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目的研究N-糖基化抑制剂衣霉素抑制乙型肝炎e抗原(HBeAg)分泌的机制,为今后探索直接抑制HBeAg分泌的高效抗HBV方法提供基础。方法观察衣霉素在HepG2.2.15细胞模型上对HBeAg分泌和内质网应激的影响;采用Western印迹比较研究衣霉素对胞质和包含内质网的非胞质中的HBeAg前体的影响。结果在HepG2.2.15细胞上,衣霉素显著减少HBeAg在培养上清中的含量,并诱导代表内质网应激的拼接xbp-1 mRNA形成。衣霉素在不显著影响胞质中HBeAg前体和β-肌动蛋白的情况下显著减少非胞质中这些蛋白的水平。结论衣霉素抑制HBeAg分泌不是糖基化抑制的直接结果,而是诱导内质网应激的效应。
Objective To study the mechanism of tunicamycin inhibition of hepatitis B e antigen (HBeAg) secretion by N-glycosylation inhibitor, and to provide a basis for exploring an efficient anti-HBV method for directly inhibiting HBeAg secretion in the future. Methods The effect of tunicamycin on HBeAg secretion and endoplasmic reticulum stress in HepG2.2.15 cell model was observed. Western blotting was used to study the effects of tunicamycin on the cytoplasm and endoplasmic reticulum-containing HBeAg precursor influences. Tunicamycin significantly reduced the content of HBeAg in the culture supernatant on HepG2.2.15 cells and induced the formation of spliced xbp-1 mRNA representing endoplasmic reticulum stress. Tunicamycin significantly reduces the level of these proteins in the non-cytoplasm without significantly affecting the cytoplasmic HBeAg precursors and β-actin. Conclusion Tunicamycin inhibition of HBeAg secretion is not a direct result of glycosylation inhibition, but the effect of inducing endoplasmic reticulum stress.