ObjectiveTo investigate the effect of emodin on the expression of hypoxia inducible factor (HIF)-1α protein in rats with severe acute pancreatitis-associated renal injury and explore the possible mechanisms. MethodsA total of 72 rats were randomly divided into sham-operated group (n=24), severe acute pancreatitis with renal injury group (injury group, n=24), and treatment group (n=24). The sham-operated and injury groups were given 1.5 mL saline through intragastric administration before operation while the treatment group was fed with the same amount of 50 mg/kg emodin diluent. The pancreas and pancreatic tail-segment was dissociated and the head of pancreas was occluded in rats to form the model, and blood vessel forceps were loosed after three hours. All the rats were sacrificed 12, 24 and 36 hours after modeling. The level of ascites, serum amylase, creatinine, blood urea nitrogen were detected. Hematoxylin-eosin staining was used to observe the pancreatic and renal pathological changes, and immunohistochemical method was used to detect the expression of HIF-1α protein level in the kidney. ResultsCompared with the sham-operated group, the level of ascites, serum amylase, creatinine, blood urea nitrogen and the expression of HIF-1α protein level increased significantly. The tissue damage of pancreas and the kidney became more serious. Compared with the injury group, the kidney and pancreas function of the treatment group had a better performance. HIF-1α protein level significantly increased in the treatment group, and the difference had a statistical significance (P<0.05). ConclusionEmodin has a good protective effect on severe acute pancreatitis-associated renal injury. It may function through up-regulation expression of HIF-1α protein level to improve the ability of the kidney to tolerate hypoxia, and then reduce the cell apoptosis and necrosis of the kidney.
This research was aimed to study the effect of Emodin gel on the hypertrophic scars of rabbit ears. A total of 18 rabbits were randomly divided into Emodin group (9 rabbits) and control group (9 rabbits) after the successful animal model for hypertrophic scars had been made. The rabbits in the Emodin group were treated with Emodin Gel,while no special treatment was given to those in the control group. The other living conditions were all kept the same in the two groups. The diameter,hardness, and expression of transforming growth factor-β (TGF-β) and interleukin-1 (IL-1) of hypertrophic scars were measured after 4 weeks. Transmission electron microscopy was applied to observe the ultra-structure of the fibroblasts of hypertrophic scars. But there was no difference between the two groups in the diameter of hypertrophic scars (P>0.05). The hardness, expression of TGF-β and IL-1 in hypertrophic scars in the Emodin group decreased, compared to the control group (P<0.05, P<0.01, P<0.05). Transmission electron microscopy showed that the fibroblast and organelle lessened in the cytoplasm and the collagen fibers dissolved obviously. The study showed that Emodin gel decreased the hardness of hypertrophic scars in the rabbit ears, and inhibited the proliferation of fibroblasts in local area. Therefore, Emodin gel treatment would be one of the methods to prevent and treat hypertrophic scars.
ObjectiveTo investigate the changes of amount of interstitial cells of Cajal (ICC) and expression of stem cell factor (SCF)/c-Kit in the process of cathartic colon induced by emodin in mice. MethodsA modified cathartic colon mouse model was established. Seventy-two healthy male Kunming (KM) mice were randomly divided into the blank control group and sustained drug delivery group.Morphological changes of colon in mice were observed; frozen section immunofluorescence was used to observed changes of amount of ICC; serum concentrations of SCF were examined by ELISA; Western blot was employed for observation of expression of SCF/c-Kit in colon. ResultsAfter the mice model were completed, the weight of mouse, length and diameter of entire colon were all reduced compared with the blank control group. The amount of ICC appeared to decline in the beginning of the first 6 weeks with emodin used, and significant decreased in 10-12 weeks. The serum concentrations of SCF first began to decline in 4 weeks with emodin used, and significantly decreased in 6 weeks, and continued at a low level after 8 weeks. The expression of c-Kit in colon began to decline in 4 weeks with emodin used and significantly reduced after 8 weeks. Conciusions The amount of ICC appear to slowly decline in the beginning of the first 12 weeks with emodin used, and significant decrease after 12 weeks.The serum concentrations of SCF and expression of c-Kit in colon have the dynamic changes in the meanwhile, and the changes of SCF are earlier than that of c-Kit. The trend of amount ofICC may have a certain relationship with changes of SCF and c-Kit.