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실험성 급성 허혈성 신손상 후 Superoxide dismutase 및 Renin 유전자의 발현양상
정태시,김형규 고려대학교 의과대학 1995 고려대 의대 잡지 Vol.32 No.1
Background. Acute renal failure(ARF) is defined as an abrupt decrease of glomerular filtration rate that is accompanied by an accumulation of nitrogenous waste products. Since tubular cell injury is the hallmark of ischemic ARF, an understanding of the mechanisms of ischemic cellular damage and dysfunction is essential to limit and possibly to prevent ischemic injury. Various pathophysiologic changes such as cellular ATP depletion, intracellular calcium alterations, mitochondrial dysfunction, oxygen free radical formation or renin-angiotensin system are proposed to be involved in the mechanism of ARF. Of these changes, the formation of reactive oxygen species in the reperfusion period and alteration of renin-angiotensin system have been suggested as a mediator of tubular cell injury and abnormal renal hemodynamics. So to investigate the expression of antioxidant superoxide dismutase (SOD) and renin genes during acute ischemic renal injury, the author performed the northern and dot hybridization of renal tissue at different reperfusion time in the ischemic ARF rats. Methods. In this experiment, 21 rats were divided into three groups ; Group Ⅰ (n=3) was a control group without any procedure, Group Ⅱ (n=3) was a sham operation group with bilateral flank incision and decapsulation of the kidneys Group Ⅲ(n=15) was an ischemic model with right nephrectomy followed by left renal artery clamping for 40minutes. In the ischemic renal injury group (Group Ⅲ), the rats were subdivided into three subgroups according to the reperfusion time such as 1, 24, and 72 hours (Group Ⅲa, Ⅲb, Ⅲc respectively). In all cases, whole blood was collected for the measurement of serum creatinine after each reperfusion time, and total renal RNA was purified by Chomczynski method after each reperfusion time. After the isolation of RNA, electrophoresis was done in a 1% agarose gel containing 2.2M formaldehyde, and confirmation of intact RNA were done by the 18S and 28S ribosomal RNA band. RNA transfer was done by vaccum transfer system and then hybridization was performed at 42℃ with isotope labelled probes for 18 hours. Autoradiographs were obtained and quantitated by computer assisted dual wave length flying spot scanner (CS-9000) at 530nm. Results. The mean levels of serum creatintne were as follows: in the control group, 0.9±0.3mg/dl; in the ischemic group after 24 hours reperfusion, 1.9±0.5mg/dl and in the ischemic group after 72hours reperfusion, 3.6±1.4mg/dl. The difference of mean serum creatinine levels between control and post-ischemic 24 and 72 hours reperfusion groups was statistically significant (P<0.05). SOD gene expression was markedly decreased by renal ischemia and showed persistently decreased pattern during reperfusion period. The expression of renin gene was markedly decreased after on ehour of reflow and progressively increased to one half of the control level 72 hours after reperfusion. Conclusion. From the above findings, SOD gene expression was rapidly decreased after ischemia and this antioxidant enzyme probably does not act as a protective mechanism of acute ischemic renal failure. Expression pattern of renin gene suggest that renin gene is not expressed as a direct mediator of acute ischemic renal injury but probably has some roles in the recovery phase of ARF. Although the specific role of SOD and renin genes are still not known in ischemic renal injury, more studies including in situ hybridization will be requested in the future.