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Objective To investigate potential effect and mechanism of dexamethasone ( DEX) on intestinal ischemia reperfusion injury. Methods A total of 18 male C57BL/6 mice were randomly divided into three groups( n=6 each): sham operation group, model control group , and DEX group. Mice in the model control and sham operation groups received intraperitoneal normal saline 0. 5 hour before ischemia, and mice in DEX group received intraperitoneal injection of DEX 10 mg·kg-1 , 0. 5 hour before ischemia. Mice in the model control and DEX groups were placed in the 32 degree infant incubator for 30 minutes after clamping superior mesenteric artery, followed by clamps removal and reperfusion for 24 hours. Mice were then sacrificed to obtain the intestinal tissues. The pathology of intestinal tissues was observed after hematoxylin-eosinstaining ( HE) staining. The mRNA expression level of pro-inflammatory cytokines IL-6, TNF-α and IFN-γ were measured by PCR. The expression of AKT and p-AKT were measured by Western blotting. Results The level of mesenteric injuries in the sham operation group, model control group and DEX group was (4±2),(13±3),(7±2) points, respectively. The mRNA level of IL-6, TNF-α and IFN-γ and the expression of p-AKT were all higher in the model control group. Compared to the model control group, the level of mesenteric injuries, the mRNA level of IL-6, TNF-αand IFN-γin DEX group were significantly attenuated, but the expression of p-AKT were further increased. Conclusion Pretreatment with DEX can reduce intestinal ischemia-reperfusion injury by activating AKT signaling pathway and suppressing inflammation.
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Acute kidney injury(AKI) is a clinical critical syndrome caused by a variety reason,sepsis is the leading cause and independently associated with mortality in critical patients.Fluid resuscitation is one of the most important treatment of spesis and AKI.Fluid overload has been shown to be associated with worse outcomes in critically ill patients.Different liquid treatment should be adopted in different stages.To carry out dynamic,noninvasive hemodynamic monitoring is the best way to critical patients with AKI liquid management.
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Background:Intestinal ischemia-reperfusion( I/R)is a surgical abdomen,which not only leads to intestinal tissue necrosis,but also induces systemic inflammatory response,resulting in a serious impact on other organs and tissues. Aims:To investigate the role and mechanism of rosiglitazone( ROS)on intestinal I/R injury. Methods:Eighteen male C57BL/6 mice were randomly divided into three groups:sham operation group,I/R injury group and ROS pretreatment group. Mice in ROS pretreatment group received ROS(0. 3 mg/kg,IV)30 minutes before I/R injury. I/R injury model was established by clamping superior mesenteric artery for 30 minutes,followed by 4 hours reperfusion. All the mice were sacrificed. The pathology of intestinal tissue was examined by HE staining. The mRNA expressions of tumor necrosis factor( TNF )-α, interferon(IFN)-γ,interleukin( IL)-1β,transforming growth factor( TGF)-β and Smad3 were measured by real-time quantitative PCR. The protein expressions of TGF-βand Smad3 were measured by Western blotting. Serum levels of TNF-α, IFN-γand IL-1βwere measured by ELISA. Results:Compared with the sham operation group,pathological score of small intestinal mucosa in I/R injury group was significantly increased(P<0. 05),and the mRNA expressions of TNF-α,IFN-γand IL-1β were significantly increased( P < 0. 05 ),the mRNA and protein expressions of TGF-β and Smad3 were significantly increased(P<0. 05),the serum levels of TNF-α,IFN-γand IL-1β were significantly increased(P<0. 05). With the pretreatment of ROS,all the above-mentioned indices were significantly ameliorated(P<0. 05). Conclusions:ROS pretreatment can attenuate intestinal I/R injury by inhibiting TGF-β/Smad3 signal pathway to reduce inflammation.