OBJECTIVE: To explore the effect of berberine(Ber) on Toll-like receptor 2(TLR2) signaling pathway and inflammatory cytokines. METHODS: RT-PCR was applied to detect effect of 100 mol?L-1 Ber on the expression of TLR2 in RAW264.7 cells stimulated by bacteria lipoprotein (BLP).Western-blot method was used to measure the level of phosphorylation of inhibitory protein of anti-nuclear factor B (I?B) and ELISA detection for the secretion of inflammatory cytokines. RESULTS: Ber promoted the expression of TLR2, the activation of I?B, IFN and secretion of TNF after 6 h and 12 h of test; Ber inhibited them after 24 h and 48 h of test. Ber induced the secretion of I?B and IL-13. CONCLUSION: Ber can dual regulate the activation of TLR2 signaling pathway and indeuce the secretion of anti-inflammatory cytokines, which play a role in fighting against bacteria and inflammatory.

OBJECTIVE:To explore the effect of rutaecarpine(Rut)on the expression of angiotensin C in the thoracic artery of hypertensive rats.METHODS:Two-kidney and one-clip goldblatt(2K1C)hypertensive model rats were enrolled in our study.The blood pressure of the model rats was measured by tail-clipping method.The model rats were assigned to receive losartan(20 mg?kg-1?d-1)or Rut(10,40 mg?kg-1?d-1)with their blood pressure was followed every week.The morphology of aorta was analyzed and the content of angiotensin C in the thoracic artery was detected by Western blotting.RESULTS:After treatment with Rut for 4 weeks,the systolic arterial pressure(SAP)in the treatment group decreased significantly;as compared with model group,the luminal diameter dilated significantly,the medium thickness of the artery decreased,angiotensin Ⅱ level in plasma and arteries decreased significantly,while the expression of angiotensin C increased significantly.CONCLUSION:Rut can effectively decrease blood pressure and improve arterial remodeling in model rats.The mechanism might be associated to the deactivation of angiotensin Ⅱ and the activation of kallikrein medicated by the enhanced expression of angiotensin C.