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Objective To explore the protective roles of Emodin in the intestinal mucosal lay of rats with severe acute pancreatitis (SAP) and its mechanism. Methods SD rats (n=30) were divided into 3 groups: sham operation group, SAP group and Emodin group (SAP rats treated with Emodin). The SAP rat models were established via retrograde injection of 3%sodium taurocholate to pancreatic duct. Rats in Emodin group were peritoneally injected with Emodin (2.5 mg/100 g) at both 1 hour and 3 hour after sodium taurocholate injection. Apoptosis of intestinal epithelial cell was detected by TUNEL analy?sis. The expression of glucose-regulated protein78 (GRP78) protein was assessed by immunohistochemistry. Results Com?pared with sham operation group, apoptosis in intestinal epithelial cells and the expression of GRP78 protein were increased significantly in SAP group(P0.05). Conclusion Emodin has a protective effect on intestinal layer in rats with SAP through inhibiting intestinal epithelial cell apoptosis. However, ER stress is not likely to be involved in this protective effect.
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[ ABSTRACT] AIM: To discuss the relevance between the pathogenesis of diabetic gastroparesis and the large-conductance calcium-activated potassium channels ( BKCa ) in gastric smooth muscle cells.METHODS:The SD rats were randomly divided into control group and model group.The gastric smooth muscle cells of the SD rats were enzymatically iso-lated in a low calcium solution containing papain.The current was recorded by patch clamp single channel recording tech-nique.The expression of KCNMA and KCNMB1 were observed by the method of immunohistochemistry.RESULTS:The value of BKCa single channel conductance was (220.10 ±10.90) pS;the channels had distinct voltage dependent and cal-cium dependent characteristics.In outside-out patch (Vm =+30 mV), the activation of BKCa was blocked by 200 nmol/L IbTX completely.Compared with control group, the open probability and amplitude of current in model group significant-ly increased, while the mean open time and mean close time significantly decreased.Compared with control group, the ex-pression of KCNMB1 in model group was significantly increased.CONCLUSION: Up-regulation of β1-subunit and in-crease in BKCa functional activities may be associated with diabetes gastroparesis in rats.
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Objective To investigate the pathogenesis of gastroparesis in diabetic rats.Methods SD rats were randomly divided into control group and diabetes group.Ten weeks later,gastroparesis model was established.The apoptosis rate and mitochondrial membrane potential of the gastric smooth muscle cells were detected by flow cytometry.Cytochrome C was detected by immunohistochemistry.Results Compared with rats in control group:(1)Typical symptoms of diabetes mellitus appeared;The rate of gastric residual pigment was significantly higher(P