ABSTRACT
Aim To observe the effect of Sinomenine on the activation of NF-?B and the degradation of its inhibitor I-?B in peritoneal macrophages of BALB/c mice in vitro and provide experimental evidence for further evaluation of the antiinflammatory and antirheumatic effects of Sinomenine. Methods Effect of Sinomenine on the activation of NF-?B p65 in the cells was investigated by using fluorescence-labelling and laser confocal scanning microscopy; Effect of Sinomenine on the degradation of I?B-? was investigated by Western blot. Results SIN (0.25,1.25 mmol?L -1) attenuated the activation of NF-?B p65 in peritoneal macrophages of BALB/c mice induced by LPS in vitro. SIN(0.25,1.25 mmol?L -1) inhibited the degradation of I-?B-? in peritoneal macrophages of BALB/c mice induced by LPS in vitro. Conclusion SIN can partially inhibit the activation of NF-?B p65 and the degradation of I?B-? in peritoneal macrophages of BALB/c mice induced by LPS in vitro.
ABSTRACT
Objective: To assess the immunological effects by orally administering chicken type Ⅱ collagen(CCⅡ) on collagen-induced arthritis(CIA)mice. To assess the effect on producing IL-1 of peritoneal macrophage in adjuvant arthritis rats by orally administering CCⅡ. Methods: Arthritis were induced in Kunming mice by immunization with chicken type Ⅱ collagen with Freund's complete adjuvant, followed by an interperitoneal injection of CCⅡ 3 weeks later.Chicken type Ⅱ collagen was orally administered from 5 days prior to the induction of arthritis to 14 days after inducing arthritis model. The animals were examined visually twice weekly for polyarthritic signs of swollen and erythemic limbs. Quantitation of antibody level of CIA mice was measured by ELISA method. Subpopulations of T lymphocytes in mice were evaluated by flow cytometry method. IL-1 assay was evaluated by ELISA method. Results: Joint swelling was significantly reduced at a dose of 5 μg.kg-1 and 50 μg.kg-1 of CCⅡ, but not at 250 μg.kg-1. The level of anti-collagen antibodies was also reduced at a dose of 5 μg.kg-1 and 50μg.kg-1 (OD value from CIA model control 0.242±0.073 to CCⅡ 5 μg.kg-1 0.123±0.029 and CCⅡ 50 μg.kg-1 0.110±0.075 respectively). Subpopulations of T-lymphocytes were changed by orally administering of CCⅡ, and the ratio of L3T4+/Lyt-2+ was lowered (the ratio from 1.71 of CIA model control to 1.21, 1.51 of administered CⅡ 5 μg.kg-1, 50μg.kg-1 respectively.) after administering CCⅡ. IL-1 level can be reduced (the value from adjuvant arthritis model control 62.8±0.9 to 43.4±1.3, 49.7±0 ng.L-1 administered CⅡ 5 μg.kg-1, 50μg.kg-1 respectively). Conclusion: Arthritis sign in CIA animal model can be suppressed by oral CCⅡ. The effects may be involved by influencing the mechanisms both humoral and cellular immunity. The effects occurred at lower doses of CCⅡ. These results demonstrated the biologic relevance of by-stander suppression associated with oral tolerance, and the potential use of this approach to treat human inflammatory joint diseases.
ABSTRACT
AIM: To discuss the influence of high glucose on the proliferation and ICAM-1 expression of human umbilical vein endothelial cells(HUVEC) within 48 h and to observe the altered effect of high glucose when high glucose and inflammatory stimulator exist at the same time.METHODS: HUVEC were cultured with different concentrations of glucose.The proliferation of HUVEC induced by high glucose was detected by MTT assay.The ICAM-1expression of HUVEC induced by high glucose was assayed by flow cytometry and cell ELISA.The difference of ICAM-1 expression between induced by LPS and by LPS together with high glucose was compared.RESULTS: 25、(45 mmol?L~(-1)) glucose did not inhibit the proliferation of HUVEC within 48 h,and they also had no effect on the expression of ICAM-1.However,when stimulated HUVEC with LPS, the proliferation of HUVEC was extremely inhibited in high glucose groups,and the expression of ICAM-1 increased significantly in those groups.CONCLUSION: In short time,high glucose has no effect on the proliferation and ICAM-1 expression of HUVEC,but when inflammatory stimulation exists,high glucose can inhibit the proliferation and increase the expression of adhesion molecules.