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《雷公藤在大鼠1型糖尿病模型中對調(diào)節(jié)性T細胞Foxp3表達的影響及意義.doc》由會員上傳分享，免費在線閱讀，更多相關內(nèi)容在工程資料-天天文庫。
1、雷公藤在大鼠1型糖尿病模型中對調(diào)節(jié)性T細胞Foxp3表達的影響及意義【摘要】目的：研究雷公藤在大鼠1型糖尿病模型中對CD4+CD25+調(diào)節(jié)性T細胞(TJFoxp3基因表達的影響及意義。方法：將48只大鼠隨機分為3組，每組各16只，II、III組采用小劑量多次腹腔注射鏈腮佐菌素(STZ)的方法制備大鼠1型糖尿病模型，I組為正常對照。III組在成模后給與雷公藤多戒(GTT)灌胃，1次/d,連續(xù)3個月。淋巴細胞轉化試驗(MTT法)檢測脾淋巴細胞增殖活性；熒光定量PCR檢測外周血及脾淋巴細胞Foxp3mRNA的表達;免疫組化檢測淋
2、巴結和脾組織F0XP3蛋白的表達。結果：II、UI組血糖水平高于I組(P<O.01);胰島中III組淋巴細胞浸潤程度較II組減輕;II、III組淋巴細胞增殖活性均較I組升高(P<0.01),用藥后皿組較II組降低;Foxp3mRNA.FOXP3蛋白表達水平H、III組均高于I組(P<0.05),III組表達水平較II組有所升高，但差別無統(tǒng)計學意義(P>0.05)o結論：Foxp3+Tr細胞參與了STZ誘導的大鼠1型糖尿病的發(fā)生發(fā)展；上調(diào)Tr細胞Foxp3基因的表達可能為雷公藤治療1型糖尿病的機制之一
3、。【關鍵詞】CD4+CD25+調(diào)節(jié)性T細胞Foxp3雷公藤1型糖尿病[Abstract]ATM:ToinvestigatethesignificanceandeffectofGlucosidorumTripterygiitororum(GTT)ontheexpressionsofFoxp3inCD4+CD25+regulatoryTcells(Tr)intype1diabeticratmodel?METHODS:48ratsweredividedevenlyinto3groupsbyrandom.Diabeticmodel
4、wasdevelopedbymultiplelowdoseintraperitonealinjectionofstreptozotociningroupII,III,andgroupIwastreatedasnormalcontrol.Aftertheestablishmentofthemodel,administrationofGTTwasconductedingroupIII,whichwasperformedonceaday,lastingthreemonthes?Lymphocyteproliferationwas
5、detectedbylymphocytetransformationtest(MTTassay)?TheexpressionofFoxp3mRNAwasmeasuredinperipheralbloodandspleenbyusingrea1timePCR?TheexpressionofFoxp3proteininlymphoidnodeandspleenwasdetectedbyimmunohistochemistry.RESULTS:ThebloodglucoselevelingroupTT,ITTwasobvious
6、lyhigherthanthatofcontrolgroup(P&11;0.01),followedwithlymphocyteinfiltratinginpancreaticislets?Theinfi1tratingdegreeingroupITTwasdecreasedthanthatofgroupTI.TheproliferationofspleniclymphocyteingroupII,IIIwasevidentlyincreasedcomparingwiththecontrolgroup(P&It;0.01)
7、.AfteradministrationofGTT,theproliferationingroupIIIwaslowerthanthatingroupII.IngroupII,III,theexpressionsofFoxp3mRNAandproteinincreasedmarkedlycomparedwithcontrolgroup(P&It;0.05)?Moreover,thelevelingroupIIIwasespeciallyenhanced,butcomparedwithgroupII，therewasnosi
8、gnificantlydifferencc(P>0.05).CONCLUSION:Foxp3+Trmayinvolveinthepathogenesyoftype1diabetesindusedbySTZ.GTTdidhavetherapeuticaleffectontype1diabetes,p
