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Objectives This work investigated the acute antinociceptive effect of a synthetic chalcone, 4-dimethylamino chalcone (DMAC), as well as its effects on vincristine-induced peripheral neuropathy (VIPN) in mice. Methods The inhibitory activity of myeloperoxidase was assessed by measuring HOCl formation. Formalin and hot plate tests were used to study the acute antinociceptive effect of DMAC. VIPN was induced through the administration of vincristine sulphate (0.1 mg/kg, i.p., 14 days). Then, DMSO, DMAC (10 or 30 mg/kg; i.p.), or pregabalin (10 mg/kg, i.p.) were administered for 14 consecutive days. Thermal hyperalgesia and mechanical allodynia were evaluated before and after VIPN induction and on days 1, 3, 7, and 14 of treatment. Neurodegeneration and neuroinflammation were assessed through immunohistochemistry for NF200, iNOS, and arginase-1 within the sciatic nerve. Key findings DMAC inhibited myeloperoxidase activity in vitro and presented an acute antinociceptive effect in both formalin and hot plate tests, with the involvement of muscarinic and opioid receptors. Treatment with 30 mg/kg of DMAC significantly attenuated thermal hyperalgesia and mechanical allodynia and prevented macrophage proinflammatory polarisation in VIPN mice. Conclusions Our results show that DMAC, acting through different mechanisms, effectively attenuates VIPN.
Objectives This work investigated the acute antinociceptive effect of a synthetic chalcone, 4-dimethylamino chalcone (DMAC), as well as its effects on vincristine-induced peripheral neuropathy (VIPN) in mice. Methods The inhibitory activity of myeloperoxidase was assessed by measuring HOCl formation. Formalin and hot plate tests were used to study the acute antinociceptive effect of DMAC. VIPN was induced through the administration of vincristine sulphate (0.1 mg/kg, i.p., 14 days). Then, DMSO, DMAC (10 or 30 mg/kg; i.p.), or pregabalin (10 mg/kg, i.p.) were administered for 14 consecutive days. Thermal hyperalgesia and mechanical allodynia were evaluated before and after VIPN induction and on days 1, 3, 7, and 14 of treatment. Neurodegeneration and neuroinflammation were assessed through immunohistochemistry for NF200, iNOS, and arginase-1 within the sciatic nerve. Key findings DMAC inhibited myeloperoxidase activity in vitro and presented an acute antinociceptive effect in both formalin and hot plate tests, with the involvement of muscarinic and opioid receptors. Treatment with 30 mg/kg of DMAC significantly attenuated thermal hyperalgesia and mechanical allodynia and prevented macrophage proinflammatory polarisation in VIPN mice. Conclusions Our results show that DMAC, acting through different mechanisms, effectively attenuates VIPN.
Background: In recent decades, all-embracing research accounting for thousands of natural bioactive compounds have been detailed on behalf of their origin, pharmacological activity, active phytoconstituents, and therapeutic applications. Chalcones, secondary metabolites have shown therapeutic potential against various forms of inflammation, pain, and cancer in multiple research papers targeting their pathway inhibition and their significant therapeutic activity. Area Covered: Diverse aspects of chalcones have been focused on with their biological source, pathway inhibition, and pharmacological activity. Objectives: This study aims to focus on the chalcones being the origin of ethnopharmacological, possess extensive pharmacological activities, including anti-neoplastic, antimicrobial, anti-inflammatory, antioxidant, anti-acne, anti-aging, hepatoprotective, neuroprotective, psychoactive, anti-parasitic, and many others. Method: Chalcones display anti-inflammatory activity via COX-2, NO synthase, and TNF-α inhibition. Furthermore, comprehensive studies will be discussed with a viewpoint of the chalcones’s role in the alleviation of inflammation. According to recent advancements, chalcones clinically have been used in the treatment of inflammation, anti-aging, oxidative stress reduction, autophagy, and apoptosis Conclusion: This article focuses on the molecular progression of inflammation and the chalcone role in combating inflammation by targeting inflammatory mediators and pathways.
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