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目的:观察两种植物多酚EGCG(表没食子儿茶素没食子酸酯)、单宁酸对5型腺病毒感染后宿主细胞膜流动性的影响,初步探讨植物多酚抑制病毒作用机制。方法:利用DPH为荧光探针,以荧光偏振法观察5型腺病毒感染对宿主细胞膜流动性的影响,EGCG、单宁酸在此过程中对宿主细胞膜流动性改变的干预作用,结合CPE法测定的EGCG,单宁酸抑制5型腺病毒感染药效试验结果,以Spearman秩相关计算EGCG,单宁酸对宿主细胞膜流动性干预作用与其抑制病毒感染作用间的关系。结果:腺病毒感染细胞可提高宿主细胞膜流动性,滴度为100TCID50病毒可使293A细胞膜流动性提高15.34%。EGCG、单宁酸可抑制宿主细胞膜流动性,高浓度下分别可使宿主细胞膜流动性下降32.61%、25.75%。在病毒吸附前、吸附后、吸附同时,以EGCG、单宁酸处理宿主细胞,均发现宿主细胞膜流动性的干预作用与其抑制病毒感染效果高度相关(相关系数均>0.900,P<0.01)。结论:5型腺病毒感染会提高宿主细胞膜的流动性,而EGCG、单宁酸在干预腺病毒感染过程中对宿主细胞膜流动性的干预作用可能是其抑制腺病毒感染的机制之一。
OBJECTIVE: To observe the effects of two plant polyphenols EGCG and tannic acid on the fluidity of host cell membrane after adenovirus type 5 infection and to explore the mechanism of plant polyphenols inhibiting virus. Methods: Fluorescence polarization method was used to observe the effect of adenovirus type 5 infection on the fluidity of host cell membrane by DPH fluorescent probe. Interference of EGCG and tannic acid in the change of host cell membrane fluidity was observed by fluorescence polarization method. Combined with CPE assay Of EGCG and tannic acid to inhibit adenovirus type 5 infection. The Spearman rank correlation was used to calculate the relationship between EGCG and the action of tannic acid on host cell membrane fluidity and the inhibition of virus infection. Results: Adenovirus-infected cells could increase the fluidity of host cell membrane. The titer of 100TCID50 virus increased the fluidity of 293A cell membrane by 15.34%. EGCG and tannic acid could inhibit the fluidity of host cell membrane, and the fluidity of host cell membrane decreased by 32.61% and 25.75% at high concentration respectively. Before virus adsorption, adsorption and adsorption, the interference of host cell membrane fluidity with EGCG and tannic acid treatment was highly correlated with its inhibitory effect on virus infection (correlation coefficient> 0.900, P <0.01). CONCLUSION: Adenovirus type 5 infection improves the fluidity of the host cell membrane. However, the intervention of EGCG and tannic acid on the fluidity of the host cell membrane during the process of adenovirus infection may be one of the mechanisms of its inhibition of adenovirus infection.