CAJ | 학술논문

目的：研究中药复方健脾清化方对慢性肾衰竭肾纤维化大鼠ATII/NADPH氧化应激通路的影响，初步探讨其发挥疗效的作用机制。方法：用5/6肾切除(Platt法)建立慢性肾衰竭大鼠模型，分为假手术组、模型组、健脾清化方组和氯沙坦组。治疗60 d后测定血清肌酐、尿素氮水平；测定各组肾组织中SOD和MDA水平；Western印迹检测各组肾组织AT1蛋白表达；RT-PCR检测各组肾组织p47phox mRNA表达。结果：与假手术组比较，模型组大鼠血清肌酐和尿素氮均有明显上升，肾组织匀浆中SOD活性降低，MDA含量升高，肾组织中AT1蛋白表达显著上调，p47phox mRNA表达显著增加，差异均具有统计学意义(P<0.05)。与模型组比较，健脾清化方组和氯沙坦组血清肌酐和尿素氮含量降低，肾组织匀浆中SOD活性上升，MDA含量下降，肾组织中AT1蛋白表达显著下调，p47phox mRNA表达显著降低，差异均具有统计学意义(P<0.05)。与氯沙坦组比较，健脾清化方组肾组织SOD活性明显升高，(P<0.05)，肾组织中AT1蛋白及p47phox mRNA表达下降趋势明显，但差异无统计学意义(P>0.05)，血清BUN，SCr水平和肾组织中MDA含量两组间比较差异也无统计学意义(P>0.05)。结论：健脾清化方可通过降低ATII及NADPH氧化酶的表达，从而改善慢性肾衰竭大鼠的氧化应激反应，延缓肾纤维化进程。
목적：연구중약복방건비청화방대만성신쇠갈신섬유화대서ATII/NADPH양화응격통로적영향，초보탐토기발휘료효적작용궤제。방법：용5/6신절제(Platt법)건립만성신쇠갈대서모형，분위가수술조、모형조、건비청화방조화록사탄조。치료60 d후측정혈청기항、뇨소담수평；측정각조신조직중SOD화MDA수평；Western인적검측각조신조직AT1단백표체；RT-PCR검측각조신조직p47phox mRNA표체。결과：여가수술조비교，모형조대서혈청기항화뇨소담균유명현상승，신조직균장중SOD활성강저，MDA함량승고，신조직중AT1단백표체현저상조，p47phox mRNA표체현저증가，차이균구유통계학의의(P<0.05)。여모형조비교，건비청화방조화록사탄조혈청기항화뇨소담함량강저，신조직균장중SOD활성상승，MDA함량하강，신조직중AT1단백표체현저하조，p47phox mRNA표체현저강저，차이균구유통계학의의(P<0.05)。여록사탄조비교，건비청화방조신조직SOD활성명현승고，(P<0.05)，신조직중AT1단백급p47phox mRNA표체하강추세명현，단차이무통계학의의(P>0.05)，혈청BUN，SCr수평화신조직중MDA함량량조간비교차이야무통계학의의(P>0.05)。결론：건비청화방가통과강저ATII급NADPH양화매적표체，종이개선만성신쇠갈대서적양화응격반응，연완신섬유화진정。
Objective:To study the effect of Jianpi Qinghua Recipe ( JPQHR) on angiotensin II/NADPH oxidase pathway in 5/6 nephrectomized rat renal failure model and the underlying mechanisms. <br> Methods:The animals were divided into 4 groups:the sham-operated group, the renal failure group, the JPQHR-treated group and the losartan-treated group. After 60-days therapy, serum nitrogen and creatinine were measured. The expression of angiotensin II type 1 receptor (AT1) protein and the expression of p47phox mRNA in renal tissue was determined. SOD and MDA were also examined. <br> Results:Compared with the sham-operated group, the levels of SCr and serum BUN and the AT1 protein and p47phox mRNA expression in the renal failure group were significantly increased. hTe activities of SOD in renal tissue from the renal failure group was signiifcantly down-regulated while MDA was up-regulated (P<0.05). Compared with the renal failure group, the levels of SCr and serum BUN and the AT1 protein and p47phox mRNA expression in both JPQHR-treated group and losartan-treated group were signiifcantly decreased. hTe activities of SOD in renal tissue from JPQHR-treated group and losartan-treated group were signiifcantly up-regulated whereas the content of MDA were down-regulated (P<0.05). Compared with the losartan-treated group, the activities of SOD in renal tissue from the JPQHR-treated group was obviously increased (P<0.05), the decrease in AT1 protein and p47phox mRNA was more evident but not statistically different (P>0.05). The level of SCr and serum BUN and the content of MDA were also not statistically different (P>0.05). <br> Conclusion:hTrough decrease the expression of angiotensin II and NADPH oxidase, JPQHR can reduce the oxidative stress in chronic renal failure and delay the renal ifbrosis progression.