- 作者: Shyun-Yeu Liu; Mei-Huei Lin; Yu-Rung Hsu; Ya-Yun Shih; Wei-Fan Chiang; Chin-Hai Lee; Ta-Hsiung Chou; Young-Chau Liu
- 作者服務機構: Oral and Maxillofacial Surgery Section, Chi Mei Medical Center, Tainan, Taiwan, ROC
- 中文摘要: --
- 英文摘要:
Areca nut (AN) is recognized as a human carcinogen; however, few studies of the cytotoxic effects of AN ingredients on cells have been reported. In Taiwan, AN, lime and inflorescence of Piper betle are the common components of betel quid (BQ). We recently noticed that
extract of AN (ANE), but not those of lime and inflorescence of Piper betle, induces rounding cell morphology and nuclear shrinkage in different types of carcinoma cells. In this study, the rounding cell activity was first traced to the partially purified C10 kDa fraction (ANE C 10 K) and subsequently to the 30–100 kDa fraction (ANE 30–100 K). ANE and ANE C10 K stimulated nuclear shrinkage (P\0.001 in both cases) and the clearance of the cytoplasm. ANE, ANE C 10 K, and ANE 30–100 K induced the cleavage of LC3-I (P\0.05, 0.01, and 0.05, respectively) and the emergence of autophagic vacuoles (AVs) and acidic vesicles. On the other hand, arecoline (Are, the major alkaloid of AN) triggered caspase-3 activation, perinuclear chromatin condensation, and micronucleation. Meanwhile, ANE 30–100 K, but not Are, inhibited the phosphorylation of the mammalian target of rapamycin (mTOR)-Ser2448. In conclusion, this study demonstrates that different AN ingredients exerting differential impact on mTOR-Ser2448 phosphorylation are capable of triggering apoptosis and autophagy. - 中文關鍵字: --
- 英文關鍵字: Arecoline; Areca nut; Apoptosis; Autophagy; Mammalian target of rapamycin (mTOR)