雷公藤内酯通过下调CⅡTA抑制BV-2小胶质细胞MHCⅡ表达

Triptolide inhibited the expression of MHC Ⅱ through downregulating the expression of CⅡTA in kainic acid-activated BV-2 microglia

目的观察雷公藤内酯对海人酸活化的BV-2小胶质细胞MHCⅡ分子表达的影响,并探讨其相关的分子机制。方法将BV-2细胞随机分为对照组、海人酸组、雷公藤內酯组,免疫组化方法检测雷公藤内酯对海人酸活化的BV-2细胞MHCⅡ和CⅡTA蛋白的影响。结果对照组MHCⅡ阳性BV-2细胞为(0.059±0.005),海人酸组MHCⅡ阳性BV-2细胞为(0.893±0.038),经统计学处理二者存在显著性差异(P<0.05)。雷公藤内酯组MHCⅡ阳性BV-2细胞率(0.089±0.013),与海人酸组比较二者存在显著性差异(P<0.05);对照组CⅡTA阳性BV-2细胞为(0.043±0.003),海人酸组CⅡTA阳性BV-2细胞为(0.692±0.015),经统计学处理二者存在显著性差异(P<0.05)。雷公藤内酯组CⅡTA阳性BV-2细胞为(0.057±0.009),与海人酸组比较存在显著性差异(P<0.05)。结论雷公藤内酯可以抑制海人酸活化的BV-2细胞MHCⅡ表达,其机制可能与下调BV-2细胞CⅡTA表达有关。

Objective To observe the effect of triptolide on the expression of MHCⅡ in kainic acid-activated BV-2microglia and investigate the related moleculsr molecular mechanism. Method BV-2 cells were divided into control group,kainic acid group and triptolide group. Immunohistochemistry techniques were used to detect the effect of triptolide on theexpressions of MHCⅡ and C ETA of kainic acid-activated BV-2 cells. Result The MHCⅡ -positive BV-2 cells in controlgroup was （0.059 ±0.005） . The MHCⅡ-positive BV-2 cells in kainic acid group was （0.893 ±0.038） and there wasobvious difference compared with that of control group （ P 〈 0. 05 ）. The MHCⅡ -positive BV-2 cells in triptolide group was（0. 089 ± 0. 013 ） and there was obvious difference compared with the kainic acid group （ P 〈 0. 05 ）. The CⅡ TA-positiveBV-2 cells in control group was （ 0. 043 ± 0. 003 ）. The CⅡ TA-positive BV-2 cells in kainic acid group was （ 0. 692 土0.015） and there was obvious difference compared with that of the control group （P 〈0. 05）. The CⅡ TA-positive BV-2cells in triptolide group was （0. 057 ±0. 009） and there was obvious difference compared with that of the kainic acid group（ P 〈 0. 05） . Conclusion Triptolide could inhibit the expression of MHCⅡ in kainic acid-activated BV-2 cells, the mechanismmay be related to downregulating the expression of C ETA in kainic acid-activated BV-2 cells.