綠茶中的多酚性化合物兒茶素,包括EGCG、ECG、EGC,在細胞培養中,被用來評估其抑制感冒病毒之複製能力與其可能地直接殺滅病毒的效果。在這些測試性化合物之中,EGCG與ECG在加入MDCK細胞培養中,被發現其對於感冒病毒之複製是強力抑制劑和此種效果對於所有感冒病毒亞型,包括A/HIN1、A/H3N2和B病毒均有測試。EGCG、ECG與EGC對付A型感冒病毒之50%有效抑制濃度(50% effective inhibition concentration, EC50)分別為22~28、22~40與309~318μM。EGCG與ECG展現出有血液凝集抑制作用力(hemagglutination inhibition activity),而EGCG更有效。然而,在3種被測試之不同的感冒病毒亞型中,其血液凝集抑制之敏感度有很大之差異。利用定量性RT-PCR分析之結果顯示在高濃度下,EGCG與ECG對在MDCK細胞之病毒性核醣核酸合成作用(viral RNA synthesis)有抑制作用,然而EGC則無類似的效果。同樣的,EGCG與ECG對神經胺酶(neuraminidase)活性之抑制效果比EGC更為有效。此結果顯示出兒茶素結構中之3-galloyl基對其抗病毒作用力為相當重要之角色,然而在結構中2~位置上trihvdroxy bezyl moiety上之5'-OH,則並非是個重要角色。結果與HA type-specific之效果,顯示出兒茶素對於感冒病毒之抗病毒作用,不僅是媒介利用其和HA之特殊的相互作用,而且亦改變了病毒外膜之物理性質。
Polyphenolic compound catechins ((-)-epigallocatechin gallate (EGCG), ( )-epicatechin gallate (ECG) and (-)-epigallocatechin (EGC)) from green tea were evaluated for their ability to inhibit influenza virus replication in cell culture and for potentially direct virucidal effect. Among the test compounds, the EGCG and ECG were found to be potent inhibitors of influenza virus replication in MDCK cell culture and this effect was observed in all influenza virus subtypes tested, including A/H1N1, A/H3N2 and B virus. The 50% effective inhibition concentration (EC50) of EGCG, ECG, and EGC for influenza A virus were 22-28, 22-40 and 309-318_M, respectively. EGCG and ECG exhibited hemagglutination inhibition activity, EGCG being more effective. However, the sensitivity in hemagglutination inhibition was widely different among three different subtypes of influenza viruses tested. Quantitative RT-PCR analysis revealed that, at high concentration, EGCG and ECG also suppressed viral RNA synthesis in MDCK cells whereas EGC failed to show similar effect. Similarly, EGCG and ECG inhibited the neuraminidase activity more effectively than the EGC. The results show that the 3-galloyl group of catechin skeleton plays an important role on the observed antiviral activity, whereas the 5-OH at the trihydroxy benzyl moiety at 2-position plays a minor role. The results, along with the HA type-specific effect, suggest that the antiviral effect of catechins on influenza virus is mediated not only by specific interaction with HA, but altering the physical properties of viral membrane.