CAJ | 학술논문

目的研究肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)与一氧化氮(nitric oxide,NO)在脑型疟(cerebral malaria,CM)发病中的作用. 方法首先建市C57BL/6J小鼠的CM动物模型.然后,取雌性(C57BL/6J 小鼠100只,随机分为:正常对照组,腹腔注射生理盐水;感染对照组,接种约氏疟原虫By265;CM模型组,腹腔注射感染们氏疟原虫K173;地塞米松处理组,于感染伯氏疟原虫K173前一天在饮水中加入地塞米松,浓度为10 ms/L;L-硝基精氰酸(L-NNA)处理组,从感染伯氏疟原虫K173当天开始每只每大腹腔注射25 g/L的L-NNA溶液0.2 ml.每组均为20只.CM 模型组鼠于CM发病时取脑组织,其他各组小鼠于感染后第10天取脑组织匀浆.观察脑组织TNF-α、NO及氧化氮合酶(nitric oxide synthase,NOS)在CM发病过程中的含量变化;同时观察TNF-α合成抑制剂地塞米松及NO合成抑制剂L-NNA对脑组织中TNF-α和NO浓度的影响. 结果 (1)CM模型组小鼠均发牛CM,地塞米松组、L-NNA 组及感染对照组小鼠至感染后第10天均末发生CM.(2)小鼠CM发病时脑组织TNF-α、NO、NOS均高于感染第5天(P＜0.01).(3)小鼠CM发病时和感染后第5天脑组织FNF-α、NO、NOS均高于感染对照组和止常对照组(P＜0.01).(4)地塞米松组小鼠感染后第10天、第5天与同时间CM模型组比较,脑组织TNF-α均明显下降(P＜0.01).(5)L-NNA组与CM模型组比较,脑组织NO、NOS均显著性降低(P＜0.01). 结论 (1)成功地建立起较理想的CM动物模型.(2)伯氏疟原虫感染小鼠给予地塞米松或L-NNA后,可有效地预防CM的发病.
목적 연구종류배사인자α(tumor necrosis factor-α,TNF-α)여일양화담(nitric oxide,NO)재뇌형학(cerebral malaria,CM)발병중적작용. 방법수선건시C57BL/6J소서적CM동물모형.연후,취자성(C57BL/6J 소서100지,수궤분위:정상대조조,복강주사생리염수;감염대조조,접충약씨학원충By265;CM모형조,복강주사감염문씨학원충K173;지새미송처리조,우감염백씨학원충K173전일천재음수중가입지새미송,농도위10 ms/L;L-초기정청산(L-NNA)처리조,종감염백씨학원충K173당천개시매지매대복강주사25 g/L적L-NNA용액0.2 ml.매조균위20지.CM 모형조서우CM발병시취뇌조직,기타각조소서우감염후제10천취뇌조직균장.관찰뇌조직TNF-α、NO급양화담합매(nitric oxide synthase,NOS)재CM발병과정중적함량변화;동시관찰TNF-α합성억제제지새미송급NO합성억제제L-NNA대뇌조직중TNF-α화NO농도적영향. 결과 (1)CM모형조소서균발우CM,지새미송조、L-NNA 조급감염대조조소서지감염후제10천균말발생CM.(2)소서CM발병시뇌조직TNF-α、NO、NOS균고우감염제5천(P＜0.01).(3)소서CM발병시화감염후제5천뇌조직FNF-α、NO、NOS균고우감염대조조화지상대조조(P＜0.01).(4)지새미송조소서감염후제10천、제5천여동시간CM모형조비교,뇌조직TNF-α균명현하강(P＜0.01).(5)L-NNA조여CM모형조비교,뇌조직NO、NOS균현저성강저(P＜0.01). 결론 (1)성공지건립기교이상적CM동물모형.(2)백씨학원충감염소서급여지새미송혹L-NNA후,가유효지예방CM적발병.
Objective To observe the role of tumor necrosis factor-α(TNF-α) and nitric oxide(NO)in pathogenesis of cerebral malaria(CM).Methods At first,C57BL/6J mice were used to be infected with Plasmodium berghei(P.berghei) K173 to establish CM animal model.Then 100 female C57 BL/6J mice were randomly divided into difierent groups,each group containe 20 mice.Normal control was injected intraperitoneally (ip) with saline,infeeted control wag,infeeted with Plasmodium yoelii,CM model group was infected with P.berghei.dexamethasone group was infeeted with P.berghei.Dexamethasone was added to the drinking water (10 mg/L) from the day before infection,N-nitro-L-arginine (L-NNA) group was infected with P.berghei.Infected mice were injected ip daily with 0.2 ml(25 g/L) L-NNA from the infeetion day.Mice of CM modeI group were killed when mice displayed the first sign of CM.other groups were killed on the 10th day after infeetion.TNF-α,NO and nitric oxide synthase (NOS) in brain tissue were measured.The influenees of dexamethasone and inhibitor of TNF-α and L-NNA,an inhibitor of NO on CM were observed.Results (1) All the mice infected with P.berghei developed CM.The P.berghei-infected mice treated with dexamethasone or treated with L-NNA did not develop CM till the 10th day after infeetion.(2)The level of TNF-α,NO and NOS in brain tissue from the mice developed CM were higher than those from the mice on the 5th day after infection (P＜0.01).(3) In the brain tissue levels of TNF-α,NO,NOS in the CM mice model group were markedly higher than those of infeetion control group and norlnal control group(P＜0.01).(4)In the brain tissue level of TNF-α in the mice of dexamethasone group was markedly lower than those in CM model group(P＜0.01).(5)In the brain tissue Ievels of NO,NOS in the mice of L-NNA group were markedly lower than those in CM model group(P＜0.01).Conclusions (1)C57BL/6L mice infected with P.berghei showed many similar characteristics with human CM.So CM animal model was established.(2)It WaS indicated that treatment with dexamethasone or L-NNA in P.berghei infeeted mice could prevent the development of CM.