Edaravone, a novel antidote against lung injury and pulmonary fibrosis induced by paraquat?

Zhi, Qiaoming; Sun, Haiyan; Xiao-ming, Qian; Yang, Litao

doi:10.1016/j.intimp.2010.10.012

Cited by 33 publications

(15 citation statements)

References 44 publications

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“…Combined with MDA, it could help to better indicate the level of oxidative stress. [21,22] In this study the intracellular levels of MDA and MPO were both significantly elevated after treatment with PQ compared to the control group, and UTI could significantly lower the extension of that increase induced by PQ, with some concentration-dependent feature. The above results led us to the conclusion that the pretreatment of UTI could significantly reduce the oxidative stress on the cells, and the effect was dose-dependent.…”

Section: Discussionmentioning

confidence: 58%

Effect of ulinastatin on paraquat-induced-oxidative stress in human type II alveolar epithelial cells

Meng¹,

Wang²,

Gao³

et al. 2013

World Journal of Emergency Medicine

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BACKGROUND:Ulinastatin (UTI) is a urinary trypsin inhibitor extracted and purified from urine of males. This study aimed to explore the effects of UTI on paraquat-induced-oxidative stress in human type II alveolar epithelial cells.METHODS:The human type II alveolar epithelial cells, A549 cells, were cultured in vitro. The A549 cells were treated with different concentrations of paraquat (200, 400, 600, 800, 1 000, 1 200 µmol/L) and ulinastatin(0, 2 000, 4 000, 6 000, 8 000 U/mL) for 24 hours, the cell viability was measured by cell counting kit-8 and the median lethal concentration was selected. In order to establish an in vitro model of paraquat intoxication and to determine the safe dose of ulinastatin, we calculated LD50 using cell counting kit-8 to determine the survival rate of the cells. A549 cells were divided into normal control group, paraquat group and paraquat+ulinastatin group. The levels of malondialdehyde (MDA) and myeloperoxidase (MPO) were detected by biochemistry colorimetry, while the level of reactive oxygen spies (ROS) was detected by DCFH-DA assay.RESULTS:The survival rate of A549 cells treated with different concentrations of paraquat decreased in a concentration-dependent manner. Whereas there was no decrease in the survival rate of cells treated with 0–4 000 U/mL ulinastatin. The levels of MDA, MPO, and ROS were significantly higher in the paraquat group than in the normal control group after 24-hour-exposure. And the survival rate of the paraquat+ulinastatin group was higher than that of the paraquat group, but lower than that of the normal control group. The levels of MDA, MPO, and ROS were lower than those of the paraquat group.CONCLUSION:Ulinastatin can alleviate the paraquat-induced A549 cell damage by reducing oxidative stress.

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Section: Discussionmentioning

confidence: 58%

Effect of ulinastatin on paraquat-induced-oxidative stress in human type II alveolar epithelial cells

Meng¹,

Wang²,

Gao³

et al. 2013

World Journal of Emergency Medicine

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“…[4] To study the antioxidant effect of edaravone, the levels of ROS, SOD and MDA were measured in the study as indicators of oxidative stress. The increased ROS level after stimulation with paraquat was detected by LSCM.…”

Section: Discussionmentioning

confidence: 99%

“…[3] Edaravone (3-methyl-1-penyl-2-pyrazolin-5-one) as a potent free-radical scavenger has the antioxidant ability to inhibit lipid peroxidation. [4] The purpose of this study was to investigate the effect of edaravone against reactive oxygen species (ROS) in A549 cells induced by paraquat. …”

Section: Introductionmentioning

confidence: 99%

Edaravone attenuates paraquat-induced lung injury by inhibiting oxidative stress in human type II alveolar epithelial cells

Cheng¹,

Han²,

Sun³

et al. 2012

World Journal of Emergency Medicine

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“…Edavarone also shown to be protective in acute pancreatitis-associated lung injury by suppression of IL-6 and TNF-α [175]. Furthermore, it has been shown that edaravone suppressed bleomycin-induced acute pulmonary injury in rabbits [176] and paraquat-induced lung injury and fibrosis in rats [177], and suppresses fibrosis in tight-skin and bleomycin-induced mouse models of systemic sclerosis [178]. This suggests an important role of edaravone in suppressing skin and lung fibrosis.…”

Section: Lipid Peroxidation and Protein Carbonylation Inhibitors/bmentioning

confidence: 99%

Pharmacological antioxidant strategies as therapeutic interventions for COPD

Rahman

2012

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

102

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Cigarette/tobacco smoke/biomass fuel-induced oxidative and aldehyde/carbonyl stress are intimately associated with the progression and exacerbation of chronic obstructive pulmonary disease (COPD). Therefore, targeting systemic and local oxidative stress with antioxidants/redox modulating agents, or boosting the endogenous levels of antioxidants are likely to have beneficial effects in the treatment/management of COPD. Various antioxidant agents, such as thiol molecules (glutathione and mucolytic drugs, such as N-acetyl-L-cysteine and N-acystelyn, erdosteine, fudosteine, ergothioneine, and carbocysteine), all have been reported to modulate various cellular and biochemical aspects of COPD. These antioxidants have been found to scavenge and detoxify free radicals and oxidants, regulate of glutathione biosynthesis, control nuclear factor-kappaB (NF-kappaB) activation, and hence inhibiting inflammatory gene expression. Synthetic molecules, such as specific spin traps like α-phenyl-N-tert-butyl nitrone, a catalytic antioxidant (ECSOD mimetic), porphyrins (AEOL 10150 and AEOL 10113), and a superoxide dismutase mimetic M40419, iNOS inhibitors, lipid peroxidation inhibitors/blockers edaravone, and lazaroids/tirilazad have also been shown to have beneficial effects by inhibiting the cigarette smoke-induced inflammatory responses and other carbonyl/oxidative stress-induced cellular alterations. A variety of oxidants, free radicals, and carbonyls/aldehydes are implicated in the pathogenesis of COPD, it is therefore, possible that therapeutic administration or supplementation of multiple antioxidants and/or boosting the endogenous levels of antioxidants will be beneficial in the treatment of COPD. This review discusses various novel pharmacological approaches adopted to enhance lung antioxidant levels, and various emerging beneficial and/or prophylactic effects of antioxidant therapeutics in halting or intervening the progression of COPD.

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Edaravone, a novel antidote against lung injury and pulmonary fibrosis induced by paraquat?

Cited by 33 publications

References 44 publications

Effect of ulinastatin on paraquat-induced-oxidative stress in human type II alveolar epithelial cells

Effect of ulinastatin on paraquat-induced-oxidative stress in human type II alveolar epithelial cells

Edaravone attenuates paraquat-induced lung injury by inhibiting oxidative stress in human type II alveolar epithelial cells

Pharmacological antioxidant strategies as therapeutic interventions for COPD

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