浙江医学
浙江醫學
절강의학
ZHEJIANG MEDICAL JOURNAL
2013年
8期
626-629
,共4页
林小春%叶晓华%林瑞霞%杨青%陈敏广
林小春%葉曉華%林瑞霞%楊青%陳敏廣
림소춘%협효화%림서하%양청%진민엄
川芎嗪%IgA 肾病%足细胞%Nephrin%大鼠
川芎嗪%IgA 腎病%足細胞%Nephrin%大鼠
천궁진%IgA 신병%족세포%Nephrin%대서
Tetramethlpyrazine%IgA nephropathy%Podocyte%Nephrin%Rat
目的研究川芎嗪对 IgA 肾病(IgAN)大鼠模型足细胞的保护作用和作用机制.方法建立 IgAN 大鼠模型,按照体重匹配原则分成正常组(A 组)8只、模型组(B 组)12只、地塞米松组(C 组)12只、川芎嗪组(D 组)12只.使用生化分析仪测定24h尿蛋白,电镜观察足细胞形态,RT-PCR 检测肾组织 Nephrin mRNA 的表达水平.结果 B、C、D 组在造模成功后第4周末均出现蛋白尿,第4、8、10、12周末时24h 尿蛋白总量均高于 A 组,偶见肉眼血尿,差异均有统计学意义(均 P<0.01),但3组间的差异无统计学意义(P >0.05);在第14、16周末时,C、D 组24h 尿蛋白总量明显低于 B 组(P<0.01).电镜下见 A 组足突形态正常,排列整齐, B 组多数肾小球足突部分融合,C 组和 D 组足突极少部分融合.RT-PCR 检测结果 C、D 组 Nephrin mRNA 表达水平较 B 组高,差异有统计学意义(P<0.01).结论川芎嗪能降低 IgAN 大鼠的24h 尿蛋白总量,减少足突的融合;Nephrin 在 IgAN 大鼠模型损伤中起重要作用,川芎嗪能增加肾组织 Nephrin mRNA 的表达水平.
目的研究川芎嗪對 IgA 腎病(IgAN)大鼠模型足細胞的保護作用和作用機製.方法建立 IgAN 大鼠模型,按照體重匹配原則分成正常組(A 組)8隻、模型組(B 組)12隻、地塞米鬆組(C 組)12隻、川芎嗪組(D 組)12隻.使用生化分析儀測定24h尿蛋白,電鏡觀察足細胞形態,RT-PCR 檢測腎組織 Nephrin mRNA 的錶達水平.結果 B、C、D 組在造模成功後第4週末均齣現蛋白尿,第4、8、10、12週末時24h 尿蛋白總量均高于 A 組,偶見肉眼血尿,差異均有統計學意義(均 P<0.01),但3組間的差異無統計學意義(P >0.05);在第14、16週末時,C、D 組24h 尿蛋白總量明顯低于 B 組(P<0.01).電鏡下見 A 組足突形態正常,排列整齊, B 組多數腎小毬足突部分融閤,C 組和 D 組足突極少部分融閤.RT-PCR 檢測結果 C、D 組 Nephrin mRNA 錶達水平較 B 組高,差異有統計學意義(P<0.01).結論川芎嗪能降低 IgAN 大鼠的24h 尿蛋白總量,減少足突的融閤;Nephrin 在 IgAN 大鼠模型損傷中起重要作用,川芎嗪能增加腎組織 Nephrin mRNA 的錶達水平.
목적연구천궁진대 IgA 신병(IgAN)대서모형족세포적보호작용화작용궤제.방법건립 IgAN 대서모형,안조체중필배원칙분성정상조(A 조)8지、모형조(B 조)12지、지새미송조(C 조)12지、천궁진조(D 조)12지.사용생화분석의측정24h뇨단백,전경관찰족세포형태,RT-PCR 검측신조직 Nephrin mRNA 적표체수평.결과 B、C、D 조재조모성공후제4주말균출현단백뇨,제4、8、10、12주말시24h 뇨단백총량균고우 A 조,우견육안혈뇨,차이균유통계학의의(균 P<0.01),단3조간적차이무통계학의의(P >0.05);재제14、16주말시,C、D 조24h 뇨단백총량명현저우 B 조(P<0.01).전경하견 A 조족돌형태정상,배렬정제, B 조다수신소구족돌부분융합,C 조화 D 조족돌겁소부분융합.RT-PCR 검측결과 C、D 조 Nephrin mRNA 표체수평교 B 조고,차이유통계학의의(P<0.01).결론천궁진능강저 IgAN 대서적24h 뇨단백총량,감소족돌적융합;Nephrin 재 IgAN 대서모형손상중기중요작용,천궁진능증가신조직 Nephrin mRNA 적표체수평.
@@@@Objective To investigate the effects of tetramethylpyrazine (TMP) on podocytes of rats with IgA nephropathy. Methods Female Sprague-Dawley(SD)rats were randomly divided into 4 groups: control group (group A, n=8), IgA nephropathy model group(group B, n=12), dexamethasone (DXM) group(group C, n=12)and TMP group(group D, n=12). IgA nephropathy was induced in groups B, C, D, DXM and TMP were given to groups C and D respectively. The 24h-urine protein was determined with a automatic biochemistry analyzer; the morphology of podocyte was observed with transmission electron microscope; and the expression of Nephrin mRNA was detected by RT-PCR. Results Proteinuria was presented in group B, C and D from week 4, the quantity of 24h urinary protein was al higher than that in group A (P<0.01); but the quantity in group C and D was signifi-cantly lower than that in group B in week 14 and 16 (P<0.01). Electron microscopy showed that most glomerular foot processes were fused in group B, but only few in group C and D. The expression of Nephrin mRNA in renal tissue of group C and group D was significantly higher than that of group B (P<0.01). Conclusion Like dexamethasone, TMP can reduce 24h-urinary protein excretion and improve foot process fusion in rat IgA nephropathy, which is associate with up-regulation of Nephrin mRNA in renal tissue.