| Objective To investigate the effects of emodin and tegaserod on the gastrointestinal motility of type 2 diabetic rats and to explore their correlated mechanisms.Methods Seventy SPF mail Wistar rats were randomly divided into two groups, i.e.,control(NOR)and model(MOD)groups.Murine type 2 diabetes model was induced by intravenous injection of a small dose of streptozotocin plus long-term high fat high caloric laboratory chow.The rats were treated with emodin(EMO),tegaserod(TEG)or domperidone(DOM)for 6 weeks.Half gastric emptying time(GET1/2)and 90 min residual rate(RIH)were measured by single photon emission computed tomography before sacrifice.The blood glucose and serum insulin,triglycerides TG),total cholesterol(TC), high density lipoprotein-cholesterol(HDL-C)were determined by biochemicaI methods.Plasma and tissue levels of substance P(sP),somatostatin(SS)were determined using radioimmunoassay.Results Gastric emptying of type 2 diabetic rats model group was significantly slower than normal group[GET1/2:(124.5±26.9min)vs.(63.5±13.9min);RIH:(54.6±7.0%) vs.(40.4±6.8%),P＜0.01],but became faster after treatment of tegaserod,emodin or domperidone(P＜0.01 or P＜0.05).In comparison with normal group,plasma and intestine levels of sP in model group were significantly reduced(P＜0.01),while plasma and intestine levels of SS were increased significantly(P＜0.01).compared with model group,plasma and intestine levels of sP were increased in tegaserod,emodin or domperidone treated groups (P＜0.01 or P＜0.05),while plasma and intestine levels of SS in both groups were significantly decreased(P＜0.01 or P＜0.05).Serum TG and TC in the model group and tegaserod or domperidone treated groups were significantly higher while HDL-C was lower than those in normal group(P＜0.01),but in emodin treated group,these detected indexes were rectified(P＜0.01).Conclusion Emodin and tegaserod can promote the gastrointestinal motility in type 2 diabetic rats.The enhancement of the gastrointestinal motility by emodin and tegaserod might be partially explained by its rectification of the abnormal expression of gastrointestinal hormones. |
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