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The role of NLRP3 in lead-induced neuroinflammation and possible underlying mechanism
CONCLUSIONS: NLRP3 is involved in the regulation of Pb-induced neurotoxicity. These findings expand mechanism research of Pb neurotoxicity and may help establish new prevention strategies for Pb neurotoxicity.PMID:34182382 | DOI:10.1016/j.envpol.2021.117520
Source: Environmental Pollution - June 28, 2021 Category: Environmental Health Authors: Peng Su Diya Wang Zipeng Cao Jingyuan Chen Jianbin Zhang Source Type: research

Minocycline prevents the inflammatory response after retinal detachment, where microglia phenotypes being regulated through A20.
Abstract Retinal detachment (RD) is a severe sight-threatening complication that can be caused by a multitude of retinal diseases. It has been evidenced that minocycline exerts neuroprotective effects by targeting microglia in the pathogenesis of massive ocular lesions including RD, but mechanisms remain elusive. We carried out this research to elucidate the potential mediators that link RD-induced vision loss with microglia reactivity by discussing effects of minocycline on cytokine levels and A20, a negative regulator of inflammation. Minocycline or vehicle was intraperitoneally administrated immediately after R...
Source: Experimental Eye Research - December 13, 2020 Category: Opthalmology Authors: Gao W, Du J, Chi Y, Zhu R, Gao X, Yang L Tags: Exp Eye Res Source Type: research

Minocycline protects against myocardial ischemia/reperfusion injury in rats by upregulating MCPIP1 to inhibit NF- κB activation.
Minocycline protects against myocardial ischemia/reperfusion injury in rats by upregulating MCPIP1 to inhibit NF-κB activation. Acta Pharmacol Sin. 2019 Feb 21;: Authors: Yi Q, Tan FH, Tan JA, Chen XH, Xiao Q, Liu YH, Zhang GP, Luo JD Abstract Minocycline is a tetracycline antibiotic and has been shown to play a protective role in cerebral and myocardial ischemia/reperfusion (I/R). However, the underlying mechanism remains unclear. Herein, we investigated whether monocyte chemotactic protein-induced protein-1 (MCPIP1), a negative regulator of inflammation, was involved in the minocycline-induced card...
Source: Acta Pharmacologica Sinica - February 21, 2019 Category: Drugs & Pharmacology Authors: Yi Q, Tan FH, Tan JA, Chen XH, Xiao Q, Liu YH, Zhang GP, Luo JD Tags: Acta Pharmacol Sin Source Type: research

Gelsemine and koumine, principal active ingredients of Gelsemium, exhibit mechanical antiallodynia via spinal glycine receptor activation-induced allopregnanolone biosynthesis.
Abstract Gelsemine, the principal active alkaloid from Gelsemium sempervirens Ait., and koumine, the most dominant alkaloids from Gelsemium elegans Benth., produced antinociception in a variety of rodent models of painful hypersensitivity. The present study explored the molecular mechanisms underlying gelsemine- and koumine-induced mechanical antiallodynia in neuropathic pain. The radioligand binding and displacement assays indicated that gelsemine and koumine, like glycine, were reversible and orthosteric agonists of glycine receptors with full efficacy and probably acted on same binding site as the glycine recep...
Source: Biochemical Pharmacology - January 19, 2019 Category: Drugs & Pharmacology Authors: Shoaib RM, Zhang JY, Mao XF, Wang YX Tags: Biochem Pharmacol Source Type: research

A Novel Role for Osteopontin in Macrophage-Mediated Amyloid- β Clearance in Alzheimer’s Models
This study demonstrates that OPN is an essential modulator of macrophage phenotype and their ability to clear pathogenic Aβ forms.
Source: Brain, Behavior, and Immunity - August 31, 2017 Category: Neurology Source Type: research

A Novel Role for Osteopontin in Macrophage-Mediated Amyloid- β Clearance in Alzheimer's Models.
This study demonstrates that OPN is an essential modulator of macrophage phenotype and their ability to clear pathogenic Aβ forms. PMID: 28860067 [PubMed - as supplied by publisher]
Source: Brain, Behavior, and Immunity - August 28, 2017 Category: Neurology Authors: Rentsendorj A, Sheyn J, Fuchs DT, Daley D, Salumbides BC, Schubloom HE, Hart NJ, Li S, Hayden EY, Teplow DB, Black KL, Koronyo Y, Koronyo-Hamaoui M Tags: Brain Behav Immun Source Type: research

Minocycline attenuates sevoflurane-induced cell  injury via activation of Nrf2.
Minocycline attenuates sevoflurane-induced cell injury via activation of Nrf2. Int J Mol Med. 2017 Feb 28;: Authors: Tian Y, Wu X, Guo S, Ma L, Huang W, Zhao X Abstract Minocycline has been demonstrated to exert neuroprotective effects in various experimental models. In the present study, we investigated the mechanisms underlying the protective effects of minocycline on cell injury induced by the inhalation of the anesthetic, sevoflurane. In our in vivo experiments using rats, minocycline attenuated sevoflurane-induced neuronal degeneration and apoptosis in the rat hippocampus, and this effect was a...
Source: International Journal of Molecular Medicine - February 27, 2017 Category: Molecular Biology Authors: Tian Y, Wu X, Guo S, Ma L, Huang W, Zhao X Tags: Int J Mol Med Source Type: research

Cynandione A attenuates neuropathic pain through p38 β MAPK-mediated spinal microglial expression of β-endorphin
This study aims to evaluate the antihypersensitivity activities of cynandione A in neuropathy and explored its mechanisms of action. Intrathecal injection of cynandione A dose-dependently attenuated spinal nerve ligation-induced mechanical allodynia and thermal hyperalgesia, with maximal possible effects of 57% and 59%, ED50s of 14.9 μg and 6.5 μg, respectively. Intrathecal injection of cynandione A significantly increased β-endorphin levels in spinal cords of neuropathic rats and its treatment concentration-dependently induced β-endorphin expression in cultured primary microglia (but not in neurons or astrocytes), wit...
Source: Brain, Behavior, and Immunity - February 8, 2017 Category: Neurology Source Type: research

Cynandione A attenuates neuropathic pain through p38 β MAPK-mediated spinal microglial expression of β-endorphin.
This study aims to evaluate the antihypersensitivity activities of cynandione A in neuropathy and explored its mechanisms of action. Intrathecal injection of cynandione A dose-dependently attenuated spinal nerve ligation-induced mechanical allodynia and thermal hyperalgesia, with maximal possible effects of 57% and 59%, ED50s of 14.9 μg and 6.5 μg, respectively. Intrathecal injection of cynandione A significantly increased β-endorphin levels in spinal cords of neuropathic rats and its treatment concentration-dependently induced β-endorphin expression in cultured primary microglia (but not in neurons or astrocytes), wit...
Source: Brain, Behavior, and Immunity - February 7, 2017 Category: Neurology Authors: Huang Q, Mao XF, Wu HY, Liu H, Sun ML, Wang X, Wang YX Tags: Brain Behav Immun Source Type: research

Minocycline ameliorates hypoxia-induced blood–brain barrier damage by inhibition of HIF-1α through SIRT-3/PHD-2 degradation pathway
Conclusions: Minocycline inhibits HIF-1α-mediated cellular responses and protects BBB integrity through SIRT-3/PHD-2 pathway, proving to be a potential drug for the prevention and treatment of hypoxic brain injuries.
Source: Neuroscience - August 7, 2015 Category: Neuroscience Source Type: research

Extracellular caspase-6 drives murine inflammatory pain via microglial TNF-α secretion
Increasing evidence indicates that the pathogenesis of neuropathic pain is mediated through spinal cord microglia activation. The intracellular protease caspase-6 (CASP6) is known to regulate neuronal apoptosis and axonal degeneration; however, the contribution of microglia and CASP6 in modulating synaptic transmission and pain is unclear. Here, we found that CASP6 is expressed specifically in C-fiber axonal terminals in the superficial spinal cord dorsal horn. Animals exposed to intraplantar formalin or bradykinin injection exhibited CASP6 activation in the dorsal horn. Casp6-null mice had normal baseline pain, but impair...
Source: Journal of Clinical Investigation - February 17, 2014 Category: Biomedical Science Authors: Temugin Berta, Chul-Kyu Park, Zhen-Zhong Xu, Ruo-Gang Xie, Tong Liu, Ning Lü, Yen-Chin Liu, Ru-Rong Ji Source Type: research