m-Trifluoromethyl-diphenyl diselenide, a multi-target selenium compound, prevented mechanical allodynia and depressive-like behavior in a mouse comorbid pain and depression model

Brüning, César Augusto; Martini, Franciele; Soares, Suelen Mendonça; Sampaio, Tuane Bazanella; Gai, Bibiana Mozzaquatro; Duarte, Marta M.M.F.; Nogueira, Cristina W.

doi:10.1016/j.pnpbp.2015.05.011

Cited by 48 publications

(15 citation statements)

References 53 publications

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“…Moreover, ( p ‐ClPhSe) 2 reversed the increase in hepatic iNOS levels in MSG–treated rats, which could be associated with an improvement in RCR and further indicating the anti‐inflammatory action of this compound. This way, it has been reported the anti‐inflammatory action of organoselenium compounds in different experimental models by regulating the levels of pro‐inflammatory proteins and cytokines [Bruning et al, , ].…”

Section: Discussionmentioning

confidence: 99%

(p-ClPhSe)₂Reduces Hepatotoxicity Induced by Monosodium Glutamate by Improving Mitochondrial Function in Rats

et al. 2017

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It is has been demonstrated that mitochondrial dysfunction, oxidative stress, and chronic inflammatory process are associated with progress of morbid obesity in human patients. For this reason, the searching for safe and effective antiobesity drugs has been the subject of intense research. In this context, the organic selenium compounds have attracted much attention due to their pharmacological properties, such as antihyperglycemic, antioxidant, and anti-inflammatory. The aim of this study was to evaluate the hepatoprotective action of p-chloro-diphenyl diselenide (p-ClPhSe) , an organic selenium compound, in a model of obesity induced by monosodium glutamate (MSG) administration in rats. Wistar rats were treated during the first ten postnatal days with MSG (4 g/kg by subcutaneous injections) and received (p-ClPhSe) (10 mg/kg, intragastrically) from 90th to 97th postnatal day. Mitochondrial function, purine content and the levels of proteins involved in apoptotic (poly [ADP-ribose] polymerase [PARP]) and inflammatory processes (inducible nitric oxide synthases [iNOS] and p38) were determined in the liver of rats. The present study, demonstrated that postnatal administration of MSG to male rats induced a mitochondrial dysfunction, accompanied by oxidative stress and an increase in the ADP levels, without altering the efficiency of phosphorylation in the liver of adult rats. Furthermore, the MSG administration also induces hepatotoxicity, through an increase in PARP, iNOS, and p38 levels. (p-ClPhSe) treatment had beneficial effects against mitochondrial dysfunction, oxidative stress, and modulated protein markers of apoptosis and inflammation in the liver of MSG-treated rats. J. Cell. Biochem. 118: 2877-2886, 2017. © 2017 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

(p-ClPhSe)₂Reduces Hepatotoxicity Induced by Monosodium Glutamate by Improving Mitochondrial Function in Rats

et al. 2017

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“…mannose receptor (MRC2), both of which are markers of the M2 phenotype, it does not inhibit the increases in IL-1β, IL-6 or suppressor of cytokine signaling 3 (SOCS3) in the PFC in a spinal nerve ligation and olfactory bulbectomy model (Burke et al, 2014). The compound m-trifluoromethyl-diphenyl diselenide (m-CF3-PhSe)2 permeates the BBB and modulates opioid receptors without inducing opioid tolerance (Brüning et al, 2015;Rosa et al, 2018). Acute and subchronic treatment with this compound improves mechanical nociceptive thresholds and depressive-like behavior, decreases COX-2 and increases BDNF in the cerebral cortex and hippocampus in a partial sciatic nerve ligation model; however, only subchronic administration decreases proinflammatory cytokines and increases IL-10 in the serum, cerebral cortex and hippocampus and decreases corticosterone in the serum (Brüning et al, 2015).…”

Section: Understanding the Anti-inflammatory Signature Of Depressive-mentioning

confidence: 99%

Neuroinflammation, Pain and Depression: An Overview of the Main Findings

et al. 2020

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Chronic pain is a serious public health problem with a strong affective-motivational component that makes it difficult to treat. Most patients with chronic pain suffer from severe depression; hence, both conditions coexist and exacerbate one another. Brain inflammatory mediators are critical for maintaining depression-pain syndrome and could be substrates for it. The goal of our paper was to review clinical and preclinical findings to identify the neuroinflammatory profile associated with the cooccurrence of pain and depression. In addition, we aimed to explore the regulatory effect of neuronal reorganization on the inflammatory response in pain and depression. We conducted a quantitative review supplemented by manual screening. Our results revealed inflammatory signatures in different preclinical models and clinical articles regarding depression-pain syndrome. We also identified that improvements in depressive symptoms and amelioration of pain can be modulated through direct targeting of inflammatory mediators, such as cytokines and molecular inhibitors of the inflammatory cascade. Additionally, therapeutic targets that improve and regulate the synaptic environment and its neurotransmitters may act as anti-inflammatory compounds, reducing local damage-associated molecular patterns and inhibiting the activation of immune and glial cells. Taken together, our data will help to better elucidate the neuroinflammatory profile in pain and depression and may help to identify pharmacological targets for effective management of depression-pain syndrome.

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“…Moreover, drugs or methods down-regulating neuroinflammation could alleviate the pain symptoms and depressive behaviors (Zhang et al, 2015; Luchting et al, 2016). Hence, modulation of neuroimmune response has been proposed for treatment of many central nervous system (CNS) disorders with an inflammatory component, including the comorbidity of neuropathic pain and depression (Kim et al, 2012; Walker et al, 2014; Bruning et al, 2015). …”

Section: Introductionmentioning

confidence: 99%

Spared Nerve Injury Increases the Expression of Microglia M1 Markers in the Prefrontal Cortex of Rats and Provokes Depression-Like Behaviors

et al. 2017

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Pain and depression are frequently co-existent in clinical practice, yet the underlying mechanisms remain largely to be determined. Microglia activation and subsequent pro-inflammatory responses play a crucial role in the development of neuropathic pain and depression. The process of microglia polarization to the pro-inflammatory M1 or anti-inflammatory M2 phenotypes often occurs during neuroinflammation. However, it remains unclear whether M1/M2 microglia polarization is involved in the neuropathic pain induced by spared nerve injury (SNI). In the present study, the mechanical withdrawal threshold, forced swim test, sucrose preference test, and open field test were performed. The levels of microglia markers including ionized calcium-binding adaptor molecule 1 (Iba1), cluster of differentiation 11b (CD11b), M1 markers including CD68, inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β), IL-6, tumor necrosis factor-a (TNF-α), 8-hydroxy-2-deoxyguanosine (8-OH-dG), and M2 markers including CD206, arginase 1 (Arg1), IL-4 in the prefrontal cortex were determined on day 14 after SNI. The results showed that SNI produced mechanical allodynia and depressive-like behaviors, and also increased the expressions of microglia markers (Iba1, CD11b) and M1 markers (CD68, iNOS, IL-1β, TNF-α, and 8-OH-dG) in the prefrontal cortex. Notably, minocycline administration reversed these abnormalities. In addition, minocycline also promoted M2 microglia polarization as evidenced by up-regulation of CD206 and Arg1. In conclusion, data from our study suggest that SNI can lead to depression-like behaviors, while M1 polarization and consequent overproduction of pro-inflammatory cytokines plays a key role in the pathogenesis of neuropathic pain. The data furthermore indicate that modulation of inflammation by inhibition of M1 polarization could be a strategy for treatment of neuropathic pain, and might prevent the induction of neuropathic pain-induced depression symptoms.

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m-Trifluoromethyl-diphenyl diselenide, a multi-target selenium compound, prevented mechanical allodynia and depressive-like behavior in a mouse comorbid pain and depression model

Cited by 48 publications

References 53 publications

(p-ClPhSe)₂Reduces Hepatotoxicity Induced by Monosodium Glutamate by Improving Mitochondrial Function in Rats

(p-ClPhSe)₂Reduces Hepatotoxicity Induced by Monosodium Glutamate by Improving Mitochondrial Function in Rats

Neuroinflammation, Pain and Depression: An Overview of the Main Findings

Spared Nerve Injury Increases the Expression of Microglia M1 Markers in the Prefrontal Cortex of Rats and Provokes Depression-Like Behaviors

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m-Trifluoromethyl-diphenyl diselenide, a multi-target selenium compound, prevented mechanical allodynia and depressive-like behavior in a mouse comorbid pain and depression model

Cited by 48 publications

References 53 publications

(p-ClPhSe)2Reduces Hepatotoxicity Induced by Monosodium Glutamate by Improving Mitochondrial Function in Rats

(p-ClPhSe)2Reduces Hepatotoxicity Induced by Monosodium Glutamate by Improving Mitochondrial Function in Rats

Neuroinflammation, Pain and Depression: An Overview of the Main Findings

Spared Nerve Injury Increases the Expression of Microglia M1 Markers in the Prefrontal Cortex of Rats and Provokes Depression-Like Behaviors

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Product

Resources

About

(p-ClPhSe)₂Reduces Hepatotoxicity Induced by Monosodium Glutamate by Improving Mitochondrial Function in Rats

(p-ClPhSe)₂Reduces Hepatotoxicity Induced by Monosodium Glutamate by Improving Mitochondrial Function in Rats