Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The paper discussed the protective effect of zinc pretreatment on renal ischemia-reperfusion injury (RIRI) and its mechanism. 50 male ICR mice were randomly divided into five groups: sham-operated group, model group, high-dose group with zinc sulfate pretreatment (60mg/kg body weight), medium-dose group with zinc sulfate pretreatment (30mg/kg body weight) and low-dose group with zinc sulfate pretreatment (15mg/kg body weight). The mice were administrated with zinc sulfate once a day for two weeks, subsequently the RIRI animal models were prepared by ligation of the left renal pedicle 30 minutes. 24h after reperfusion, the kidney tissue was removed and pathological results by HE staining showed that in the model group, kidney surface covered with a large number of red exudates, renal tubular dilatated, disorganized, renal tubular epithelial cell vacuolar degenerated, nuclear pyknosis and necrosis appeared; congestive and necrosis were visible in medullary junction. The pathological changes of renal ischemia- reperfusion were obviously relieved in the animals with medium and low-dose zinc pretreatment. The superoxide dismutase (SOD) activity in the lowdose zinc sulfate pretreatment group was significantly higher than that in the model and high-dose groups (P <0.05). The malondialdehyde (MDA) content of renal tissue, the apoptotic cells percentage in the medium and low dose groups were significantly lower than those in the model group (P <0.05), and MDA content in the low-dose group was significantly lower than that in the medium dose group (P <0.05). The ratio of BCL-2/BAX protein expression in the medium and low dose groups was significantly higher than that in the model group (P<0.05), the ratio in the low groups was significantly higher than that in the medium dose and high dose group by double immunofluorescence staining (P <0.05). In conclusion, zinc has a protective effect on the renal ischemia-reperfusion injury by antioxidant capacity and inhibition of apoptosis in the kidney.
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PMID:Protective effect of zinc on mouse renal ischemia-reperfusion injury by anti-apoptosis and antioxidation. 2515 71

Acute kidney failure is the main cause of death among patients with severe trauma due to massive blood loss and hemorrhagic shock (HS). Renal cell injury is caused by tissue ischemia. Renal ischemia initiates a complex and interconnected chain of events resulting in cell injury and renal cell necrosis. Nitric oxide plays a crucial role in renal function and can be inhibited by aminoguanidine (AG). We studied whether AG can ameliorate pathological renal changes associated with HS syndrome in a rat model and explored the AG protection mechanism. Rats were intraperitoneally injected with heparin sodium and mean arterial blood pressure was monitored. Animals were divided into three groups: control (without hemorrhage), with or without intra-arterially injected AG; HS (blood continuously withdrawn or reinfused to maintain an MABP of 35-40 mmHg); and HS with AG. We found that AG decreased plasma concentrations of urea, creatinine, and nitrates; ameliorated histological changes of HS-induced rats; and decreased the expressions of inducible nitrogen oxide synthase (iNOS), proapoptotic protein (BAX), and vitamin D receptors (VDR). AG ameliorated kidney injury by inhibiting iNOS resulting in decreased BAX and VDR expressions. Therefore, a therapeutic strategy targeting AG may provide new insights into kidney injury during severe shock.
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PMID:Histological and Immunohistochemical Basis of the Effect of Aminoguanidine on Renal Changes Associated with Hemorrhagic Shock in a Rat Model. 2838 46