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)

Effect of hepatic ischemia and reperfusion on hepatic regeneration after 70% partial hepatectomy was evaluated in rats. Total hepatic ischemia by portal triad cross clamping (15 minutes) and reperfusion (15 minutes) was repeated two times during partial hepatectomy in the PS, non-PS, and G groups. In the C group, partial hepatectomy was made as a control without ischemia and reperfusion. In order to evaluate the effect of portal pooling, portal systemic shunt (PS shunt) was made by splenic transposition to subcutaneous space in the PS group, and compared with the non-PS group. Gadolinium chloride (GdCl3), the selective blocker of Kupffer (K) cell, was intravenously administered to the rat in the G group. Hepatic regeneration rates, labelling index of liver cells, rates of bacterial infection of mesenteric lymph nodes (MLN), blood levels of endotoxin (Ex) and tumor necrosis factor-alpha (TNF) were compared. Hepatic regeneration at 28 days was suppressed by total hepatic ischemia in the non-PS group. Increased positive rates of MLN culture and blood levels of Ex showed bacterial translocation induced by the portal pooling during portal triad clamping. PS shunt reduced both bacterial translocation and the suppression of hepatic regeneration occurred in the PS group. Hepatic regeneration was not suppressed and blood TNF level did not increased in the G group by the inhibition of K cell function. In conclusion, repeated total hepatic ischemia and reperfusion induced portal pooling, bacterial translocation, and activated K cell, then inhibited hepatic regeneration after partial hepatectomy.
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PMID:[Inhibitory effect of portal pooling, bacterial translocation, and Kupffer cell activation on hepatic regeneration after partial hepatectomy by repeated portal triad cross clamping in rats]. 828 11

This study examined the role of Kupffer cells in altering the hepatic secretory and microsomal function during ischemia and reperfusion (Is/Rp). Rats were subjected to 60 min of hepatic ischemia, followed by 1 and 5 h of reperfusion. Gadolinium chloride (GdCl3, 7.5 mg/kg body weight, intravenously) was used to inactivate the Kupffer cells 1 day prior to ischemia. Is/Rp markedly increased the serum aminotransferase level and the extent of lipid peroxidation. GdCl3 significantly attenuated these increases. Is/Rp markedly decreased the bile flow and cholate output, and GdCl3 restored their secretion. The cytochrome P450 content was decreased by Is/Rp. However, these decreases were not prevented by GdCl3. The aminopyrine N-demethylase activity was decreased by Is/Rp, while the aniline p-hydroxylase activity was increased. GdCl3 prevented the increase in the aniline p-hydroxylase activity. Overall, Is/Rp diminishes the hepatic secretory and microsomal drug-metabolizing functions, and Kupffer cells are involved in this hepatobiliary dysfunction.
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PMID:The roles of Kupffer cells in hepatic dysfunction induced by ischemia/reperfusion in rats. 1639 73

Exact mechanism of cerebral ischemic stroke remains unclear. The calcium-sensing receptor (CaSR), a G-protein coupled receptor, has been reported to participate in the pathology of myocardial ischemia-reperfusion (I/R) injury and myocardial hypertrophy. Nevertheless, only a limited number of studies have been conducted to investigate the role of CaSR in cerebral ischemic stroke. This study was to investigate the effect of CaSR activation on cerebral ischemic stroke. Male adult Kunming mice were subjected to 2-h focal cerebral ischemia followed by 22-h reperfusion. Then, the brain was collected, and the expression of CaSR, JNK, p38, Bcl-2, and Bax was detected by Western blot assay. The morphology of neurons in the brain was evaluated by HE staining. Neurological function was scored, and the infarct volume was determined by TTC (triphenyltetrazolium chloride) staining. Results showed that ischemia/reperfusion (I/R) increased CaSR expression and induced neuronal apoptosis in the brain. Gadolinium trichloride (GdCl3), an agonist of CaSR, further deteriorated neurological dysfunction, increased infarct volume, enhanced CaSR expression, and promoted neuronal apoptosis. In addition, GdCl3 unregulated expression of Bax, p-JNK, and p-p38, and down-regulated Bcl-2 expression during I/R, which were attenuated by NPS2390, an inhibitor of CaSR. In conclusion, the CaSR activation promotes apoptosis in focal cerebral I/R in mice, which may be related to the activation of JNK/p38 MAPK signalling pathway. Targeting CaSR may be a novel strategy for the prevention and treatment of cerebral ischemic stroke.
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PMID:Activation of the calcium-sensing receptor promotes apoptosis by modulating the JNK/p38 MAPK pathway in focal cerebral ischemia-reperfusion in mice. 2715 78