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OBJECTIVE： To study on the effects of prophylactic administration of Ramulus mori polysaccharides （RMP） on inflammatory response of renal ischemia reperfusion injury （RIRI） model mice and to explore its possible mechanism. METHODS： Totally 60 C57BL/6 mice were randomly divided to sham operation group， model group， atorvastatin group （positive control， 15 mg/kg）， RMP low-dose， medium-dose and high-dose groups （300， 600， 1 200 mg/kg）. Except for sham operation group， RIRI model was induced in other 5 groups. 24 h before surgery， they were given relevant medicine intragastrically， once a day， for consecutive one week. 24 h after reperfusion， the mice were sacrificed. The serum levels of Scr and BUN were detected. The morphological changes of renal tissue were observed under optical microscope. The serum levels of IL-1β， IL-6， IL-10 and TNF-α were determined by ELISA. Western blot assay was used to determine the protein expressions of Toll-like receptor 4 （TLR4）， p38 mitogen-activation protein kinase （p38MAPK） and p-p38MAPK. RESULTS： Compared with sham operation group， the serum levels of Scr and BUN were significantly elevated in model group （P＜0.01）. RIRI led to typical inflammatory response of renal tissue， widespread renal tubular epithelial cell degeneration and necrosis， and inflammatory cells infiltration. Serum levels of IL-1β， IL-6， IL-10 and TNF-α were increased significantly （P＜0.01）. The protein expressions of TLR4， p38MAPK and p-p38MAPK were increased significantly in renal cortex （P＜0.01）. Compared with model group， serum levels of Scr and BUN were decreased significantly in administration groups （P＜0.05 or P＜0.01）. The pathological damage of renal tissue was improved in varying degrees， especially in the RMP medium-dose and high-dose groups. Serum levels of IL-1β and IL-6 were decreased significantly in administration groups （P＜0.05 or P＜0.01）. Serum levels of IL-10 were further increased in atorvastatin group and RMP high-dose group （P＜0.01）， and serum level of TNF-α was decreased significantly in atorvastatin group and RMP medium-dose and high-dose groups （P＜0.05 or P＜0.01）. The protein expressions of TLR4 and p-p38MAPK in renal cortex were decreased significantly in administration groups （P＜0.05 or P＜0.01）. CONCLUSIONS： RMP prophylactic administration can improve RIRI of mice， the mechanism of which may be associated with relieving the inflammatory response through inhibition of TLR4/p38MAPK signaling pathway.
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OBJECTIVE:To study the protective effect of fingolimod on renal ischemia reperfusion injury (RIRI) model mice and its mechanism.METHODS:A total of 60 mice were randomly divided into sham operation group,model group,fingolimod group (1 mg/kg) and fingolimod+wortmannin group [fingolimod 1 mg/kg+phosphatidylinositol 3-kinase (PI3K) specific blocker wortmarmin 1.4 mg/kg],with 15 mice in each group.Except for sham operation group,RIRI model was induced in other 3 groups,and those model mice were given relevant medicine via caudal vein at once 24 h before surgery.Serum of mice were collected in each group after 24 h perfusion.Serum levels of Scr and BUN were measured by automatic biochemical analyzer.The pathological changes of renal tissue were observed under light microscope.The protein expression of intercellular cell adhesion molecule-1 (ICAM-1),monocyte chemoattractant protein-1 (MCP-1) and phosphorylated protein kinase B (p-Akt) in renal tissue were measured by Western blot assay.RESULTS:Compared with sham operation group,the serum levels of Scr and BUN in model group were increased significantly (P＜0.01).Pathological changes were found in the kidney,and RIRI led to widespread renal tubular epithelial cell injury,apoptosis and inflammatory cells infiltration.The protein expression of ICAM-1 and MCP-1 in renal tissue were increased significantly (P＜0.01),the protein expression of p-Akt was increased slightly (P＞0.05).Compared with model group,other indexes of fingolimod group were improved significantly (P＜0.01) except that the protein expression of p-Akt in renal tissue was increased significantly (P＜0.01).Compared with fingolimod group,above indexes of fingolimod+wortmannin group were reversed (P＜0.05 or P＜0.01).CONCLUSIONS:Fingolimod can obviously ameliorate renal injury induced by RIRI in mice,the mechanism of which may be associated with the activation of PI3K/Akt signaling pathway.
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In light of the unfulfilled docking of the previous curriculum system of clinical medicine science specialty in higher vocational colleges and with the requirement of being a first-line physician,we put forward our reform sketch for Clinical Medicine Transboundary Curriculum System targeting at fostering technical and skilled genius that will be qualified for the post of clinical physician in primary heahh-care institution,following the principle of quality-first,capability-centered and knowledge-based and attempting to establish a unified system combining quality,capability and knowledge,and analyze the difficulty during the implementation of the reform ideas and measures that could be taken.In this way,it will be possible for us to comprehensively dock curriculum initiatives with the capability of the post,curriculum content with professional criteria,professional teaching with clinical applications,vocational education and lifelong study,and hence,it will be helpful for us to foster qualified genius for first-line medical institution.
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Objective:To explore the influence of percutaneous coronary intervention (PCI) on plasma levels of brain natri‐uretic peptide (BNP) and aldosterone (Ald) and short‐term prognosis in patients with acute left ventricular inferior and an‐terior wall myocardial infarction .Methods:A total of 212 patients were divided into acute inferior myocardial infarction (AIMI) group (n=140) and acute anterior myocardial infarction (AAMI) group (n=72) .Relationship among plasma lev‐els of BNP and Ald and coronary artery disease were analyzed in two groups .Changes of plasma levels of BNP and Ald after direct/delayed PCI and influence of PCI on short‐term prognosis were compared between two groups .Results:Compared with AIMI group before PCI ,there were significant rise in plasma levels of BNP [ (642.06 ± 235.08) ng/L vs .(856.54 ± 223.50) ng/L] and Ald [(50.26 ± 5.23) ng/dl vs .(88.34 ± 8.52) ng/dl] ,extent of coronary stenosis [(82.28 ± 7.65)%vs .(90.64 ± 7.54)% ] and incidence rate of triple‐vessel coronary disease (22.52% vs .39.66% ) in AAMI group , P<0.05 all;plasma levels of BNP and Ald significantly reduced in both groups after direct /delayed PCI (P<0.01 both) ,com‐pared with delayed PCI group ,there were significant reductions in plasma levels of BNP [AIMI group:(453.75 ± 107.54) ng/L vs .(216.93 ± 119.86) ng/L ,AAMI group:(483.04 ± 164.65) ng/L vs .(245.754 ± 121.52) ng/L] and Ald [AIMI group:(45.34 ± 8.15) ng/dl vs .(40.09 ± 6.55) ng/dl ,AAMI group:(50.43 ± 9.21) ng/dl vs .(43.65 ± 3.50) ng/dl] in direct PCI group , P<0.01 all;short‐term mortality rate of patients not undergoing PCI was significantly higher than those of patients undergoing direct PCI and delayed PCI (11.63% vs .2.78% vs .3.28% , P<0.05 both ) .Conclusion:Plasma levels of BNP and Ald are higher and coronary disease is more severe in AAMI patients ;compared with delayed PCI ,plas‐ma concentrations of BNP and Ald possess higher decreasing extent after undergoing direct PCI ;patients not receiving PCI possess higher mortality rate .