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目的:通过观察芪冬活血饮大鼠药物血清对NF-κB抑制巨噬细胞炎症细胞因子及TLR4、Cav-1、NF-κBp65 mRNA表达的影响,探讨其炎症调控的机制。方法:将巨噬细胞分为空白对照组(UT组)、LPS组、NF-κB抑制组(NI组)、NF-κB抑制+LPS组(NL组)、LPS加空白血清组(LB组)、LPS加药物血清组(LD组)、NF-κB抑制+LPS+空白血清组(NLB组),NF-κB抑制+LPS+药物血清组(NLD组)8组。巨噬细胞予阻断剂阻断0.5 h后加入LPS致炎,并予药物血清干预,LPS处理12 h后测定各组细胞上清液TNF-α、IL-1β、IL-10水平,及TLR4、Cav-1、NF-κBp65 mRNA相对表达量。结果:LD组TNF-α、IL-1β、IL-10水平及NF-κBp65、Cav-1、TLR4 mRNA相对表达量均低于LB组和LPS组,比较有统计学意义;NLD组TNF-α、IL-1β、IL-10水平及NF-κBp65、Cav-1、TLR4mRNA相对表达量均低于NL组,两组TNF-α、IL-1β有显著统计学差异,NF-κBp65mRNA、IL-10比较差异无统计学意义,Cav-1、TLR4mRNA比较差异有统计学意义。结论:芪冬活血饮药物血清可减轻LPS刺激的巨噬细胞炎性反应;除TLR4/Cav-1/NF-κBp65途径外,芪冬活血饮还可以通过非NF-κBp65途径降低炎症反应。
OBJECTIVE: To investigate the effect of Qi Dong Huoxue Yin serum on the inflammatory cytokines and the expression of TLR4, Cav-1 and NF-κBp65 mRNA induced by NF-κB in macrophages. Methods: Macrophages were divided into four groups: untreated group (UT), LPS group, NF-κB inhibitory group (NI group), NF-κB inhibition + LPS group (NL group), LPS plus blank serum group , LPS plus drug serum group (LD group), NF-κB inhibition + LPS + blank serum group (NLB group) and NF-κB inhibition + LPS + drug serum group (NLD group). After macrophages were blocked for 0.5 h, LPS was added to induce inflammation and serum was given to the mice. After 12 h of LPS treatment, the levels of TNF-α, IL-1β, IL-10 and TLR4 , Cav-1, NF-κBp65 mRNA relative expression level. Results: The relative expression of TNF-α, IL-1β, IL-10 and the expressions of NF-κBp65, Cav-1 and TLR4 in LD group were lower than those in LB group and LPS group , IL-1β, IL-10 and the relative expressions of NF-κBp65, Cav-1 and TLR4 mRNA in NL group were significantly lower than those in NL group. The levels of TNF-α and IL- The difference was not statistically significant, Cav-1, TLR4 mRNA differences were statistically significant. Conclusion: Qidudonghuoxueyin serum can reduce the LPS-stimulated macrophage inflammatory reaction. In addition to the TLR4 / Cav-1 / NF-κBp65 pathway, Qidudong Huoxue Yin can also reduce the inflammatory reaction through the non-NF-κBp65 pathway.