m+Medelevator.RU
← Поиск публикаций
Zhongguo shi yan xue ye xue za zhi · 2021

[Costunolide Induces Apoptosis of K562/ADR Cells through PI3K/AKT Pathway].

СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…

История · было → стало

Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.

Cai Hong, Hu Hong

Аннотация

OBJECTIVE: To explore the effects of costunolide on the proliferation and apoptosis of human chronic myeloid leukemia drug resisitant cell line K562/ADR and its mechanism.

METHODS: The proliferation of the cells was assessed by CCK-8 assay, while flow cytometry was used to detect the apoptosis of the cells. The related-proteins were detected by using Western blot.

RESULTS: The proliferation of K526/ADR cells was significantly inhibited by costunolide in a dose-dependent manner (r=0.9886) after treated by 0.01, 0.1, 0.25, 0.5, 1, 2.5, 5, 10, 25, 50 and 100 μmol/L costunolide for 72 h, and IC50 value of costunolide on K562/ADR cells was about (10.86±0.99) μmol/L (P<0.05). The apoptosis of K562/ADR cells could be induced by costunolide (10 and 15 μmol/L) significantly, the rate of apoptosis was 14.80%±3.27%, 33.2%±5.03%, respectively, which in comparison with a significantly difference as compared with the control group (4.30%±0.62%) (P<0.05). Western blot showed that costunolide could down-regulated the expression of p-AKT, p-PI3K, BCL-2, and up-regulated the expression of cleaved-caspase-3, cleaved-PARP significantly.

CONCLUSION: Costunolide could inhibit the proliferation and apoptosis of K562/ADR cells through regulation of PI3K/AKT pathway.

Предметные рубрики MeSH

ИП Урсолов Владлен Сергеевич

ИНН 500118482352 · ОГРНИП 314500117700049

Реквизиты и контакты