Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxygen free radicals have been implicated in the pathogenesis of tissue injury consequent to ischemia/reperfusion in several different organs, including heart, bowel, and kidney. In this study, the protective effect of FOY, SOD, and PEG-SOD against kidney damage resulting from warm ischemia and reperfusion was investigated in the rat. FOY (Gabexate mesilate), one of protease inhibitor, has been suggested to inhibit the activity of superoxide in polymorphonuclear leucocyte in recent reports. PEG-SOD (polyethyleneglycol-modified SOD), recently synthesized on the basis of SOD, has an additional value in comparison with SOD. WKA rats underwent right nephrectomy, and occlusion of the left renal artery, vein, and ureter for 60 minutes. FOY (50mg/kg, DIV.) was administrated from 5 minutes before reperfusion to 5 minutes after reperfusion to the rat. SOD (2mg/kg, 5mg/kg, 10mg/kg, IV.) and PEG-SOD (2mg/kg, 5mg/kg, IV.) were administrated at 10 minutes before reperfusion. 48 hours after operation, the measurement of urine output (60 minutes) was made, and BUN, Cr, K, UUN, UCr were measured at this point. Creatinine clearance was calculated from these results. The left kidney was removed and histological examination was performed. Serum BUN, Cr level were greatly elevated, and creatinine was diminished in the group of ischemic untreated rats (n = 8). In the groups of rats treated with FOY (n = 9), SOD (5mg/kg, 10mg/kg; n = 5, respectively), and PEG-SOD (2mg/kg, 5mg/kg; n = 5, respectively), serum Cr was significantly lower and creatinine clearance was significantly higher than control untreated group. Furthermore, tubular injury was less in histological examination in these groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Experimental study on renal protection against damage in kidneys subjected warm ischemia--protective effect of FOY, SOD, and PEG-SOD on ischemic acute renal failure]. 251 Nov 30

Liver failure due to ischemia-reperfusion injury, believed to be closely related to the generation of oxygen-free radicals, is a serious problem during liver surgery. Gabexate mesilate, a synthetic protease inhibitor, suppresses the extracellular release of oxygen-free radicals in the microvascular endothelium. To determine its effects on ischemia-reperfusion injury to the liver, we performed experiments with rats. We divided the animals into two ischemia-reperfusion groups: an experimental group, which underwent ischemic injury for 30 minutes, along with the infusion of gabexate mesilate, and a control group, which underwent injury only. Each group was then divided into four subgroups: ischemic injury only and 60-, 120-, and 180-minute reperfusion injury. The test parameters were tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) in serum and superoxide dismutase (SOD), catalase, and malondialdehyde (MDA) in liver and lung tissues. The experimental group had a significantly higher liver SOD and catalase levels and a significantly lower level of liver and lung MDA than the control groups. TNFalpha levels in the experimental groups were significantly lower during the early phase, but a comparison of IL-6 levels between the two groups yielded no differences. Levels of lung catalase and SOD were not significantly different between the two groups. We concluded that protease inhibitor suppressed liver ischemia-reperfusion injury, and that it was due to an increase of antioxidant or suppression of oxygen-free radicals. The roles of TNFalpha and IL-6 in liver reperfusion injury were not clear, though TNFalpha might have had an effect during the early phase. With liver ischemia-reperfusion injury, the mechanism of lung involvement might be different from that of liver involvement.
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PMID:Effect of protease inhibitor on ischemia-reperfusion injury to rat liver. 1051 42