Chronic pancreatitis (CP) is characterized by progressive pancreatic fibrosis, which can lead to irreversible pancreatic endocrine and exocrine dysfunction. Previous reported studies suggested that in patients with CP, there are varying degrees of intestinal bacteria imbalance. In addition, intestinal bacteria have been found to associate with a variety of fibrosis-related diseases. The purpose of this study is to analyze the possible mechanisms of intestinal bacteria in progression of pancreatic fibrosis in CP, by investigating regulation of intestinal barrier, regulation of immunity, and synthesis and release of metabolites, to provide further references in exploring the clinical value of intestinal bacteria in diagnosis and treatment of CP.

【Objective】 To clarify the role and molecular mechanism of Tanshinone ⅡA (TanⅡA) in the pathological integration of granule cells in the dentate gyrus (DG) by using the mouse model of temporal lobe epilepsy (TLE). 【Methods】 Status epilepticus (SE) was induced in the mice with pilocarpine and treated with TanⅡA 5 mg/kg. After two months, Morris water maze was used to examine the spatial learning and memory ability and video surveillance was used to monitor spontaneous seizures. The DG was removed for staining of Timm, Prox-1, DCX and SynⅠ. PTEN, p-AKT, and p-S6 expressions were observed by Western blotting. 【Results】 TanⅡA decreased Timm score, SynⅠ, PSD-95 and pS6 levels, and increased the level of PTEN in the DG, and attenuated the formation of mossy fiber sproutings and basal dendrites of the granule cells. Video surveillance showed that TanⅡA reduced the frequency of Racine’ grade 5 seizures. 【Conclusion】 TanⅡA can effectively attenuate the abnormal integration of the granule cells in the DG by regulating PTEN/AKT/mTOR pathway and thus plays an anti-epileptic role.