Effect of iopromide on glomerular visceral epithelium cells
10.11659/jjssx.10E015118
- VernacularTitle:碘普罗胺对大鼠肾小球脏层上皮细胞的影响
- Author:
Fengxia YU
;
Lijie WANG
;
Shuwu LIN
;
Zilong LI
- Publication Type:Journal Article
- Keywords:
contrast-induced nephropathy iopromide;
iopromide;
glomerular visceral epithelium cells
- From:
Journal of Regional Anatomy and Operative Surgery
2016;(2):83-86
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the mechanism of contrast-induced nephropathy (CIN) caused by Iopromide.Methods Two-four female SD rats were randomly divided into two groups which were control group and CIN group .The rats in CIN group were injected Io-promide via caudal vein ,the rats in control group were injected the equal amount of solvent .After 24 hours,all the rats were euthanized and tested.The excretion of 24 h urinary protein was detected using biochemistry assay .The expression of related cell cycle regulatory protein such as P21,P27 and TGF-β1 in glomerular visceral epithelium cells were measured using immunohistochemical technique .A semiquantitative score was used to evaluate the injure degree of glomerular and tubulointerstitium .Renal glomerular cell apoptosis was evaluated by TUNEL . Results Compared with control group ,CIN group rat glomerular epithelial cells of P 21,P27 and TGF beta 1 positive expression rate signifi-cantly increased,[(12.86 ±0.98) %vs (0.46 ±0.21)%,P=0.004 5],[(21.76 ±2.75)% vs (9.57 ±1.86)%,P =0.0071], [(12.85 ±5.54) vs (7.63 ±0.84),P=0.003 7)] respectively,24 h urine protein significantly increase [(23.44 ±5.22) mg/d vs (2.13 ±0.52) mg/d,P=0.007 0,P=0.005 0],CIN pathological damage of rat glomerular epithelial cells and apoptotic rate significantly more serious [(52.5 ±6.4)%vs (4.2 ±0.3) %,P =0.007 5].In addition,the renal pathologic scores were positively correlated with the excretion of 24hr urinary protein and the expression of P 21,P27,and TGF-β1(r=0.765,0.701,0.842,0.651,P<0.01).Conclusion Io-dine amine via increased glomerular epithelial cells P 27 and TGF-beta 1expression and urinary protein excretion , aggravating pathological damage and apoptosis .
