Effect of astragalus polysacharin on bone resorption in experimental periodontitis / 中草药

Objective To analyze the effect of astragalus polysacharin (APC) on bone resorption in experimental periodontitis, and evaluate its protective function of inflammatory resorption of alveolar bone in periodontits. Methods SD rats were randomly divided into five equal groups: contorol group, model group, and APC low [LD: 100 mg/(kg∙d)], medium [MD: 200 mg/(kg∙d)], and high dose [HD: 500 mg/(kg∙d)] treatment groups. The periodontitis models were established through Porphyromonas gingivalis attracting. APC [LD: 100 mg/(kg∙d); MD: 200 mg/(kg∙d); HD: 500 mg/(kg∙d)] gavage was given to treatment groups, and the same amount of normal saline was given to control and model groups. The rats executed after four weeks, their CEJ-ABC distance (CAD) and expression of IL-1β, IL-6, TNF-α, TOS, TAS, RANKL, OPG in their serum was evaluated, and the oxidative stress index (OSI) was calculated. Results As APC amount increased, CAD, TOS, and OSI levels were declined significantly; While TAS, RANKL, RANKL/OPG levels were improved significantly; There was no significantly change on IL-1β, IL-6, TNF-α, and OPG levesl among groups. Conclusion APC prevents alveolar bone from oxidative stress and inflammatory damage by down-regulating OSI and RANKL/OPG.

Effects of astragalus polysacharin on fibroblast proliferation and adhesion between HUVECs and white cells / 中国病理生理杂志

AIM: To investigate the effects of Astragalus polysacharin(APS) on human fibroblast and human umbilical vein endothelia cell (HUVEC) proliferation, as well as its acts on adhesion between white cells and HUVECs. METHODS: Human fibroblasts from distal and proximal skin away the ulcer were cultured as normal fibroblasts(NF) and wounded fibroblasts(WF). MTT assay was used for detecting cell proliferation, Rose Bengal staining and fluorescence immunohistology assay were used for examining the adhesion of human polymorpho-nuclear cell(PMN) and TPH-1 to HUVECs. RESULTS: 2 44-156 mg/L APS promoted WF proliferation, and 2 44-39 mg/L APS also promoted NF proliferation, but it did not show any proliferating effect on HUVECs. APS inhibited the adhesion of PMN or TPH-1 to HUVECs induced by tumor necrosis factor(TNF). At 25-100 mg/L, it also inhibited both VCAM-1 and ICAM-1 expression in HUVECs induced by TNF. Treatment with APS for 12 h also inhibited CD44 expression in HUVECs. CONCLUSION: APS shows mitogenic activity on both human normal and wounded fibroblasts. It also exerts anti-inflammation effects by inhibiting adhesion molecule expression and adhesion of white cells to HUVECs. [