Ethyl Acetate Extract from Celastrus aculeatus Merr. Suppresses Synovial Inflammation in Adjuvant Arthritis Rats through Apoptosis Induction of CD4(+)CD25(+)FOXP3(+) T Cells.

Celastrus aculeatus Merr. has been widely used in traditional Chinese medicine to treat rheumatoid arthritis (RA) in clinic. However, the main active fraction of this plant is still unclear. In this study, we attempted to evaluate the suppressive effect of ethyl acetate extract (EAE) from Celastrus aculeatus Merr. on synovial inflammation in adjuvant arthritis (AA) rats induced by Mycobacterium tuberculosis H37Ra (Mtb) and to explore the underlying mechanisms. SD rats immunized with heat-killed Mtb were fed with EAE and observed for erythema, swelling, and induration of each paw. The pathologic changes in joint synovium were tested by hematoxylin-eosin staining. Apoptosis induction of synoviocytes was tested immunohistochemically. Apoptosis of peripheral lymphocytes and the level of regulatory T cells were analyzed by flow cytometry. After treatment with EAE, the joint inflammation in rats with AA was alleviated. Both apoptotic ratios of synoviocytes and peripheral lymphocytes and the ratio of CD4(+)CD25(+)FOXP3(+) to CD4 regulatory T cells were significantly increased. In summary, we first demonstrated that EAE of Celastrus aculeatus Merr. can inhibit synovial inflammation in AA rats through apoptosis induction of CD4(+)CD25(+)FOXP3(+) T cells. Our study provides a rationale for the application of Celastrus aculeatus Merr. to treat RA.

[Protective effect of licoflavone on gastric mucosa in rats with chronic superficial gastritis].

OBJECTIVE: To evaluate the protective effect of licoflavone on gastric mucosa in rats with chronic superficial gastritis and explore the possible mechanism. METHODS: SD rat models of chronic superficial gastritis was established by intragastric administration of 0.02% ammonia and long-term irregular diet. The rat models were then randomized into model group, vitacoenzyme group and 3 licoflavone groups of high, medium, and low doses. After 30 days of treatment, the gastric histopathology, mucosal lesions, scanning electron microscopy, mucin function production by the gastric mucosa epithelial cells, serum PGE(2) level and gastric microcirculation were assessed to evaluate the protective effect of licoflavone on gastric mucosa. RESULTS: Compared with normal control rats, the rat models of chronic superficial gastritis showed significantly higher gastric mucosal injury rate, histopathological scores and gastric mucin content. Licoflavone significantly ameliorated gastric pathology and increased serum PGE(2) level, enhanced acidic mucin secretion by the epithelial cells, and improved gastric microcirculation in the rat models. CONCLUSION: Licoflavone feeding suppresses gastric mucosa injury, protects and restores the injured mucosa in rats with chronic superficial gastritis, and these effects are related with the up-regulation of serum PGE(2) level.