TNF-αwere lower than those in the model group (P<0.05).Immunohistochemical findings showed that the expression of NF-κB(p65 )in synovium of joint in the model group was greater than that in the control group (P<0.05).The expression of NF-κB(p65)in respective ATO groups decreased with the increased dose of ATO,yet still greater than that in the control group (P<0.05).Conclusions ATO has therapeutical effect on rheumatoid arthritis model of rabbits,the mecha-nism of which may be associated with the inhibition of NF-κB(p65 )in synovium of joint and decreasing levels of IL-1 and TNF-α.