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1.
Int J Mol Sci ; 24(3)2023 Feb 02.
Artigo em Inglês | MEDLINE | ID: mdl-36769233

RESUMO

Neuron-glia interactions are essential for the central nervous system's homeostasis. Microglial cells are one of the key support cells in the brain that respond to disruptions in such homeostasis. Although their participation in neuroinflammation is well known, studies investigating their role in ferroptosis, an iron-dependent form of nonapoptotic cell death, are lacking. To address this issue, we explored whether microglial (BV-2 cells) activation products can intensify, mitigate or block oxidative and/or ferroptotic damage in neuronal cells (HT22 cell line). Cultured BV-2 microglial cells were stimulated with 5-100 ng/mL lipopolysaccharide (LPS) for 24 h and, after confirmation of microglial activation, their culture medium (conditioned media; CM) was transferred to neuronal cells, which was subsequently (6 h later) exposed to glutamate or tert-butyl hydroperoxide (t-BuOOH). As a major finding, HT22 cells pretreated for 6 h with CM exhibited a significant ferroptosis-resistant phenotype characterized by decreased sensitivity to glutamate (15 mM)-induced cytotoxicity. However, no significant protective effects of LPS-activated microglial cell-derived CM were observed in t-BuOOH (30 µM)-challenged cells. In summary, activated microglia-derived molecules may protect neuronal cells against ferroptosis. The phenomenon observed in this work highlights the beneficial relationship between microglia and neurons, highlighting new possibilities for the control of ferroptosis.


Assuntos
Ferroptose , Microglia , Microglia/metabolismo , Meios de Cultivo Condicionados/farmacologia , Meios de Cultivo Condicionados/metabolismo , Lipopolissacarídeos/toxicidade , Lipopolissacarídeos/metabolismo , Ácido Glutâmico/toxicidade , Ácido Glutâmico/metabolismo , Células Cultivadas , Neurônios/metabolismo
2.
R. bras. Ci. avíc. ; 18(4): 593-597, Out-Dez. 2016. tab
Artigo em Inglês | VETINDEX | ID: vti-683978

RESUMO

An experiment was conducted to determine the effects of the dietary inclusion of different levels of thymoquinone (TQ) of broilers subjected to oxidative stress or not on the antibody titers against Newcastle disease and on the gene expression of interleukine-1 and interferon gamma. A total of 320 one-day-old broilers was randomly assigned to eight treatments with four replicates of 10 birds each, in a 4 × 2 factorial arrangement, consisting of four thymoquinone (TQ) levels (0, 5, 8, or 11 mg/kg body weight) and two levels tert-butyl hydroperoxide (t-BHP) injection (0 or 0.02 mmol/kg of body weight). Blood samples were collected from two birds per replicate to determine antibody titers against Newcastle disease. At the end of experiment, two birds per replicate were randomly selected, sacrificed and their spleens were collected to evaluate the genes expressioninterleukin-1 and interferon gamma (p 0.05). The dietary inclusion of TQ of broilers subjected or not oxidative stress increased antibody production against Newcastle disease (p 0.05). Both individual and combined dietary inclusion of t-BHP and TQ promote the differentiation and proliferation of spleen cells and the gene expression of interleukin-1 and interferon gamma (p 0.05). (AU)


Assuntos
Animais , Plantas Medicinais/fisiologia , Proteínas do Fator Nuclear 90/fisiologia , Proteínas do Fator Nuclear 90/uso terapêutico , Interferons/fisiologia , Anticorpos/fisiologia , Doença de Newcastle/fisiopatologia , Estresse Oxidativo , Dieta/veterinária , Coleta de Amostras Sanguíneas , Baço/anatomia & histologia , Expressão Gênica , Autopsia/veterinária
3.
Rev. bras. ciênc. avic ; 18(4): 593-597, Out-Dez. 2016. tab
Artigo em Inglês | VETINDEX | ID: biblio-1490307

RESUMO

An experiment was conducted to determine the effects of the dietary inclusion of different levels of thymoquinone (TQ) of broilers subjected to oxidative stress or not on the antibody titers against Newcastle disease and on the gene expression of interleukine-1 and interferon gamma. A total of 320 one-day-old broilers was randomly assigned to eight treatments with four replicates of 10 birds each, in a 4 × 2 factorial arrangement, consisting of four thymoquinone (TQ) levels (0, 5, 8, or 11 mg/kg body weight) and two levels tert-butyl hydroperoxide (t-BHP) injection (0 or 0.02 mmol/kg of body weight). Blood samples were collected from two birds per replicate to determine antibody titers against Newcastle disease. At the end of experiment, two birds per replicate were randomly selected, sacrificed and their spleens were collected to evaluate the genes expressioninterleukin-1 and interferon gamma (p 0.05). The dietary inclusion of TQ of broilers subjected or not oxidative stress increased antibody production against Newcastle disease (p 0.05). Both individual and combined dietary inclusion of t-BHP and TQ promote the differentiation and proliferation of spleen cells and the gene expression of interleukin-1 and interferon gamma (p 0.05).


Assuntos
Animais , Anticorpos/fisiologia , Dieta/veterinária , Doença de Newcastle/fisiopatologia , Estresse Oxidativo , Interferons/fisiologia , Plantas Medicinais/fisiologia , Proteínas do Fator Nuclear 90/fisiologia , Proteínas do Fator Nuclear 90/uso terapêutico , Autopsia/veterinária , Baço/anatomia & histologia , Coleta de Amostras Sanguíneas , Expressão Gênica
4.
Free Radic Biol Med ; 63: 446-56, 2013 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-23747984

RESUMO

NADPH is the reducing agent for mitochondrial H2O2 detoxification systems. Nicotinamide nucleotide transhydrogenase (NNT), an integral protein located in the inner mitochondrial membrane, contributes to an elevated mitochondrial NADPH/NADP(+) ratio. This enzyme catalyzes the reduction of NADP(+) at the expense of NADH oxidation and H(+) reentry to the mitochondrial matrix. A spontaneous Nnt mutation in C57BL/6J (B6J-Nnt(MUT)) mice arose nearly 3 decades ago but was only discovered in 2005. Here, we characterize the consequences of the Nnt mutation on the mitochondrial redox functions of B6J-Nnt(MUT) mice. Liver mitochondria were isolated both from an Nnt wild-type C57BL/6 substrain (B6JUnib-Nnt(W)) and from B6J-Nnt(MUT) mice. The functional evaluation of respiring mitochondria revealed major redox alterations in B6J-Nnt(MUT) mice, including an absence of transhydrogenation between NAD and NADP, higher rates of H2O2 release, the spontaneous oxidation of NADPH, the poor ability to metabolize organic peroxide, and a higher susceptibility to undergo Ca(2+)-induced mitochondrial permeability transition. In addition, the mitochondria of B6J-Nnt(MUT) mice exhibited increased oxidized/reduced glutathione ratios as compared to B6JUnib-Nnt(W) mice. Nonetheless, the maximal activity of NADP-dependent isocitrate dehydrogenase, which is a coexisting source of mitochondrial NADPH, was similar between both groups. Altogether, our data suggest that NNT functions as a high-capacity source of mitochondrial NADPH and that its functional loss due to the Nnt mutation results in mitochondrial redox abnormalities, most notably a poor ability to sustain NADP and glutathione in their reduced states. In light of these alterations, the potential drawbacks of using B6J-Nnt(MUT) mice in biomedical research should not be overlooked.


Assuntos
Mitocôndrias Hepáticas/metabolismo , Membranas Mitocondriais/metabolismo , NADP Trans-Hidrogenases/metabolismo , NADP/metabolismo , Animais , Glutationa/metabolismo , Peróxido de Hidrogênio/metabolismo , Peróxido de Hidrogênio/farmacologia , Camundongos , Mitocôndrias Hepáticas/efeitos dos fármacos , Mitocôndrias Hepáticas/patologia , Membranas Mitocondriais/efeitos dos fármacos , Membranas Mitocondriais/enzimologia , Mutação , NADP Trans-Hidrogenases/genética , Oxirredução/efeitos dos fármacos
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