Objective To investigate the effect of rebamipide on chronic non-atrophic gastritis (NAG) with erosion and its protection of gastric mucosa from Helicobacter priori(Hp) associated lesions.Methods Patients(n=452)with endoscopically confirmed NAG with erosion from 11 hospitals in China were enrolled and randomly assigned at a ratio of 3:1 to receive either rebamipide(100 mg t.i.d.)or sucralfate(1.0 t.i.d.)for 8 weeks.Hp infected patients received eradication treatment before randomization.Symptoms,endoscopic scores and histological changes were recorded before and after therapy.Concentrations of serum prostaglandin E(PGE:)and oxygen free radical(MDA)were measured in patients from 2 centers.Results Per-protocol analysis(n=415)showed that the dyspeptic symptom score in rebamipide group decreased significantly after eight weeks of treatment. The endoscopic inflammation score in rebamipide group also decreased from 2.65 ±0.09 to 0.60±0.10(P<0.001),which was,significantly better than that of sucralfate group(P<0.001).Histological findings were consistent with the endoscopic findings.There Was a significant elevation(P=0.002)in PGE2 concentration in mucesa from rebamipide-treated subjects [(225.4±18.3) pg/g vs.(266.7±14.7)Pg/g] compared with that in sucralfate group.The concentration of MDA significantly decreased from(325.9±65.6)mmoL/g to(216.5±61.5)mmol/g,which is markedly different from that of sucralfate group(P=0.046).No statistical difference was found between Hp eradication group,Hp infection group and Hp negative group,regarding the effect of Rebamipide.Conclusion Compared to sucralfate,Rebamipide demonstrates a superior effect on improvement of dyspepsia symptom and endoscopic findings in erosive NAG,which is not influenced by Hp infection.

Objective To clarify the changes of ultrastructure of interstitial cells of Cajal in the small intestine of diabetic rats. Methods Rats were randomly divided into diabetic group and control group. The rate of the small intestinal transit was measured and the tissues of the small intestine were observed by transmission electron microscopy at 3 months after the establishment of rat model of diabetics. Results In the diabetic rats, the rate of small intestinal transit was delayed as compared with that in the control group. The number of the gap junction of interstitial cells of Cajal in the small intestine of diabetic rats decreased significantly, and the rest structures were damaged. Damaged organelles and formation of vacuoles were also found. Conclusion The changes of ultrastructure of interstitial cells of Cajal in the small intestine may be one of the mechanisms resulting in slow rate of the small intestinal transit in diabetic rats.

Objective To study the effect of carbachol(CCH) on membrane potential of smooth muscle cells of gastric antrum of diabetic rats to verify the mechanism of gastric motility disturbance.Methods Fifty healthy Wistar rats of 2-month old,weighing 100-160 g,were divided into the control group(n=20) and diabetes mellitus group(n=30).Three months after the establishment of the rat model of diabetes by intraperitoneal injection of 60 mg/kg streptozotocin,gastric emptying time and gastric electrical activity were measured,and the resting membrane potentials of smooth muscle cells in antrum were measured by confocal laser scanning microscopy,then treated with carbachol of 10~(-9) mmol/L,10~(-8) mmol/L,10~(-7) mmol/L,the membrane potentials were measured.Results As compared with the normal rats,gastric emptying time in diabetic rats was significantly longer and abnormal gastric electric rhythm was significantly increased,the abnormal rhythm index(ARI) and the coefficient of variation(CV) of slow wave frequency in diabetic rats were significantly higher,but the resting membrane potentials remained unchanged and the sensitivity of CCH-induced membrane depolarization was increased.Conclusion The increase of sensitivity of CCH-induced membrane depolarization may be involved in the diabetes-induced gastric motor disorders.

Objective To study the role of gastric mitochondrial DNA cytochrome C oxidases (COX) subunit Ⅱ gene and its expression in diabetic gastric motility dysfunction. Methods Seventy Wister rats were randomly divided into 2 groups: diabetic group (STZ 60mg/Kg intraperitonealy) and control group. The changes in expressions of COX protein were assayed by Westernblot. Mitochondrial DNA COX mRNA was assayed with reverse-transcriptional polymerase chain reaction(RT-PCR). Cytochrome C oxidase activity was determined by ultraviolet spectrophotometer. Results Gastricelectric dysrythmia was more frequently delected in diabetic rats, and the COX activity in diabetic rats was 0.41?0.21/min, which was significantly lower than that in normal rats (0.78?0.37/min). The expression of gastrointestinal COX protein and COX gene in diabetic gastroparesis rats were markedly decreased compared with normal rats. Conclusion Cytochrome C oxidases activity was greatly reduced in diabetic rats. Diabetic gastroparesis was associated with down-regulation of the expression of gastrointestinal mtDNA encoding COX gene and protein. These changes might play a key role in pathogenesis of diabetic gastroparesis

Objective To investigate the relationship between mitochondrial membrane potential change and apoptosis of smooth muscle cells of the small intestine in diabetic rats. Methods Seventy Wistar rats were randomly divided into two groups: diabetic group(STZ60mg/kg intraperitonealy) and control group.The gastric empty time and intestinal transit were determined in diabetic rats 2 months after the reproduction of diabetes. Mitochondrial membrane potential in small intestinal smooth muscle cells was determined by the change in the intensity of labeling rhodamine 123 with lasor scanning confocal micrographs, and apoptosis index was assessed with the technique of terminal deoxynucleotidyl transferase mediated d-UTP nick end labeling(TUNEL) test and flow cytometry.The changes in expression of cytochrome C were determined by Western blotting. Results The mitochondrial membrane potential of small intestine smooth musele cells was significantly lowered in diabetic rats compared with normal rats. Apoptosis index in diabetic rats was significantly higher than that of normal as shown by TUNEL technic. Apoptosis rate in diabetic rats was 15%, and it was significantly higher than that of normal rat (P

Objective To study the change in cytosolic Ca 2+ in smooth muscle cells in gastric antrum of diabetic rat. Methods Rats were randomly divided into diabetic group and control group. Gastric empty time was determined 3 months after diabetes was reproduced in rats, the apoptosis rate of smooth muscle cells in the gastric antrum was assessed by flow cytometry, and the content of cytosolic Ca 2+ in smooth muscle cells was measured by laser scanning confocal microscopy. Results In diabetic rats, gastric emptying was significantly delayed. Compared the normal rats, the content of cytosolic Ca 2+ in smooth muscle cells from the antrum of diabetic rats was increased. The apoptosis rate of smooth muscle cells in the antrum of diabetic rats was 15%, and it was higher than that in normal rats. Conclusion With the increase in the content of cytosolic Ca 2+ in smooth muscle cells, smooth muscles were damaged and therefore their contraction was also impaired.

Objective To study the role of nitriergic nerves in the myenteric plexus of the gastric antrum in diabetic rats with motor disorder. Methods Rats were randomly divided into diabetic group and control group. Electrogastrogram was recorded, and the number of cholinergic nerves in the myenteric plexus of the gastric antrum was counted 3 months after reproducing diabetes in the model group. Results In the rats of diabetic group, gastro-electric dysrhythmia was observed more frequently, and the number of nitriergic cells in the myenteric nerves was significantly decreased compared with control group. Conclusion The changes in nitriergic nerves in the myenteric plexus of the gastric antrum might be one of the mechanisms of gastro-electric dysrhythmia and gastric motility disorders in diabetic rats.