Nepenthes Ethyl Acetate Extract Provides Oxidative Stress-Dependent Anti-Leukemia Effects

Bibliographic Details
Title: Nepenthes Ethyl Acetate Extract Provides Oxidative Stress-Dependent Anti-Leukemia Effects
Authors: Wangta Liu, Li-Ching Lin, Pei-Ju Wang, Yan-Ning Chen, Sheng-Chieh Wang, Ya-Ting Chuang, I-Hsuan Tsai, Szu-Yin Yu, Fang-Rong Chang, Yuan-Bin Cheng, Li-Chen Huang, Ming-Yii Huang, Hsueh-Wei Chang
Source: Antioxidants, Vol 10, Iss 9, p 1410 (2021)
Publisher Information: MDPI AG, 2021.
Publication Year: 2021
Collection: LCC:Therapeutics. Pharmacology
Subject Terms: Nepenthes, leukemia cells, antioxidant, DNA damage, apoptosis, oxidative stress, Therapeutics. Pharmacology, RM1-950
More Details: Several kinds of solvents have been applied to Nepenthes extractions exhibiting antioxidant and anticancer effects. However, they were rarely investigated for Nepenthes ethyl acetate extract (EANT), especially leukemia cells. The purpose of the present study was to evaluate the antioxidant properties and explore the antiproliferation impact and mechanism of EANT in leukemia cells. Five standard assays demonstrated that EANT exhibits antioxidant capability. In the cell line model, EANT dose-responsively inhibited cell viabilities of three leukemia cell lines (HL-60, K-562, and MOLT-4) based on 24 h MTS assays, which were reverted by pretreating oxidative stress and apoptosis inhibitors (N-acetylcysteine and Z-VAD-FMK). Due to similar sensitivities among the three cell lines, leukemia HL-60 cells were chosen for exploring antiproliferation mechanisms. EANT caused subG1 and G1 cumulations, triggered annexin V-detected apoptosis, activated apoptotic caspase 3/7 activity, and induced poly ADP-ribose polymerase expression. Moreover, reactive oxygen species, mitochondrial superoxide, and mitochondrial membrane depolarization were generated by EANT, which was reverted by N-acetylcysteine. The antioxidant response to oxidative stress showed that EANT upregulated mRNA expressions for nuclear factor erythroid 2-like 2 (NFE2L2), catalase (CAT), thioredoxin (TXN), heme oxygenase 1 (HMOX1), and NAD(P)H quinone dehydrogenase 1 (NQO1) genes. Moreover, these oxidative stresses led to DNA damage (γH2AX and 8-hydroxy-2-deoxyguanosine) and were alleviated by N-acetylcysteine. Taken together, EANT demonstrated oxidative stress-dependent anti-leukemia ability to HL-60 cells associated with apoptosis and DNA damage.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2076-3921
Relation: https://www.mdpi.com/2076-3921/10/9/1410; https://doaj.org/toc/2076-3921
DOI: 10.3390/antiox10091410
Access URL: https://doaj.org/article/4a5d3c1ad4dd47529aa67beb38cf4b2f
Accession Number: edsdoj.4a5d3c1ad4dd47529aa67beb38cf4b2f
Database: Directory of Open Access Journals
More Details
ISSN:20763921
DOI:10.3390/antiox10091410
Published in:Antioxidants
Language:English