Interleukin-1beta: a common thread between inflammation, pain and opioid tolerance

Mohan, Shekher

doi:10.20517/2347-8659.2016.37

Cited by 2 publications

(3 citation statements)

References 35 publications

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“…Tumor necrosis factor-α (TNF-α) is an inflammatory cytokine that resulted from macrophages/monocytes during acute inflammation and is responsible for a diverse range of cell signaling events (Hartupee and Mann 2013 ). While IL-1β is a proinflammatory cytokine that has been involved in inflammation, pain, and autoimmune conditions (Mohan 2016 ). This work showed a significant increase in both heart and brain TNF-α and IL-1β by Cyclo (100 mg/kg, i.p.)…”

Section: Discussionmentioning

confidence: 99%

Ameliorative effect of flavocoxid on cyclophosphamide-induced cardio and neurotoxicity via targeting the GM-CSF/NF-κB signaling pathway

Elsayed

Elshenawy

Khalifa

et al. 2022

Environ Sci Pollut Res

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Cyclophosphamide (Cyclo) is a chemotherapeutic agent used as an immunosuppressant and as a treatment for many cancerous diseases. Many previous pieces of literature proved the marked cardio and neurotoxicity of the drug. Thus, this research provides evidence on the alleviative effect of flavocoxid on the cardiac and brain toxicity of cyclophosphamide in mice and determines its underlying mechanisms. Flavocoxid (Flavo) is a potent antioxidant and anti-inflammatory agent that inhibits the peroxidase activity of cyclooxygenase (COX-1 and COX-2) enzymes and 5-lipooxygenase (5-LOX). Flavo was administered orally (20 mg/kg) for 2 weeks, followed by Cyclo (100 mg/kg, i.p.) on day 14. Higher heart and brain weight indices, serum lactate dehydrogenase (LDH), creatine kinase (CK-MB), and nitric oxide (NO) were mitigated following Flavo administration. Flavo modulated oxidative stress biomarkers (malonaldehyde (MDA), glutathione (GSH), and superoxide dismutase (SOD)), tumor necrosis factor-α (TNF-α), and interleukin (IL)-1β. Additionally, cardiac troponin I (cTn-I), nuclear factor kappa B (NF-κB), brain amyloid precursor protein (APP), and granulocyte macrophage colony-stimulating factor (GM-CSF) were decreased by Flavo administration. Moreover, Flavo ameliorated heart and brain histopathological changes and caspase-3 levels. Collectively, Flavo (20 mg/kg) for 14 days showed significant cardio and neuroprotective effects due to its antioxidant, anti-inflammatory, and antiapoptotic activities via modulation of oxidative stress, inflammation, and the GM-CSF/NF-κB signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Ameliorative effect of flavocoxid on cyclophosphamide-induced cardio and neurotoxicity via targeting the GM-CSF/NF-κB signaling pathway

Elsayed

Elshenawy

Khalifa

et al. 2022

Environ Sci Pollut Res

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“…For instance, major inflammatory cytokines such as TNFα and IL-1β modulate glutamate receptor (NMDA/AMPA) conductance and/or surface expression resulting in changes in neuronal excitability (42). In parallel, cytokine-induced glutamate transporter (e.g., GLT-1, GLAST) downregulation by opioid administration can contribute to tolerance by increasing synaptic glutamate and modulating neuronal excitability (6,30). The immunoregulatory aspect of opioids is supported by a multitude of publications describing changes in various cytokines and chemokines in response to opioid administration particularly with morphine (3,14).…”

Section: Advances In Drug and Alcohol Researchmentioning

confidence: 99%

“…The analgesic and addictive attributes of common opioids are largely driven by the mu opioid receptor (MOR) subtype. MORs are G-coupled receptors that regulate expression of proteins central to neuronal activity such ion co-transporters (K+/Cl-), glutamate transporter (GLT-1), glutamate receptors (NMDA) among other mediators and targets (3)(4)(5)(6)(7). However, evidence suggests that glial cells (astrocytes and microglia) also express MOR where they indirectly regulate neuronal excitation (e.g., glutamatergic/GABA-ergic tone) as well as glial reactivity (pro-inflammatory cytokine and chemokine production).…”

Section: Introductionmentioning

confidence: 99%

Microglial knockdown does not affect acute withdrawal but delays analgesic tolerance from oxycodone in male and female C57BL/6J mice

Jordi¹,

Fischer²,

Meyer³

et al. 2022

Adv. Drug Alcohol Res.

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Opioid Use Disorder (OUD) affects approximately 8%–12% of the population. In dependent individuals, abrupt cessation of opioid taking results in adverse withdrawal symptoms that reinforce drug taking behavior. Considerable unmet clinical need exists for new pharmacotherapies to treat opioid withdrawal as well as improve long-term abstinence. The neuroimmune system has received much scientific attention in recent years as a potential therapeutic target to combat various neurodegenerative and psychiatric disorders including addiction. However, the specific contribution of microglia has not been investigated in oxycodone dependence. Chronic daily treatment with the CSF1R inhibitor Pexidartinib (PLX3397) was administered to knockdown microglia expression and evaluate consequences on analgesia and on naloxone induced withdrawal from oxycodone. In vivo results indicated that an approximately 40% reduction in brain IBA1 staining was achieved in the PLX treatment group, which was associated with a delay in the development of analgesic tolerance to oxycodone and maintained antinociceptive efficacy. Acute withdrawal behavioral symptoms, brain astrocyte expression, and levels of many neuroinflammatory markers were not affected by PLX treatment. KC/GRO (also known as CXCL1) was significantly enhanced in the somatosensory cortex in oxycodone‐treated mice receiving PLX. Microglial knock-down did not affect the expression of naloxoneinduced opioid withdrawal but affected antinociceptive responsivity. The consequences of increased KC/GRO expression within the somatosensory cortex due to microglial reduction during opioid dependence are unclear but may be important for neural pathways mediating opioid‐induced analgesia.

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Interleukin-1beta: a common thread between inflammation, pain and opioid tolerance

Cited by 2 publications

References 35 publications

Ameliorative effect of flavocoxid on cyclophosphamide-induced cardio and neurotoxicity via targeting the GM-CSF/NF-κB signaling pathway

Ameliorative effect of flavocoxid on cyclophosphamide-induced cardio and neurotoxicity via targeting the GM-CSF/NF-κB signaling pathway

Microglial knockdown does not affect acute withdrawal but delays analgesic tolerance from oxycodone in male and female C57BL/6J mice

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