摘要
目的:探讨干扰素α-2b(IFNα-2b)对丙肝患者血清铁调素(Hepcidin)的影响及分析其可能机制。方法:(1)按3个月内曾否接受IFNα-2b治疗把37例丙肝患者归为治疗组(n=25)及未治疗组(n=12),分析2组血清Hepcidin的差异。(2)用逐渐增量(0、50、100、200、400μL)的IFNα-2b处理Hep G2及LO2细胞24 h,real-time PCR检测细胞Hepcidin、白细胞介素6(IL-6)、信号转导与转录激活子3(STAT3)的mRNA表达量,Western blot检测细胞STAT3及磷酸化STAT3(pSTAT3)蛋白水平,分析其变化。结果:治疗组血清Hepcidin低于未治疗组(P<0.05)。随IFNα-2b浓度增加,HepG2及LO2细胞Hepcidin mRNA表达逐渐下调(P<0.05),IL-6和STAT3的mRNA变化趋势不明显;pSTAT3蛋白水平逐步下降(P<0.05),STAT3蛋白水平不呈递减改变。结论:丙肝患者接受IFNα-2b治疗后血清Hepcidin浓度降低可能是由于IFNα-2b抑制了肝细胞Hepcidin基因表达,其机制可能与STAT3通路磷酸活化受阻有关。
Objective To investigate the effects of interferon alpha-2b （IFNα-2b） on serum Hepcidin in hepatitis C patients and its mechanism. Methods Hepatitis C patients were divided evenly into treatment group and control group according to whether they had received treatment with IFNα-2b in the past 3 months. The serum hepci- din was compared between the two groups. HepG2 cells and LO2 cells were treated for 24 hours at varied levels of IFNα-2b （0, 50, 100,200,400 μL） and real-time PCR was used to detect the hepcidin, interleukin-6 （IL-6） and signal transduction and transcription activator 3 （STAT3） mRNA expression of cells. The protein levels of STAT3 and phosphorylated STAT3 （pSTAT3） were measured by Western blot. The changes of these indexes were observed with the gradual increase of IFNα-2b levels. Results Serum Hepcidin level in the treatment group was significantly lower than the control （P 〈 0.05）. IFNα-2b inhibited the Hepeidin mRNA in HepG2 cells and LO2 cells, pSTAT3 was significantly decreased with the increased levels of IFNα-2b （P 〈 0.05）, and the expression of IL-6 and STAT3 had no significant changes with the increase of IFNα-2b. Conclusion The serum Hepcidin levels can be decreased because IFNα-2b suppresses the expression of Hepeidin, and its mechanism may be related with inhibited STAT3 pathway activation.
出处
《实用医学杂志》
CAS
北大核心
2017年第5期785-788,共4页
The Journal of Practical Medicine
基金
广州市科技和信息化局项目(编号:2014J4100063)
