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作 者:郭建友[1] 杨元霄 赵保胜[1] 刘洪斌[1] 李兰芳[1] 郭淑英[1] 霍海如[1] 姜廷良[1]
机构地区:[1]中国中医科学院中药研究所唐氏中药研究中心,北京100700 [2]浙江中医学院,杭州310053
出 处:《中国药学杂志》2006年第8期596-599,共4页Chinese Pharmaceutical Journal
基 金:国家自然科学基金资助项目(90209006)
摘 要:目的观察桂枝汤中分离获得的单体成分桂皮醇对发热相关的环氧酶(COX)和前列腺素E2(PGE2)的影响。方法建立大鼠脑微血管内皮细胞(rCMEC)培养,进行Ⅷ因子相关抗原鉴定。待细胞生长至融合状态后加入不同终浓度的桂皮醇(0.093,0.186,0.372,0.744,1.488 mmol.L-1)孵育3 h,之后以30μg.L-1的IL-1刺激12 h。ELISA方法检测细胞培养液中PGE2的含量及细胞内COX-1,COX-2的活性。结果Ⅷ因子抗体免疫组化染色可见95%的培养细胞呈阳性,确认为rCMEC。暴露于质量浓度为30μg.L-1IL-1后,rCMEC内COX-2活性及释放的PGE2量显著增加(P<0.01),COX-1活性变化无统计学差异(P>0.05)。加入不同浓度的桂皮醇后,随浓度增加可下调COX-1、COX-2活性及PGE2量,且呈浓度依赖关系;至浓度为0.744mmol.L-1时,COX-2活性及释放的PGE2与IL-1单独作用组相比均有显著性差异(P<0.05),COX-1活性虽有所降低,但无统计学上的显著差异(P>0.05)。结论桂皮醇能下调IL-1刺激rCMEC释放升高的PGE2,作用机制可能与抑制COX-2活性有关。OBJECTIVE To observe the effect of cinnamyl alcohol on the activity of COX and PGE2 release in rat cerebral microvascular endothelial cells (rCMEC) stimulated by 1L-1. METHODS rCMEC were cultured, and identified by immunohistochemistry for Von Willebrand Factor (Ⅷ factor, a marker for all endothelial cells) in the cytoplasm of the cells. Different concentrations of cinnamyl alcohol were added respectively and incubated for 3 h, then IL-1 stimulated for another 12 h. The activity of COX-1 and COX-2 in rCMEC, and production of PGE2 in the conditioned media were measured by ELISA. RESULTS Positive immunostaining for Ⅷ factor was present diffusely in the cytoplasm of 〉 95 % rCMEC. After heing exposed to 30μg· L^-1 IL, the activity of COX-2 in rCMEC and the production of PGE2 in conditioned media were higher than those in control group ( P 〈 0.01 ), while there was no difference on the activity of COX- 1 hetween the two groups ( P 〉 0.05). Cinnamyl alcohol down-regulated them with a concentration-dependen manner, and significant differences on the activity of COX- 2 and amount of PG2 were showed as the concentration reached 0. 744 mmol· L^- 1 ( p 〈 0.05). CONCLUSION Cinnamyl alcohol can affect the PGE2 release in rCMEC induced by IL-1, which might he related with its inhibition on the activity of COX-2.
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