Verbascoside inhibits paraquate-induced pulmonary toxicity via modulating oxidative stress, inflammation, apoptosis and DNA damage in A549 cell

活力测定 毛蕊糖甙 A549电池 氧化应激 细胞凋亡 化学 程序性细胞死亡 抗氧化剂 MTT法 分子生物学 药理学 生物化学 生物 有机化学 糖苷
作者
Nastaran Khorashadizadeh,Ali Neamati,Mohammad Moshiri,Leila Etemad
出处
期刊:Drug and Chemical Toxicology [Taylor & Francis]
卷期号:45 (5): 2212-2220 被引量:10
标识
DOI:10.1080/01480545.2021.1917467
摘要

Paraquat (PQ), one of the most frequently used herbicides, can cause serious health problems in an exposed individual. In the present study, we investigated the protective effect of verbascoside (VB), a phenylpropanoid glycoside from lemon verbena, against PQ-induced A549 cell injury with a particular focus on the possible molecular pathways involved. A549 cells were exposed to PQ (300 µM) and different concentrations of VB (12.5, 25, and 50 µM). Cell viability, ROS content, the level of antioxidant enzymes (SOD, CAT and GPx) and inflammatory markers (IL-6 and TNF-α), as well as 8-OHdG, were detected using MTT assay and an ELISA kit. Western blotting and qRT-PCR were performed to measure the levels of caspase3 and NF-κB mRNA and protein expression. Exposure of cells to PQ caused viability loss and ROS increase. PQ also increased the levels of IL-6, TNF-α and 8-OHdG and decreased the antioxidant enzymes content. PQ treatment resulted in cell death by increasing the gene and protein expression level of caspase 3 and NF-κB. Treatment with VB notably increased cell survival, antioxidant enzymes activity, which concomitantly attenuated ROS, NF-κB and inflammatory mediator production. VB also inhibited apoptosis expression markers. These results indicated that VB could protect A549 cells against PQ induced cell injury by attenuation of ROS and inflammatory marker production and modulation of antioxidant enzymes. VB efficiently suppressed increased NF-κB and caspase-3 activity and formation of 8-OHdG and ultimately improved cell viability. Therefore, VB may be useful in the development of a new therapy for PQ-induced pulmonary toxicity.
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