Meloxicam inhibits fipronil‐induced apoptosis via modulation of the oxidative stress and inflammatory response in SH‐SY5Y cells

Park, Jae Hyeon; Park, Youn Sun; Lee, Je-Bong; Park, Kyung-Hun; Paik, Min-Kyoung; Jeong, Mihye; Koh, Hyun Chul

doi:10.1002/jat.3136

Cited by 40 publications

(18 citation statements)

References 61 publications

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“…Recent alarming reports suggest that chronic FPN in rodents at 30 but not 10 mg/kg by daily oral gavage causes memory impairment in parts associated with the modulation of the GABAergic system [ 9 ] and the deposition of amyloid plaques [ 10 ]. FPN oral administration raises the oxidative stress in various tissues, including the adipose tissue, the liver, and the brain, in a range of doses of 5–30 mg/kg [ 8 , 11 , 12 , 13 ]. Upon intra-nigral administration in rats, FPN reduced the dopamine (DA) content in the striatum as well as the tyrosine hydroxylase (TH) levels in the striatum and the substantia nigra (SN) pars compacta, and impaired motor coordination [ 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

Chronic Administration of Fipronil Heterogeneously Alters the Neurochemistry of Monoaminergic Systems in the Rat Brain

Bharatiya

Chagraoui

Deurwaerdere

et al. 2020

IJMS

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Fipronil (FPN), a widely used pesticide for agricultural and non-agricultural pest control, is possibly neurotoxic for mammals. Brain monoaminergic systems, involved in virtually all brain functions, have been shown to be sensitive to numerous pesticides. Here, we addressed the hypothesis that chronic exposure to FPN could modify brain monoamine neurochemistry. FPN (10 mg/kg) was chronically administered for 21 days through oral gavage in rats. Thereafter, the tissue concentrations of dopamine (DA) and its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid; serotonin (5-HT) and its metabolite, 5-hydroxyindoleacetic acid (5-HIAA); and noradrenaline (NA) were measured in 30 distinct brain regions. FPN significantly decreased DA and its metabolite levels in most striatal territories, including the nucleus accumbens and the substantia nigra (SN). FPN also diminished 5-HT levels in some striatal regions and the SN. The indirect index of the turnovers, DOPAC/DA and 5-HIAA/5-HT ratios, was increased in numerous brain regions. FPN reduced the NA content only in the nucleus accumbens core. Using the Bravais–Pearson test to study the neurochemical organization of monoamines through multiple correlative analyses across the brain, we found fewer correlations for NA, DOPAC/DA, and 5-HIAA/5-HT ratios, and an altered pattern of correlations within and between monoamine systems. We therefore conclude that the chronic administration of FPN in rats induces massive and inhomogeneous changes in the DA and 5-HT systems in the brain.

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Section: Introductionmentioning

confidence: 99%

Chronic Administration of Fipronil Heterogeneously Alters the Neurochemistry of Monoaminergic Systems in the Rat Brain

Bharatiya

Chagraoui

Deurwaerdere

et al. 2020

IJMS

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“…Surprisingly, meloxicam revealed comparable neuroprotective effects to low-dose G-CSF regarding antiapoptosis, inhibition of macrophage infiltration, and macrophage M2 polarization in this model. Meloxicam breaks the inflammatory cascade via inhibition of MAPK and p53 signaling pathway and owns antiapoptotic effects evidenced by alleviating oxidative stress, avoiding mitochondrial dysfunction, and reducing endoplasmic reticulum stress response in vitro 25,26 . A recent study reported that meloxicam's neuroprotective effects maintained cell survival via the upregulation of the PI3K/Akt pathway instead of COX-2 inhibition 26 .…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effects of low-dose G-CSF plus meloxicam in a rat model of anterior ischemic optic neuropathy

Liu

Wen²,

Lin

et al. 2020

Sci Rep

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Non-arteritic anterior ischemic optic neuropathy (NAION) causes a sudden loss of vision and lacks effective treatment. Granulocyte colony-stimulating factor (G-CSF) provides neuroprotection against the experimental optic nerve injuries but also induce leukocytosis upon typical administration. We found synergetic neuroprotective effects of meloxicam and low dose G-CSF without leukocytosis in a rat model of anterior ischemic optic neuropathy (rAION). The WBC counts in the low-dose G-CSF-plus meloxicam-treated group were similar to the sham-operated group. Combination treatment of lowdose G-CSF plus meloxicam preserved RGCs survival and visual function, reduced RGC apoptosis and the macrophages infiltration, and promote more M2 phenotype of macrophage/microglial transition than the low-dose GCSF treatment or the meloxicam treatment. Moreover, the combination treatment induced higher serine/threonine kinase 1 (Akt1) expression. The combination treatment of low-dose G-CSF plus meloxicam lessened the leukocytotic side effect and provided neuroprotective effects via Akt1 activation in the rAION model. This approach provides crucial preclinical information for the development of alternative therapy in AION. Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common acute optic neuropathy in people older than 50 years. The estimated mean annual incidence rates of NAION are 2.3-10.3 per 100,000 in the United States and 3.72 per 100,000 in Taiwan 1-3. The debilitating consequences for patients with NAION include severe vision impairment and visual field defect. The primarily proposed pathogenesis of NAION is the transient nonperfusion or hypoperfusion of the optic nerve head and loss of retinal ganglion cells (RGCs) following ischemic insults. The histologic evidence in an early clinical case of human NAION demonstrated the presence of apoptotic cells in the RGC layer by 30 days after the event. This reaction eventually results in RGC death and vision loss 4. Currently, no definite treatment for NAION is available. Halting the injury and loss of RGCs may, therefore, rescue the visual deterioration and be a potential treatment strategy. Granulocyte colony-stimulating factor (G-CSF), a member of the cytokine family of growth factors, is a 19.6-kDa glycoprotein. It is commonly applied clinically to treat neutropenia 5. G-CSF can induce the mobilization of CD34 + hematopoietic stem cells from the bone marrow into the peripheral blood. G-CSF is commonly used in clinics for stem cell mobilization and bone marrow reconstitution 6-8. Our previous studies have demonstrated that G-CSF exerts neuroprotective effects on a rat model of anterior ischemic optic neuropathy (rAION). The protective effects of G-CSF on the rAION model are achieved through dual mechanisms of anti-inflammation and antiapoptosis 9,10. The antiapoptotic effect of G-CSF occurs through the activation of a variety of intracellular

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“…Reactive oxygen species [4] which include hydrogen peroxide (H 2 O 2 ), superoxide anion and hydroxyl radicals are generated by many mechanisms in organisms under physiological conditions [17,18].Pesticide can induce production of ROS which results in lipid peroxidation, protein oxidations, modulation of gene expression, alterations of redox status and certain disease conditions [7,19]. The peroxidation of lipid is particularly damaging because of the formation of aldehyde -products of ω3 and ω6 of polyunsaturated fatty acid [17]. In this present study we demonstrated that increasing the concentration of glyphosate induced lipid peroxidation significantly compared with the control.…”

Section: Discussionmentioning

confidence: 99%

Toxic Effect of Glyphosate-Pesticide on Lipid Peroxidation Superoxide Dismutase and Catalase of Clarias Gariepinus

Ogochukwu¹,

Achikanu²

2020

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The oxidative stress indices lipid peroxidation (LPO), superoxide dismutase (SOD) and catalase (CAT) in juvenile Clarias gariepinus (average weight 200.15 g) exposed to sub - lethal dose 2.40mg/L and 4.98mg/L of glyphosate was investigated over a period of days 1,5,10 and 15 in three replicates. The colorimetric analysis showed increase in lipid peroxidation from 4.55 ±2.14a1 to 12.12± 10.00a1at 2.40mg/L but remain the same at 4.98mg/L (4.55±2.14a1) compared with control (3.03±0.01a1 to 1.51±2.14b1) from day 1 to 15. The SOD activity decreased significantly with time and concentration compared with control. The Catalase activity at day 15 decreased to 0.17±0.05a1 in 2.40mg/L but further increased to 0.28±0.05b1 in 4.98mg/L compared to 0.28±0.02a1 catalase activity as control. The result suggests that glyphosate induce oxidative stress that may overwhelm the antioxidant system in juvenile catfish especially at higher concentrations with long exposure.

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Meloxicam inhibits fipronil‐induced apoptosis via modulation of the oxidative stress and inflammatory response in SH‐SY5Y cells

Cited by 40 publications

References 61 publications

Chronic Administration of Fipronil Heterogeneously Alters the Neurochemistry of Monoaminergic Systems in the Rat Brain

Chronic Administration of Fipronil Heterogeneously Alters the Neurochemistry of Monoaminergic Systems in the Rat Brain

Neuroprotective effects of low-dose G-CSF plus meloxicam in a rat model of anterior ischemic optic neuropathy

Toxic Effect of Glyphosate-Pesticide on Lipid Peroxidation Superoxide Dismutase and Catalase of Clarias Gariepinus

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