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Evaluation of anticancer activity of Cordia dichotoma leaves against a human prostate carcinoma cell line PC3

机译:香茅叶片对人前列腺癌细胞系PC3的抗癌活性评估

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摘要

Mechanisms of antioxidant and apoptosis induction may be involved in the management of cancer by medicinal plants. Aim of the study was designed to evaluate anticancer activity of the methanolic extract of Cordia dichotoma leaves (MECD) against a human prostate carcinoma cell line, PC3. Flavonoid content was determined by colorimetric principle and antioxidant activity by various in vitro assays. MTT, DCFH-DA and DAPI staining assays were performed for the evaluation of cytotoxicity, analysis of induction of apoptosis and intracellular reactive oxygen species (ROS) activity level by MECD against human prostate carcinoma cell line, PC3. Flavonoid content was found to be 160 mg QE/g extract. IC50 values for MECD treatment in various assays based on scavenging of 2,2-diphenyl-1-picrylhydrazyl, 2,2-azinobis(3-ethylenebenzothiazoline-6-sulfonic acid), nitric oxide, peroxy radical, superoxide anion, hydroxy radical were found to be 315.5, 38, 476, 523, 197, 82 μg/ml respectively. MECD exposure to PC3 cells significantly increased the cell death (p < 0.001, IC50 = 74.5 μg/ml), nuclear condensation, apoptosis (p < 0.001) and induced production of ROS (p < 0.001) initiating apoptotic cascade in a dose dependent manner. This study confirms that MECD possesses antioxidant property and can prevent carcinogenesis by reducing oxidative stress. MECD possesses anticancer activity and lead to PC3 cell death via induction of apoptosis mediated through excessive ROS generation. Flavonoids in MECD may be responsible for these activities due to dual antioxidant and pro-oxidant properties.
机译:抗氧化剂和细胞凋亡的诱导机制可能与药用植物对癌症的控制有关。设计该研究的目的是评估二香Cordia dichotoma叶子(MECD)的甲醇提取物对人前列腺癌细胞系PC3的抗癌活性。类比黄酮含量由比色原理确定,抗氧化剂活性由各种体外测定确定。进行了MTT,DCFH-DA和DAPI染色测定,以评价细胞毒性,MECD对人前列腺癌细胞株PC3诱导的凋亡诱导和细胞内活性氧(ROS)活性水平。发现黄酮含量为160 mg QE / g提取物。基于清除2,2-二苯基-1-吡啶并肼,2,2-叠氮基双(3-乙烯苯并噻唑啉-6-磺酸),一氧化氮,过氧自由基,超氧阴离子,羟基自由基的各种检测方法,MECD处理的IC50值分别为分别为315.5、38、476、523、197、82μg/ ml。 MECD暴露于PC3细胞会显着增加细胞死亡(p <0.001,IC50 = 74.5μg/ ml),核浓缩,细胞凋亡(p <0.001)和诱导ROS的产生(p <0.001),并以剂量​​依赖性方式引发凋亡级联反应。 。这项研究证实,MECD具有抗氧化性能,并可以通过降低氧化应激来防止癌变。 MECD具有抗癌活性,并通过诱导过多的ROS产生介导的凋亡诱导PC3细胞死亡。由于具有双重抗氧化剂和促氧化剂特性,MECD中的类黄酮可能负责这些活动。

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