Tamba Yukihiro, Sugita Naoya, Terada Mika, Yamazaki Masahito
General Education, National Institute of Technology, Suzuka College, Suzuka 510-0294, Japan.
Department of Chemistry and Biochemistry, National Institute of Technology, Suzuka College, Suzuka 510-0294, Japan.
Biochim Biophys Acta Biomembr. 2025 Jun;1867(5-6):184427. doi: 10.1016/j.bbamem.2025.184427. Epub 2025 May 26.
(-)-Epigallocatechin gallate (EGCg), a tea catechin, exhibits antimicrobial activity. EGCg induces burst of giant unilamellar vesicles (GUVs), resulting in leakage of their internal contents. Here, we examined the effect of membrane tension on the EGCg-induced burst of dioleoylphosphatidylcholine (DOPC)-GUVs. The observation of the EGCg-induced burst of GUVs without membrane tension indicated that first a micropore was formed in the membrane and then its radius rapidly increased with time within ~10 ms without a change in the GUV diameter, and then the GUV diameter decreased to a lipid membrane aggregate. Next, we examined the effect of membrane tension on the EGCg-induced fractional area change (δ) of GUVs and its burst. During the interaction of EGCg with a GUV with low tension (≤ 0.5 mN/m), the δ initially increased slightly and then decreased to negative values, concomitant with the appearance of invaginated structures such as dense particles and narrow tubes in the GUV membrane and lumen, resulting in pore formation and subsequent GUV burst. By contrast, at higher tension, δ increased with time. The fraction of burst GUV after 5 min of interaction, P (5 min), decreased with increasing tension up to 3.0 mN/m, indicating that membrane tension suppressed the burst. The P (5 min) increased with increasing the fraction of GUVs in which invaginated structures appeared within 5 min of interaction, suggesting that the formation of invaginated structures may cause the initial EGCg-induced pore formation. We have proposed a mechanism of the tension effect on the EGCg-induced pore formation.
（-）-表没食子儿茶素没食子酸酯（EGCg）是一种茶儿茶素，具有抗菌活性。EGCg可诱导巨型单层囊泡（GUVs）破裂，导致其内部内容物泄漏。在此，我们研究了膜张力对EGCg诱导的二油酰磷脂酰胆碱（DOPC）-GUVs破裂的影响。在没有膜张力的情况下观察EGCg诱导的GUVs破裂，结果表明，首先在膜中形成一个微孔，然后其半径在约10毫秒内随时间迅速增加，而GUV直径不变，随后GUV直径减小至脂质膜聚集体。接下来，我们研究了膜张力对EGCg诱导的GUVs分数面积变化（δ）及其破裂的影响。在EGCg与低张力（≤0.5 mN/m）的GUV相互作用期间，δ最初略有增加，然后降至负值，同时GUV膜和内腔中出现密集颗粒和细管等内陷结构，导致孔形成和随后的GUV破裂。相比之下，在较高张力下，δ随时间增加。相互作用5分钟后破裂的GUV分数P（5分钟）随着张力增加至3.0 mN/m而降低，表明膜张力抑制了破裂。P（5分钟）随着相互作用5分钟内出现内陷结构的GUVs分数增加而增加，这表明内陷结构的形成可能导致最初EGCg诱导的孔形成。我们提出了一种关于张力对EGCg诱导的孔形成影响的机制。
