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韩国山茱萸果实提取物的馏分对 A549 肺癌细胞的增殖抑制和 p53 依赖性凋亡的作用。

Effects of fraction obtained from Korean Corni Fructus extracts causing anti-proliferation and p53-dependent apoptosis in A549 lung cancer cells.

机构信息

Department of Medical Zoology, Kyung Hee University School of Medicine, Seoul, Republic of Korea.

出版信息

Nutr Cancer. 2011;63(1):121-9. doi: 10.1080/01635581.2010.516475.

Abstract

Corni Fructus has traditionally been used as herbal medicine for the treatment of tuberculosis, asthma, hepatitis, and chronic nephritis in Korea, Japan, and China. This research was carried out to evaluate the proliferative-inhibitory effect of CF extracts against cancer cells and to identify the new pro-substance from medicinal plants. Among these herbal extracts extracted from KCF (Korean Corni Fructus), JCF (Japanese Corni Fructus) and CCF (Chinese Corni Fructus), KCF extracts strongly induced anti-proliferation of cancer cells in a dose-dependent manner compared with other extracts. Moreover, after treatment with CM/F3 (fraction 3 obtained from KCF extracts) for 24 h, A549 cells were evaluated by several indicators such as cell viability, LDH release, DNA fragmentation, nuclear condensation, and apoptotic proteins in vitro. CM/F3 showed the tumor-selective growth inhibitory activity in a dose- and time-dependent manner in A549 cells. Consistently, CM/F3 effectively induced the activation of bax, cytochrome-c, caspase-3, -8, -9, p53, and p21 causing apoptosis, and caused the suppression of Cdk2, pRb, and E2F1 related to cell arrest in A549 cells. These results demonstrate that CM/F3 caused not only anti-proliferation but also cell death involving cell arrest through interaction between apoptotic proteins and the upregulation of p53 in A549 cells.

摘要

山茱萸在韩国、日本和中国传统上被用作草药,用于治疗肺结核、哮喘、肝炎和慢性肾炎。这项研究旨在评估 CF 提取物对癌细胞的增殖抑制作用,并从药用植物中鉴定新的前体物质。在这些从 KCF(韩国山茱萸)、JCF(日本山茱萸)和 CCF(中国山茱萸)中提取的草药提取物中,与其他提取物相比,KCF 提取物强烈地以剂量依赖的方式诱导癌细胞的抗增殖作用。此外,在用 CM/F3(从 KCF 提取物中获得的第 3 馏分)处理 24 小时后,通过体外细胞活力、LDH 释放、DNA 片段化、核浓缩和凋亡蛋白等几种指标评估 A549 细胞。CM/F3 以剂量和时间依赖的方式在 A549 细胞中显示出肿瘤选择性生长抑制活性。一致地,CM/F3 有效地诱导 bax、细胞色素-c、caspase-3、-8、-9、p53 和 p21 的激活,导致凋亡,并导致与细胞停滞相关的 Cdk2、pRb 和 E2F1 的抑制在 A549 细胞中。这些结果表明,CM/F3 不仅引起增殖抑制,而且通过凋亡蛋白之间的相互作用和 p53 的上调导致 A549 细胞中的细胞死亡涉及细胞停滞。

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