中国免疫学杂志
中國免疫學雜誌
중국면역학잡지
CHINESE JOURNAL OF IMMUNOLOGY
2015年
9期
1169-1172
,共4页
晏现丽%张颖%郑立运%任凌燕%周雅丽%权松霞%邢国兰
晏現麗%張穎%鄭立運%任凌燕%週雅麗%權鬆霞%邢國蘭
안현려%장영%정립운%임릉연%주아려%권송하%형국란
IgA肾病%C3a%C5a%受体
IgA腎病%C3a%C5a%受體
IgA신병%C3a%C5a%수체
IgA nephropathy%C3a,C5a%Receptors
目的：探讨C3a、C5a及其受体在IgA肾病发病中作用及潜在机制。方法：6～8周清洁级雌性BALB／c小鼠28只，阴性对照组、野生型组、C3 a受体敲除组、C5 a受体敲除组各7只，采用有活性的仙台病毒滴鼻经鼻黏膜感染联合尾静脉注射建立小鼠IgA肾病模型，测定24 h尿蛋白量、血清尿素氮、血清肌酐；留取肾组织标本，通过直接免疫荧光法检测肾组织IgA、C3沉积；采用PAS染色光镜下观察肾组织病理改变；采用RT-qPCR法检测肾组织中TNF-α、TGF-β、IL-1β、IL-6、MCP-1 mRNA相对表达量。结果：15周后野生型组、C3a受体敲除组、C5a受体敲除组（实验组）24 h尿蛋白量高于阴性对照组，野生型组高于C3 a受体敲除组及C5 a受体敲除组，差异具有统计学意义；血清尿素氮及血清肌酐差异无统计学意义；实验组小鼠可见肾脏组织病理改变，且野生型组重于C3 a受体敲除组及C5 a受体敲除组，阴性对照组肾脏组织病理则无明显异常。实验组小鼠肾组织TNF-α、TGF-β、IL-1β、IL-6、MCP-1 mRNA相对表达量高于阴性对照组，同时野生型组高于C5a受体敲除组及C3a受体敲除组，另外IL-1β、IL-6、MCP-1的mRNA相对表达量C5a受体敲除组高于C3a受体敲除组。结论：C3a及C5a受体缺失可减轻IgA肾病肾损伤，并且C3a受体缺失作用更加显著。
目的：探討C3a、C5a及其受體在IgA腎病髮病中作用及潛在機製。方法：6～8週清潔級雌性BALB／c小鼠28隻，陰性對照組、野生型組、C3 a受體敲除組、C5 a受體敲除組各7隻，採用有活性的仙檯病毒滴鼻經鼻黏膜感染聯閤尾靜脈註射建立小鼠IgA腎病模型，測定24 h尿蛋白量、血清尿素氮、血清肌酐；留取腎組織標本，通過直接免疫熒光法檢測腎組織IgA、C3沉積；採用PAS染色光鏡下觀察腎組織病理改變；採用RT-qPCR法檢測腎組織中TNF-α、TGF-β、IL-1β、IL-6、MCP-1 mRNA相對錶達量。結果：15週後野生型組、C3a受體敲除組、C5a受體敲除組（實驗組）24 h尿蛋白量高于陰性對照組，野生型組高于C3 a受體敲除組及C5 a受體敲除組，差異具有統計學意義；血清尿素氮及血清肌酐差異無統計學意義；實驗組小鼠可見腎髒組織病理改變，且野生型組重于C3 a受體敲除組及C5 a受體敲除組，陰性對照組腎髒組織病理則無明顯異常。實驗組小鼠腎組織TNF-α、TGF-β、IL-1β、IL-6、MCP-1 mRNA相對錶達量高于陰性對照組，同時野生型組高于C5a受體敲除組及C3a受體敲除組，另外IL-1β、IL-6、MCP-1的mRNA相對錶達量C5a受體敲除組高于C3a受體敲除組。結論：C3a及C5a受體缺失可減輕IgA腎病腎損傷，併且C3a受體缺失作用更加顯著。
목적：탐토C3a、C5a급기수체재IgA신병발병중작용급잠재궤제。방법：6～8주청길급자성BALB／c소서28지，음성대조조、야생형조、C3 a수체고제조、C5 a수체고제조각7지，채용유활성적선태병독적비경비점막감염연합미정맥주사건립소서IgA신병모형，측정24 h뇨단백량、혈청뇨소담、혈청기항；류취신조직표본，통과직접면역형광법검측신조직IgA、C3침적；채용PAS염색광경하관찰신조직병리개변；채용RT-qPCR법검측신조직중TNF-α、TGF-β、IL-1β、IL-6、MCP-1 mRNA상대표체량。결과：15주후야생형조、C3a수체고제조、C5a수체고제조（실험조）24 h뇨단백량고우음성대조조，야생형조고우C3 a수체고제조급C5 a수체고제조，차이구유통계학의의；혈청뇨소담급혈청기항차이무통계학의의；실험조소서가견신장조직병리개변，차야생형조중우C3 a수체고제조급C5 a수체고제조，음성대조조신장조직병리칙무명현이상。실험조소서신조직TNF-α、TGF-β、IL-1β、IL-6、MCP-1 mRNA상대표체량고우음성대조조，동시야생형조고우C5a수체고제조급C3a수체고제조，령외IL-1β、IL-6、MCP-1적mRNA상대표체량C5a수체고제조고우C3a수체고제조。결론：C3a급C5a수체결실가감경IgA신병신손상，병차C3a수체결실작용경가현저。
Objective:To investigate the role of C3a,C5a and their receptors in the pathogenesis of IgA nephropathy (IgAN). Methods:A total of twenty-eight 6-8 weeks old female BALB/c mice were investigated.And they were negative control group , WT group,C3aR-/-group,C5aR-/-group(the latter three groups were named as experimental groups ),seven mice in each group.All the mice were infected through respiratory tract with infectious SV (experimental groups) or PBS(negative control group),combined with tail vein challenge to make IgAN animal model.Testing 24 h total urinary protein , serum urea nitrogen ( BUN ) and creatinine ( Cr ) , using direct immunofluorescence to test the renal deposition of IgA and C 3,observing renal pathologic lesion under PAS staining with light microscopy.RT-qPCR was used to test the relative mRNA expression of TNF-α,TGF-β,IL-1β,IL-6,MCP-1.Results: After 15 weeks,the level of UTP in experimental group was significantly higher than negative control group ,and the same results as WT group than C3aR-/-group and C5aR-/-group.There was no significant difference among groups for BUN and Cr.Combined with negative control group , experimental groups had significant renal pathological lesions , and the changes of WT group was more severe than C3aR-/-group and C5aR-/-group.The results of relative mRNA expression of TNF-α,TGF-β,IL-1β,IL-6,MCP-1 was the same as the level of 24 h UTP,at the same time,the relative mRNA expression of IL-1β,IL-6,MCP-1 in C3aR-/-group was significantly less than C5aR-/-group.Conclusion:The deficiency of C3a/C5a receptors can protect kidney from injury in IgAN ,and C3a receptor has more significant role in protect kidney from injury in IgAN.
