| Objective: To investigate the protective and functionalmechanism of emodin on intestinal motility dysfunction in rats withsevere acute pancreatitis through establishing rat model withsevere acute pancreatitis, testing morphological markers of pancreas,detecting the pushing rate of small bowel and apoptosis of smooth musclecells.Methods: Forty-five SD rats were randomly divided into3groups:severe acute pancreatitis group（SAP group in short）, emodin treatmentgroup (Emodin group in short) and sham operation group (SO group inshort),15in each group. For SAP group and Emodin group, rats modelswere established through uniformly injecting3.8％sodium taurocholatesolution into pancreas subcapsule, while the model in SO group was setthrough merely turning rats’ pancreas after opening abdomens.Rats inEmodin group were injected emodin solution10cm away frompylorus(0.5ml/100g，concentration5mg/ml), while rats in other groupswere injected the same amount of Sodium Chloride at the same place.Forty-eight hours after setting up models, rats’ stomachs were per-fused with methyl cellulose and then pushing rates of small bowels weredetected thirty minutes later. After killing rats, the pancreas wereembedded, sliced and stained and then examined histologically. Intestinal tissue was fixed with glutaraldehyde and its ultrastructural changes wereobserved by electron microscope. After embedding and slicing rats’ smallintestine tissues, TUNEL method was used for detecting apoptosis andimmunohistochemistry for detecting cytochrome C. Then small intestinetissues were taken out, mucosa,submucosa and serosa layer weremechanically separated to obtain smooth muscle tissues to preparesingle-cell suspension and test the mitochondria membrane potential. Themeasurement data were described by means±standard deviations(x±S),with SPSS13.0statistics software for one-way ANOVA analysis and LSDmethod for comparison between groups at various levels. There wassignificant difference between groups (P <0.05) with the inspectionlevel α=0.05. Results:1. Pushing rate of rats’ small intestine revealedthe pushing rate in SAP group decreased obviously compared withEmodin and SO groups(P<0.05); whereas, the pushing rate in Emodingroup was obviously higher than that of the SAP group and the differenceis quite remarkable（P<0.05）.2. After the laparotomy of rats in SO group,there were no bloody ascites and no necrosis bleeding of pancreatic tissue.However, after that in SAP group, large amount of bloody ascites wasquite visible to naked eyes, gastrointestinal pneumatosis was obvious,bleeding and necrosis of pancreatic tissue were sharp and hemorrhage andnecrosis were visible in the greater omentum; while as for rats in Emodingroup, a little reddish ascites was visible and gastrointestinal pneumatosis was significantly reduced compared with SAP group and rat pancreaticnecrosis bleeding was also reduced. Pancreatic pathology score suggestedthat there are significant differences between pathology scores of SAPgroup, SO group and Emodin group（P<0.001）, and the pathology scoresof Emodin group are significantly lower than SAP group (P <0.001).3.The ultramicrostructure of smooth muscle in small intestine showed thatin SAP group, their cell mitochondria decreased significantlyaccompanied with edema and rupture; while in Emodin group, their cellmitochondria decreased insignificantly with merely slight edema; in SOgroup, the ultramicrostructure remained quite normal.4. The results ofcell apoptosis and cytochrome C of smooth muscle in small intestineindicated the positive expression degree in SAP group was much higherthan that of Emodin group and SO group（P<0.001）, whereas. thepositive expression degree in Emodin group decreased obviouslycompared with that of SAP group（P<0.05）.5. The results of cellmitochondrial membrane potential of Small intestinal smooth muscleshowed that the mitochondrial membrane potential in SAP group (greenfluorescence intensity:5.07±0.92) was obviously lower than that of SOgroup (green fluorescence intensity:2.40±0.5) and the mitochondrialmembrane potential in Emodin group (green fluorescence intensity:3.28±0.28) increased greatly compared with SO group (green fluorescenceintensity:5.07±0.92). Conclusion:1. Injecting3.8％sodium taurocholate solution into pancreas subcapsule can successfully induce ratmodel with severe acute pancreatitis.2. Intestinal motility dysfunctionappeared in SAP, which can be protected effectively by emodin.3.Emodin may have a protective effect on intestinal motility dysfunction bymeans of improving the ultramicrostructure of smooth muscle in smallintestine and inhibiting the apoptosis of small intestinal smooth musclecells. |
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