Objective:To explore the role and the intervention effect of emodin in intestinal neuropathy in rats with severe acute pancreatitis (SAP) through the nucleotide binding oligomerization domain like receptor protein 3/cysteine containing aspartic acid protease-1 (NLRP3/Caspase-1) pathway.Methods:Forty male healthy SD rats aged 6-8 weeks with a weight of approximately 200g were randomly divided into control group, SAP model group, emodin treatment (EMO) group, and NLRP3 knockdown group. SAP were induced by retrograde injection of sodium deoxycholate into the pancreatic duct of rats and serum amylase of which were detected. The effective NLRP3 knockdown sequence was screened for NLRP3 knockdown animal experiments. Fluorescence quantitative polymerase chain reaction was used to detect the expression of NLRP3, Caspase-1, gasdermin-D (GSDMD), interleukin (IL)-1β, IL-18 and tumor necrosis factor-α(TNF-α) in the small intestine of each group. Immunofluorescence staining was used to detect the expression of glial fibrillary acidic protein (GFAP) in the small intestine of each group.Results:The amylase levels of the control group, SAP group, EMO group, and NLRP3 knockdown group were (277.73±24.92) U/L, (1018.57±282.89) U/L, (625.43±134.40) U/L, and (391.01±27.63) U/L, respectively. The SAP and EMO groups were significantly higher than the control group ( P<0.001), while the EMO and NLRP3 knockdown groups were significantly lower than the SAP group (all P<0.001). Compared with control group, the expression levels of NLRP3, Caspase-1, IL-1β, IL-18, TNF-α and GSDMD in SAP group were increased, with statistical significance (all P<0.001). Compared with SAP group, the NLRP3 knockdown group showed the expressionlevels of the above 6 genes were all decreased, and EMO group showed decreased gene expressing levels of NLRP3, IL-1β, IL-18 and TNF-α, with statistical significance (all P<0.05). The relative expression of GFAP in small intestine of control group, SAP group, EMO group and NLRP3 knockdown group were (1.00±0), (1.66±0.11), (1.13±0.02) and (1.13±0.02), respectively. Among them, the expression of GFAP in SAP group was increased compared with the control group; The expression of GFAP in EMO group and NLRP3 knockdown group was lower than that in model group, and the differences were statistically significant (all P<0.05). Conclusions:Emodin and knocking down NLRP3 can both promote the repair of SAP small intestine injury through the NLRP3/Caspase-1 signaling pathway, and thus play a protective role in the intestine.

OBJECTIVE To explore t he protective mechanism of Yangxin dingji capsules on the cardiomyocytes of diabetic cardiomyopathy（DCM）model golden hamsters. METHODS In this study ，golden hamsters were divided into control group （n＝ 10，no modeling ，no drug administration ），model group （n＝9，modeling，no drug administration ），TCM high-dose group [ n＝8， modeling，Yangxin dingji capsules 2 g/（kg·d）]，TCM low-dose group [ n＝8，modeling，Yangxin dingji capsules 1 g/（kg·d）] and empagliflozin group [ n＝9，positive control ，modeling，10 mg/（kg·d）]. All the golden hamsters were gavaged continuously for 8 weeks. The general conditions of golden hamsters were observed during the experiment. Blood glucose ，total cholesterol （TC）and creatine kinase MB （CK-MB），ejection fraction （EF），fractional shortening （FS），interleukin 1β（IL-1β）and transforming growth factor β1（TGF-β1）were detected ；the histopathological changes of myocardium were observed. mRNA and protein expression of nucleotide-binding oligomerization domain-like receptor protein 3（NLRP3），caspase-1，aspirin D （GSDMD），nuclear factor κB （NF-κB）and IL- 1β were detected and observed；DNA damage in myocardial was detected. RESULTS Compared with control group，the blood glucose ，TC，CK-MB，serum IL- 1β，TGF-β1 levels，the mRNA expressions and positive protein expression of NLRP 3，caspase-1，GSDMD，NF-κ B and IL-1 β and protein expression of GSDMD in golden hamsters were significantly increased in model group （P＜0.05 or P＜0.01） EF and FS were significantly decreased （P＜0.01）；the fibers of myocardial cells was disordered ， and the blue-stained collagen fibers between the myocardium increased ； DNA damaged positive cells in myocardial tiss ue of gold hamsters increased significantly. Compared with model group，the above indexes of administration groups were reversed to varying degrees ；the gap of myocardial cells were clear ，and the fibers disorder was improved ；the DNA damaged positive cells in the myocardial tissue were reduced to varying degrees. CONCLUSIONS Yangxin dingji capsule can inhibit the cardiomyocyte pyroptosis and relieve the inflammatory injury of DCM in DCM model golden hamsters by regulating the NLRP 3/caspase-1/GSDMD signaling pathway ，so as to protect the cardiomyocytes.