Ameliorative role of aspirin in paraquat‐induced lung toxicity via mitochondrial mechanisms

Marashi, Sayed Mahdi; Hosseini, Seyede Fatemeh; Hosseinzadeh, Massood; Qadir, Muhammad Farhan; Khodaei, Forouzan

doi:10.1002/jbt.22370

Cited by 10 publications

(6 citation statements)

References 54 publications

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“…[ 45 ] Oxidative stress is an important risk factor for tissue damage and organ dysfunction. [ 45–47 ] In addition, there is an important interaction between oxidative stress and the function of antioxidant enzymes in various tissues. [ 48 ] Oxidative stress is involved in activating several messaging pathways that activate the factors of transcription, gene expression, and the induction of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

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The effect of ellagic acid on spinal cord and sciatica function in a mice model of multiple sclerosis

Khodaei

Khoshnoud

Heidaryfar

et al. 2020

J Biochem & Molecular Tox

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Multiple sclerosis (MS) is a well‐known neurodegenerative disorder, causing toxicity in different organs, such as spinal cord tissue. The goal of this study was to investigate the protective effect of ellagic acid (EA) against spinal cord and sciatica function in cuprizone (Cup)‐induced demyelination model. Animals were divided into six equal groups. The first group received tap water as the control. Cup group was treated with Cup (0.2% w/w in fed). EA 100 group was orally treated with EA (100 mg/kg). EA + Cup groups were orally treated with three doses of 5, 50, and 100 mg/kg of EA plus Cup (0.2% w/w). All groups received treatment for 42 days. Open field, rotarod, and gait tests were done to evaluate the behavioral changes following Cup and/or EA treatment. Also, lipid peroxidation, reactive oxygen species (ROS) content, antioxidant capacity, superoxide dismutase (SOD), and catalase enzymes activity in spinal cord was evaluated. Luxol fast blue (LFB) staining also the behavioral tests were performed to evaluate the model. Cup increased ROS levels and oxidative stress in their spinal cord tissues. Also, Cup reduced antioxidant capacity, SOD, and catalase activity. EA (especially at 100 mg/kg) prevented these abnormal changes. EA co‐treatment dose‐dependently was able to ameliorate behavioral impairments in mice that received Cup. EA might act as a protective agent in MS by modulating spinal cord function.

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Section: Discussionmentioning

confidence: 99%

“…Finally, the fluorescence intensity of the samples was measured (at excitation = 485 nm and emission=525 nm,) by microplate reader (FLUOstar Omega multifunctional). [ 22 ]…”

Section: Methodsmentioning

confidence: 99%

The effect of ellagic acid on spinal cord and sciatica function in a mice model of multiple sclerosis

Khodaei

Khoshnoud

Heidaryfar

et al. 2020

J Biochem & Molecular Tox

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“…The control group received PBS. Before inducing the model, the animals were orally pretreated with ASA (aspirin 200 mg/kg/day [27], as a positive control) or ATR (10 mg/kg/day [21,28]) prepared in 0.5% CMC-Na for 7 days. The vehicle-treated control group received equal volume of 0.5% CMC-Na.…”

Section: Experimental Design and Mouse Model Of Alimentioning

confidence: 99%

Pretreatment with atorvastatin ameliorates cobra venom factor-induced acute lung inflammation in mice

Guo

Yang

et al. 2020

BMC Pulm Med

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Background The complement system plays a critical role as the pathogenic factor in the models of acute lung injury due to various causes. Cobra venom factor (CVF) is a commonly used complement research tool. The CVF can cause acute inflammation in the lung by producing complement activation components. Atorvastatin (ATR) is a 3-hydroxy-3-methylglutaryl coenzyme A inhibitor approved for control of plasma cholesterol levels. This inhibitor can reduce the acute pulmonary inflammatory response. However, the ability of ATR in treating acute lung inflammation caused by complement activation is still unknown. Therefore, we investigated the effect of ATR on lung inflammation in mice induced by activation of the complement alternative pathway in this study. Methods ATR (10 mg/kg/day via oral gavage) was administered for 7 days before tail vein injection of CVF (25 μg/kg). On the seventh day, all mice were sacrificed 1 h after injection. The lung lobe, bronchoalveolar lavage fluid (BALF), and blood samples were collected. The myeloperoxidase (MPO) activity of the lung homogenate, the leukocyte cell count, and the protein content of BALF were measured. The levels of interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), P-selectin, and Intercellular cell adhesion molecule-1 (ICAM-1) in BALF and serum were determined by enzyme-linked immunosorbent assay. The pathological change of the lung tissue was observed by hematoxylin and eosin staining. The deposition of C5b-9 in the lung tissue was detected by immunohistochemistry. The phosphorylation of NF-κB p65 in the lung tissues was examined by immunohistochemistry and western blotting. Results The lung inflammation levels were determined by measuring the leukocyte cell numbers and protein content of BALF, the lung MPO activity, and expression and staining of the inflammatory mediators (IL-6 and TNF-α), and adhesion molecules (P-selectin and ICAM-1) for lung lesion. A significant reduction in the lung inflammation levels was observed after 7 days in ATR pre-treated mice with a CVF-induced lung disease. Deposition of C5b-9 was significantly alleviated by ATR pretreatment. Early intervention with ATR significantly reduced the development of acute lung inflammation on the basis of phosphorylation of NF-κB p65 in the lung. Conclusion These findings suggest the identification of ATR treatment for the lung inflammation induced by activating the complement system on the basis of its anti-inflammatory response. Together with the model replicating the complement activating characteristics of acute lung injury, the results may be translatable to the overactivated complement relevant diseases.

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“…The concentration of 50 mg/kg was applied in this study. This concentration of PQ has been largely reported to induce lung injury 26‐29 . Thalidomide has been reported to be applied at different doses in multiple diseases.…”

Section: Methodsmentioning

confidence: 99%

Thal protects against paraquat‐induced lung injury through a microRNA‐141/HDAC6/IκBα‐NF‐κB axis in rat and cell models

Zheng

Zhu

Zhang

et al. 2020

Basic Clin Pharma Tox

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Paraquat (1,1-dichloro-4,4-bipyridine, PQ) is a widely used herbicide in agriculture and with extremely potent toxicity that leads to serious public health problem once misused. By accidental or voluntary ingestion, PQ poisoning results in numerous deaths annually, mainly in developing countries where PQ is more largely used. 2 In oral ingestion cases, the mortality rate is over 90%. 3 PQ poisoning through oral, skin and respiratory tracts contributes to multiple organ failure including lungs, kidneys, liver and nervous system, in which the lung is the primary target organ. 4,5 This phenomenon was attributed to high affinity of PQ to alveolar cells. 6 Therefore, PQ poisonings usually cause acute lung injury and, ultimately, acute respiratory distress syndrome and death. 7 Unfortunately, despite the large volume of studies in the past

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Ameliorative role of aspirin in paraquat‐induced lung toxicity via mitochondrial mechanisms

Cited by 10 publications

References 54 publications

The effect of ellagic acid on spinal cord and sciatica function in a mice model of multiple sclerosis

The effect of ellagic acid on spinal cord and sciatica function in a mice model of multiple sclerosis

Pretreatment with atorvastatin ameliorates cobra venom factor-induced acute lung inflammation in mice

Thal protects against paraquat‐induced lung injury through a microRNA‐141/HDAC6/IκBα‐NF‐κB axis in rat and cell models

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