PPARα通过抑制IL-17细胞因子的表达改善自身免疫性心肌炎

更新时间:2023-06-01 22:35:19 阅读: 评论:0

目录
1.中文摘要…………………………………………………………………………I
2.英文摘要………………………………………………………………………… II
3.主要缩略词……………………………………………………………………… IV
4.前言 (1)吃饭英文
5.材料与方法 (04)
个性美女头像6.实验结果 (18)
7.讨论 (27)
9.结论 (29)
10.参考文献(1) (30)
11.致谢 (33)
12.综述 (34)
13.参考文献(2) (41)
PPARα通过抑制IL-17细胞因子的表达改善自身免疫性心肌炎
【摘要】目的探讨PPARα在大鼠自身免疫性心肌炎(EAM)病程中的变化及其作用机制.方法将提纯精制后的猪心室肌球蛋白加等体积含灭活的结核杆菌的完全弗氏免疫佐剂充分混匀后,于Lewis大鼠双后足皮下注射制作大鼠EAM模型。首先体内试验,应用PPARα激动剂非诺贝特给予大鼠灌胃17天后,通过HE染色进行心脏病理评估心脏炎症;应用实时荧光定量PCR, 检测ANP,BNP,IL-17,IL-6,TGF-β,PPARαmRNA的表达; 应用WB技术检测PPARα蛋白的表达水平;ELASA技术,流式细胞技术分别检测血清中IL-17蛋白及CD4T细胞中IL-17的合成情况,其次是体外实验, 应用非诺贝特及PPARα阻断剂mk886以不同组合分别进行脾细胞培养后,再应用实时荧光定量PCR,ELASA技术检测IL-17炎性因子表达.结果在心肌炎急性期,即大鼠免疫2周后(第14天),心脏HE染色示心肌间大量炎症细胞浸润,心肌炎症相关的炎性因子,如ANP,BNP,IL-17,IL-6,TGF-β,基因及蛋白表达量在心肌炎时程中最高,而此时PPARα的表达量较低,这种趋势在EAM免疫第17天时最明显.而在心肌炎症3周(21天)时,上诉心肌炎症相关因子表达量下降,而此时PPARα的表达量上升并达整个病程中达高峰.给予EAM大鼠PPARα菲诺贝特灌胃治疗后,大鼠心肌炎症减轻,炎性因子表达减少, PPARα的表达增加;体外实验也证实了上诉作用.结论激活PPARα可抑制IL-17细胞因子分泌,从而改善自身免疫性心肌炎。
【关键词】PPARα;Th17细胞;IL-17 ;实验性自身免疫性心肌炎.
PPARα ameliorates experimental autoimmune myocarditis by inhibiting IL-17
cytokine expression
【Abstract】Objective This study was designed to explore the function and the effect of PPARα on EAM rats and the mechanism of it. Methods Experimental autoimmune myocarditis (EAM) rats were injected with porcine cardiac myosin and complete Freund's adjuvant in double feet. Fenofibrate(100/200 mg /kg/d) or vehic was administered orally from D0 to D17, while physiological saline was administered. orally from D0 to D17 On control group. On day 17, the verity of myocarditis was evaluated by hematoxylin and eosin (HE) staining. the mRNA expression of Atrium natriuretic peptide (ANP)and brain natriuretic peptide(BNP),Th17-type cytokines (IL-17) and the related cytokines(IL-6,TGF-β)were determined by Quantative RT-PCR, and the rum level of IL-17 were measured by ELISA.PPARαprotein determined by western blot and its Mrna determined by RT-PCR.In addition,CD4T cells isolated from rats spleen cutured with fenobrate(PPARαagonist) and mk886(a inhibitor of PPARα)in different combination. And detected the level of IL-17 by Quantative RT-PCR, ELISA and FASC. Results HW/BW and the relative expression of ANP、BNP started to ris
e on day 14(2W),prenting a highest level on day 21(3w). The relative expression of IL-17、IL-1 prented a higher leval on day 14the.HE staining showed that a large number of inflammatory cells infiltrated cardiac muscle tissues, which was the most rious stage on day 14 of the whole dia cour .At the same time, PPARa prent a lower level on day 14 but a higher level on day 21.The expression of ANP、BNP、HW/BW were elevated in EAM group but decresd in fenofibrate group on day 17. In addition, treatment with fenofibrate decread the expression of Th17-type cytokines (IL-17) and the related cytokines(IL-6,TGF-β).In cultured spleen cells, The IL-17 and its related cytokines prented a low level in the group cultured with fenobrate than the group cultured
with fenobrate and mk886.Conclusions Activiting PPARAαcan inhibiting IL-17 cytokine which ameliorates the experimental autoimmune myocarditis.
【Keywords】PPARα; TH17; IL-17; EAM
主要英文缩略词表
缩略词英文全称中文注释
EAM Experimantal autoimmune myocarditis 实验室自身免疫性心肌
ANP CFA BNP PPARs
GAPDH
DEPC PCR RT-PCR mRNA DNA cDNA COX2 IL ELISA Atrium natriuretic peptide
Complete freund's adjuvant
Brain natriuretic peptide
Peroxisome Proliferators
上水石
activation receptors
Glyceraldehyde-3-phosphate
Dehydrogenate
Diethyl pyrocarbonate
Polymera chain reaction残留的回忆
Rever transcription PCR
mesnger RNA
Deoxyribonucleic acid
Complementary Deoxyribonucleic acid
Cyclooxygena
Interlukin
Enzyme Linked Immunosorbent Assay
心房钠尿肽
完全免疫弗氏佐剂
脑钠尿肽
lol设置过氧化物酶体增生物活
化受体
甘油醛-3-磷酸脱氢酶
生日祝福语大全简短10个字
二乙基焦磷酰胺
聚合酶链反应
逆转录PCR
奢侈品代购利润信使RNA
脱氧核糖核酸
四大名注互补DNA
环氧合酶
白介素
酶联免疫吸附试验
FCM      Flow Cytometry                          流式细胞技术

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