[Sijunzi Decoction Promote the Repair of Intestinal Epithelial Cell Injury via Activating TLR-2/My D88 Signaling Pathway].

Objective: To study the effect and mechanism of Sijunzi decoction( SJZD) containing serum on the repairing of gastrointestinal mucosal damage. Methods: SJZD containing serum was prepared by serum pharmacological method. Cell migration model was established by tips scratch method, Real-time-cell-analyzer( RTCA) was used to mensurate IEC-6 cell proliferation, the mRNA and protein expression of TLR-2 and My D88 mRNA were detected by qRT-PCR and Western blot analysis,respectively. Results: Medium dose( 10%) and high dose( 20%) of SJZD containing serum stimulated IEC-6 cell migration at 8 h after cell damage; medium dose( 10%)and high dose( 20%) of SJZD containing serum increased IEC-6 cell proliferation at 12 h after cell damage; low dose( 5%),medium dose( 10%) and high dose( 20%) of SJZD containing serum enhanced IEC-6 proliferation both at 24 h and 36 h after cell damage. Medium dose( 10%) and high dose( 20%) of SJZD containing serum upregulated TLR-2 and My D88 mRNA and protein expression,respectively. Conclusion: Sijunzi decoction can repair the injury of gastrointestinal mucosal barrier,the mechanism may be related to its effect on activating TLR-2 / My D88 signaling pathway,and promoting IEC-6 cell migration and proliferation.

Phenotypic characterization of type II collagen-induced arthritis in Wistar rats.

The aim of the present study was to determine a more specific, efficient and simple method for the induction of collagen-induced arthritis (CIA) in rats. Different strains of rats were injected at the base of the tail with bovine type II collagen (CII) emulsified in incomplete Freund's adjuvant (IFA). The onset and severity of arthritis were evaluated by clinical assessment. The established CIA model was analyzed using a comprehensive examination of clinical, hematological, histological and radiological parameters. The results demonstrated that Wistar rats were the most susceptible strain to CIA followed by Wistar Furth rats, with Sprague Dawley rats being the least susceptible. Following primary and booster immunization, female Wistar rats developed severe arthritis, with an incidence of >83% and low variability in clinical signs. The development of arthritis was accompanied by a significantly elevated erythrocyte sedimentation rate compared with that in the control rats. The radiographic examination revealed bone matrix resorption, considerable soft tissue swelling, periosteal new bone formation and bone erosion in the arthritic joints of the CIA rats. Histopathologically, the synovial joints of CIA rats were characterized by synovial hyperplasia, pannus formation, marked cellular infiltration, bone and cartilage erosion and narrowing of the joint space. The administration of an intradermal injection of only 200 µg bovine CII emulsified in IFA at the base of the tail therefore leads to the successful development of a CIA rat model. This well-characterized CIA rat model could be specifically used to study the pathophysiology of human rheumatoid arthritis as well as to test and develop anti-arthritic agents for humans.