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为观察小鼠脾巨噬细胞内的TLR4和TLR2在脂多糖 (LPS )刺激后 ,地塞米松 (Dx )对其表达量的影响 ,在向BALB/c小鼠腹腔内注射LPS和Dx后采用贴壁法分离小鼠脾巨噬细胞 ,通过半定量RT PCR方法测定了TLR4和TLR2mRNA的表达量。结果显示 :①LPS刺激后 ,小鼠脾巨噬细胞内TLR4mRNA显著上调 (吸光度比为 0 11) ,TLR2上调不明显 (吸光度比为0 0 0 8) ;②预先注射不同剂量Dx ,分别为 0 1mg/kg、 1mg/kg、 10mg/kg ,再用LPS刺激小鼠。注射了Dx后巨噬细胞TLR4mRNA表达量较单纯注射LPS的小鼠显著降低 (吸光度比分别为 0 0 93、 0 0 5 0和 0 0 14 ) ;但TLR2mRNA表达量随着Dx使用剂量增加而增加 (吸光度比分别为 0 0 5 4、 0 0 80和 0 16 1)。该项研究表明TLR4是参与LPS引起炎症反应的主要Toll样受体 ,而TLR2不起主要作用 ;Dx对LPS刺激后TLR 4mRNA的表达有抑制作用 ,而对TLR2mRNA的表达有增强作用 ;Dx抑制LPS引起的炎症反应可能与抑制TLR4的表达有关
To observe the effect of dexamethasone (Dx) on the expression of TLR4 and TLR2 in splenic macrophages after lipopolysaccharide (LPS) stimulation in mice, intraperitoneal injection of LPS and Dx into BALB / c mice Mice splenic macrophages were isolated by adherent method. The expression of TLR4 and TLR2 mRNA was determined by semi-quantitative RT-PCR. The results showed that: (1) TLR4mRNA was significantly up-regulated in splenic macrophages after LPS stimulation (absorbance ratio was 0 11), TLR2 upregulation was not obvious (absorbance ratio was 0 0 0 8); ② pre-injection of different doses of Dx were 0 1mg / kg, 1 mg / kg, 10 mg / kg, and then stimulated with LPS. The expression of TLR4 mRNA in macrophages after Dx injection was significantly lower than that in mice injected with LPS alone (absorbance ratios were 0 0 93, 0 0 0 0 0 and 0 0 14, respectively); however, TLR2 mRNA expression increased with Dx dose (Absorbance ratios of 0 0 5 4, 0 0 80 and 0 16 1, respectively). This study shows that TLR4 is the major Toll-like receptor involved in LPS-induced inflammation, whereas TLR2 has no major role. Dx can inhibit the expression of TLR4 mRNA and enhance the expression of TLR2 mRNA after LPS stimulation. Dx inhibits LPS The inflammatory reaction may be related to the inhibition of TLR4 expression