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目的:探究白介素-33(interleukin-33,IL-33)在子痫前期(preeclampsia,PE)胎盘中的表达以及自噬通过调节IL-33的表达参与PE发病的分子机制。方法:应用免疫组化法及Western blot检测PE患者与正常妊娠胎盘中IL-33,微管相关蛋白LC3(LC3)的表达,应用Western blot检测PE患者与正常妊娠胎盘中IL-33受体ST2和核转录因子-κB(nuclear factor,NF-κB)的表达。使用3-Methyladenine(3-MA)、巴佛洛霉素A1(bafilomycin A1,BAF)处理人类绒毛膜外滋养细胞株HTR8/SVneo,检测IL-33、ST2和NF-κB蛋白表达情况以及自噬水平的高低。结果:(1)Western blot检测结果显示IL-33平均吸光度(absorbance,A)值PE组低于对照组(t=2.830,P=0.010),LC3B/A平均A值PE组高于对照组(t=3.470,P=0.005),ST2蛋白表达PE组高于对照组(t=2.650,P=0.026),NF-κB表达水平PE组高于对照组(t=3.180,P=0.005);(2)BAF处理HTR8/SVneo细胞株,IL-33蛋白水平较正常对照组明显降低(ta=3.740,Pa=0.006),LC3B/A比值水平较二甲基甲砜(dimethyl sulphoxide,DMSO)组明显升高(td=2.500,Pd=0.032)。3-MA对IL-33、NF-κB以及自噬水平的表达情况影响不明显。结论:过度自噬可能降低IL-33水平,导致IL-33抗炎作用减弱,进而出现过度炎症反应,并且这一过程与PE的发病存在一定关系。
Objective: To investigate the expression of interleukin-33 (IL-33) in the placenta of preeclampsia (PE) and the molecular mechanism of autophagy involved in the pathogenesis of PE by regulating the expression of IL-33. Methods: The expression of IL-33 and LC3 in placentae of PE patients and normal pregnant women were detected by immunohistochemistry and Western blot. Western blot was used to detect the expression of IL-33 receptor ST2 And nuclear factor-κB (NF-κB) expression. Human chorionic villus trophoblast cell line HTR8 / SVneo was treated with 3-Methyladenine (3-MA) and bafilomycin A1 (BAF) to detect the expression of IL-33, ST2 and NF- The level of the level. Results: (1) Western blot results showed that the average absorbance (A) value of IL-33 in PE group was lower than that in control group (t = 2.830, P = 0.010) (t = 3.470, P = 0.005). The expression of ST2 protein in PE group was higher than that in control group (t = 2.650, P = 0.026) 2) BAF treatment of HTR8 / SVneo cell line, IL-33 protein levels were significantly lower than the normal control group (ta = 3.740, Pa = 0.006), LC3B / A ratio was significantly higher than the dimethyl sulphoxide Rise (td = 2.500, Pd = 0.032). 3-MA had no obvious effect on the expression of IL-33, NF-κB and autophagy. Conclusion: Over-autophagy may reduce the level of IL-33, lead to the weakened anti-inflammatory effect of IL-33, leading to excessive inflammatory reaction, and this process has a certain relationship with the pathogenesis of PE.