Modulatory effect of methylsulfonylmethane against BPA/γ-radiation induced neurodegenerative alterations in rats: Influence of TREM-2/DAP-12/Syk pathway

Abdel-Rafei, Mohamed K.; Thabet, Noura M

doi:10.1016/j.lfs.2020.118410

Cited by 11 publications

(4 citation statements)

References 104 publications

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“…Ionizing radiation, one of the exogenous environmental stressors, is threatening healthy and causes damage in tissues which eventually results in diseases. Workers in the nuclear power industry, researchers in radiological laboratories, and patients undergoing diagnostic procedures or routine therapeutic radiation are among those who are inevitably exposed to the deleterious effects of radiation (Azzam et al 2012 ; Abdel-Rafei and Thabet 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Fractionated whole body γ-irradiation aggravates arthritic severity via boosting NLRP3 and RANKL expression in adjuvant-induced arthritis model: the mitigative potential of ebselen

2023

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Rheumatoid arthritis (RA) is an autoimmune chronic inflammatory disease associated with oxidative stress that causes excruciating pain, discomfort, and joint destruction. Ebselen (EB), a synthesized versatile organo-selenium compound, protects cells from reactive oxygen species (ROS)-induced injury by mimicking glutathione peroxidase (GPx) action. This study aimed to investigate the antioxidant and anti-inflammatory effects of EB in an arthritic irradiated model. This goal was achieved by subjecting adjuvant-induced arthritis (AIA) rats to fractionated whole body γ-irradiation (2 Gy/fraction once per week for 3 consecutive weeks, for a total dose of 6 Gy) and treating them with EB (20 mg/kg/day, p.o) or methotrexate (MTX; 0.05 mg/kg; twice/week, i.p) as a reference anti-RA drug. The arthritic clinical signs, oxidative stress and antioxidant biomarkers, inflammatory response, expression of NOD-like receptor protein-3 (NLRP-3) inflammasome, receptor activator of nuclear factor κB ligand (RANKL), nuclear factor-κB (NF-κB), apoptotic indicators (caspase 1 and caspase 3), cartilage integrity marker (collagen-II), and histopathological examination of ankle joints were assessed. EB notably improved the severity of arthritic clinical signs, alleviated joint histopathological lesions, modulated oxidative stress and inflammation in serum and synovium, as well as reduced NLRP-3, RANKL, and caspase3 expression while boosting collagen-II expression in the ankle joints of arthritic and arthritic irradiated rats with comparable potency to MTX. Our findings suggest that EB, through its antioxidant and anti-inflammatory properties, has anti-arthritic and radioprotective properties in an arthritic irradiated model.

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Section: Introductionmentioning

confidence: 99%

Fractionated whole body γ-irradiation aggravates arthritic severity via boosting NLRP3 and RANKL expression in adjuvant-induced arthritis model: the mitigative potential of ebselen

2023

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“…- Augmented secretion of IFN-γ and IL-4. DBA/1J mice [ 125 ] BPA 150 mg/kg TREM-2/DAP-12/Syk Pathway Upregulation of hippocampal signaling pathway with tau phosphorylation; increased oxidative stress; altered antioxidant machinery; disrupted Nrf-2/HO-1 signaling and Trx-1/Grx-1 system Wistar albino rats [ 126 ] BPA & Nonylphenol 100 μM Apoptosis Increased Ca2+, PLC activation, and ADAM17 activation Reproductive tract cancer cell lines [ 127 ] BPA 50 μg/kg Cognitive dysfunction and oxidative stress Oxidative stress in brain areas, reduced NMDA receptor expression, increased MDA levels Male Swiss albino mice [ 128 ] BPA 50 μg/kg Estrogen Receptor Alpha Regulation Altered ER mRNA and protein expression, reduced ER phosphorylation Male rats [ 129 ] BPA 50 μg/kg Apoptosis & Inflammatory response Increased ROS, RNS, MDA, and H2O2; decreased antioxidant enzyme activity; elevated proinflammatory cytokines; enhanced caspase activity CD-1 male mice [ 130 ] BPA & Nonylphenol 50 mg/kg Apoptosis Increased TUNEL-positive cells, cleaved PARP, and active caspase-3 Male Sprague–Dawley rats [ 131 ] BPA & BPS 50 μg BPA & BPS/kg Glucose Intolerance & Hepatic Mitochondrial Changes Elevated HDL-C levels; mitochondrial H2O2 production; DRP1 expression; reduced mitochondria; altered PGC1 expression …”

Section: The Therapeutic Target Of Nlrp3 In Bpa Toxicitymentioning

confidence: 99%

Deciphering the molecular mechanism of NLRP3 in BPA-mediated toxicity: Implications for targeted therapies

Charles,

Prince

2024

Heliyon

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“…It was found that co-exposure of BPA and γ-IR induces hallmarks typical of neurodegenerative disorders, due to rather high oxidative stress, extensive neuroinflammation, elevated Alzheimer’s markers in the cortex and hippocampus, as well as up-regulation of microglial pro-inflammatory triggering receptor expressed on the myeloid cell-2/DNAX-activating protein of 12 kDa/spleen-tyrosine kinase pathway and its downstream targets (PLC-γ/DAG/p38-MAPK) in the hippocampus. In addition, neurodegenerative lesions were detected on histopathological examination of the cortex and hippocampus along with marked Aβ deposition in the hippocampus (Abdel-Rafei and Thabet 2020 ). Moreover, in male Sprague–Dawley rats, the research group of Kobayashi analysed the exposure effect of 100 mg/kg/day of BPA or 3 mg/kg/day of Rotenone on the cerebrovascular system.…”

Section: Effects Of Bpa On Animal Modelsmentioning

confidence: 99%

Effect of bisphenol A on the neurological system: a review update

Costa,

Cairrao

2023

Arch Toxicol

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Bisphenol A (BPA) is an endocrine-disrupting chemical (EDC) and one of the most produced synthetic compounds worldwide. BPA can be found in epoxy resins and polycarbonate plastics, which are frequently used in food storage and baby bottles. However, BPA can bind mainly to estrogen receptors, interfering with various neurologic functions, its use is a topic of significant concern. Nonetheless, the neurotoxicity of BPA has not been fully understood despite numerous investigations on its disruptive effects. Therefore, this review aims to highlight the most recent studies on the implications of BPA on the neurologic system. Our findings suggest that BPA exposure impairs various structural and molecular brain changes, promoting oxidative stress, changing expression levels of several crucial genes and proteins, destructive effects on neurotransmitters, excitotoxicity and neuroinflammation, damaged blood–brain barrier function, neuronal damage, apoptosis effects, disruption of intracellular Ca2+ homeostasis, increase in reactive oxygen species, promoted apoptosis and intracellular lactate dehydrogenase release, a decrease of axon length, microglial DNA damage, astrogliosis, and significantly reduced myelination. Moreover, BPA exposure increases the risk of developing neurologic diseases, including neurovascular (e.g. stroke) and neurodegenerative (e.g. Alzheimer’s and Parkinson’s) diseases. Furthermore, epidemiological studies showed that the adverse effects of BPA on neurodevelopment in children contributed to the emergence of serious neurological diseases like attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), depression, emotional problems, anxiety, and cognitive disorders. In summary, BPA exposure compromises human health, promoting the development and progression of neurologic disorders. More research is required to fully understand how BPA-induced neurotoxicity affects human health.

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Modulatory effect of methylsulfonylmethane against BPA/γ-radiation induced neurodegenerative alterations in rats: Influence of TREM-2/DAP-12/Syk pathway

Cited by 11 publications

References 104 publications

Fractionated whole body γ-irradiation aggravates arthritic severity via boosting NLRP3 and RANKL expression in adjuvant-induced arthritis model: the mitigative potential of ebselen

Fractionated whole body γ-irradiation aggravates arthritic severity via boosting NLRP3 and RANKL expression in adjuvant-induced arthritis model: the mitigative potential of ebselen

Deciphering the molecular mechanism of NLRP3 in BPA-mediated toxicity: Implications for targeted therapies

Effect of bisphenol A on the neurological system: a review update

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