In vitro anticancer potential of dill seed extract against human hepatocellular carcinoma (Huh-7) cells

被引:0
|
作者
Al-Oqail, Mai M. [1 ]
Al-Sheddi, Ebtesam S. [1 ]
Farshori, Nida N. [1 ]
Al-Massarani, Shaza M. [1 ]
Alsultan, Ebtesam N. [1 ]
Ahmad, Javed [2 ]
Al-Khedhairy, Abdulaziz A. [2 ]
Siddiqui, Maqsood A. [2 ]
机构
[1] King Saud Univ, Coll Pharm, Dept Pharmacognosy, POB 22452, Riyadh 11495, Saudi Arabia
[2] King Saud Univ, Coll Sci, Chair DNA Res, Dept Zool, POB 2455, Riyadh 11451, Saudi Arabia
关键词
Dill seeds; Huh-7; cells; Cytotoxicity; Oxidative damage; ROS generation; Gene expression; MEDICINAL-PLANTS; APOPTOSIS; OIL;
D O I
10.1016/j.jksus.2024.103390
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Background: Hepatocellular carcinoma is the most prevalent type of primary liver cancer and remains the foremost cause of cancer-related deaths globally. Dill (Anethum graveolens) seeds, rich in phytoconstituents, is renowned for their pharmacological properties. Objectives: This study performed an in vitro evaluation to assess the cytotoxic effects of dill seed extract (DS-EE) on the Huh-7 hepatocellular carcinoma cell line. Moreover, the study investigated its effects on cell viability, cellular morphology, oxidative damage, levels of intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and the expression of apoptosis-related genes in Huh-7 cells. Methods: Huh-7 cells were treated with DS-EE at concentrations ranging from 5 to 100 mu g/mL for a duration of 24 h. Results: The cytotoxicity findings showed that DS-EE decreased cell viability and suppressed the growth of Huh-7 cells in a dose-dependent way, with an IC50 value of 60 mu g/mL. Exposure to DS-EE extract for 24 h resulted in a significant elevation in lipid peroxidation (LPO) and a notable decrease in glutathione (GSH) content compared to the control. Furthermore, DS-EE significantly increased ROS production while notably decreasing the MMP level in Huh-7 cells. Moreover, DS-EE induces cell apoptosis by upregulating the expression of proapoptotic genes (p53, caspase-3, caspase-9, and Bax) and downregulating the expression of the antiapoptotic gene, Bcl-2. Conclusion: DS-EE exhibited a notable cytotoxic effect on Huh-7 cells by increasing oxidative damage and subsequently modulating the expression of apoptosis-related genes. The results of this study highlight the anticancer effectiveness of DS-EE, indicating its potential as a promising agent for hepatocellular carcinoma management.
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页数:7
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