Scholarlink

<p>14,15-Dihydroclerodin, or dihydroclerodin-I (DCLR), is a natural product that can also be synthesized through catalytic hydrogenation of clerodin. In this study, dihydroclerodin, purified from <i>Clerodendrum viscosum</i> leaves, was evaluated for its cell cycle arrest and cytotoxic effects in <i>Allium cepa</i> root tip cells and compared with colchicine-induced antimitotic activity. Treatments with dihydroclerodin at concentrations of 100, 200, and 300&#xa0;µg&#xa0;mL<sup>−1</sup>, and colchicine at 150&#xa0;µg&#xa0;mL<sup>−1</sup> (as a positive control), were administered for 2, 4, and 4 + 16&#xa0;h (4-hour treatment followed by 16&#xa0;h of recovery). The highest frequency of metaphase cells was observed with dihydroclerodin (300&#xa0;µg&#xa0;mL<sup>−1</sup>) and colchicine (150&#xa0;µg&#xa0;mL<sup>−1</sup>) at 4&#xa0;h, with values of 75.09 ± 0.93% and 78.31 ± 0.49%, respectively. Both treatments significantly increased the percentages of aberrant cells, chromosomal aberrations (CA), micronuclei (MN), C-metaphases (C-Met), and polyploid (PP) cells. These findings suggest that dihydroclerodin exhibits strong antimitotic effects, warranting further investigation of its potential in cancer chemotherapy due to its ability to induce cell cycle delay and cytotoxicity.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

14,15-dihydroclerodin (C24H36O7) induced cell cycle delay, antimitotic and cytotoxic effects in Allium cepa L. root tip cells

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年11月6日

查看全文
  • Poulomi Ghosh,
  • Sujit Roy,
  • Sanjib Ray

摘要

14,15-Dihydroclerodin, or dihydroclerodin-I (DCLR), is a natural product that can also be synthesized through catalytic hydrogenation of clerodin. In this study, dihydroclerodin, purified from Clerodendrum viscosum leaves, was evaluated for its cell cycle arrest and cytotoxic effects in Allium cepa root tip cells and compared with colchicine-induced antimitotic activity. Treatments with dihydroclerodin at concentrations of 100, 200, and 300 µg mL−1, and colchicine at 150 µg mL−1 (as a positive control), were administered for 2, 4, and 4 + 16 h (4-hour treatment followed by 16 h of recovery). The highest frequency of metaphase cells was observed with dihydroclerodin (300 µg mL−1) and colchicine (150 µg mL−1) at 4 h, with values of 75.09 ± 0.93% and 78.31 ± 0.49%, respectively. Both treatments significantly increased the percentages of aberrant cells, chromosomal aberrations (CA), micronuclei (MN), C-metaphases (C-Met), and polyploid (PP) cells. These findings suggest that dihydroclerodin exhibits strong antimitotic effects, warranting further investigation of its potential in cancer chemotherapy due to its ability to induce cell cycle delay and cytotoxicity.