The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
Naloxone Protects Rat Dopaminergic Neurons against Inflammatory Damage through Inhibition of Microglia Activation and Superoxide Generation
Abstract
Degeneration of dopaminergicrgic neurons in the substantia nigra of the brain is a hallmark of Parkinson's disease and inflammation and oxidative stress are closely associated with the pathogenesis of degenerative neurological disorders. Treatment of rat mesencephalic mixed neuron-glia cultures with lipopolysaccharide (LPS)-activated microglia, resident immune cells of the brain, to release proinflammatory and neurotoxic factors tumor necrosis factor-alpha, interleukin-1beta, nitric oxide, and superoxide and subsequently caused damage to midbrain neurons, including dopaminergic neurons. The LPS-induced degeneration of the midbrain neurons was significantly reduced by cotreatment with naloxone, an opioid receptor antagonist. This study focused on understanding the mechanism of action for the protective effect of naloxone on dopaminergic neurons because of relevance to Parkinson's disease. Both naloxone and its opioid receptor inactive stereoisomer (+)-naloxone protected the dopaminergic neurons with equal potency. Naloxone inhibited LPS-induced activation of microglia and release of proinflammatory factors, and inhibition of microglia generation of superoxide free radical best correlated with the neuroprotective effect of naloxone isomers. To further delineate the site of action, naloxone was found to partially inhibit the binding of [(3)H]LPS to cell membranes, whereas it failed to prevent damage to dopaminergic neurons by peroxynitrite, a product of nitric oxide and superoxide. These results suggest that naloxone at least in part interferes with the binding of LPS to cell membranes to inhibit microglia activation and protect dopaminergic neurons as well as other neurons in the midbrain cultures from inflammatory damage.
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“Alternative drugs with anti-inflammatory properties, including dexamethasone, minocycline, naloxone, are going to be or have already been tested in preclinical and clinical trials.560–562”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [562]
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“Cells were seeded in maintenance media and treated with the treatment media described previously (28).”
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Self-citationMicroglial cells and Parkinson’s disease
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“Support for this conclusion comes from the following sets of observations: 1) our previous studies have shown that inhibiting microglia production of superoxide was critical in eliciting a neuroprotective effect against microglia-mediated inflammatory damage, indicating that superoxide is a key element associated with…”
MethodResultSelf-citationMorales-Garcia, J. A., Susín, C., Alonso‐Gil, S., Pérez, D. I., Palomo, V., Pérez, C., Conde, S., Santos, Á., Gil, C., Martı́nez, A., et al. (2012) · ACS Chemical Neuroscience · doi:10.1021/cn300182g · Cited by 83
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“Evidence for a toxic role comes from numerous in vitro studies demonstrating that activated microglial cells release neurotoxic substances, including nitric oxide, superoxide anion, glutamate, and toxic cytokines (Chao et al., 1992, Boje et al., 1992; Piani et al., 1992; Viviani et al., 1998; Liu et al., 2000).”
BackgroundMicroglial NADPH oxidase is a novel target for femtomolar neuroprotection against oxidative stress
Qin, L., Block, M. L., Liu, Y., Bienstock, R. J., Pei, Z., Zhang, W., Wu, X., Wilson, B. C., Burka, T., & Hong, J. (2005) · The FASEB Journal · doi:10.1096/fj.04-2857com · Cited by 81
“Primary enriched-microglia cultures were prepared from the whole brains of 1-day-old Fisher 344 rat pups, using a described procedure (12).”
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“In our previous publications, the H-dopamine uptake is paralleled well with the number of dopaminergic neurons (TH-immunoreactive cells) (Liu et al., 2000; Yang et al., 2006)”
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“This culture composition is in consistence with that described by others (Liu et al. 2000; Gao et al. 2003; Qin et al. 2004).”
ResultDistinct modulation of microglial amyloid β phagocytosis and migration by neuropeptidesi
Fleisher‐Berkovich, S., Filipovich‐Rimon, T., Ben-Shmuel, S., Hülsmann, C., Kummer, M. P., & Heneka, M. T. (2010) · Journal of Neuroinflammation · doi:10.1186/1742-2094-7-61 · Cited by 82
“The medium containing detached microglia was collected and the isolated microglia were reseeded and allowed to settle for 24 h [24].”
MethodTGF-β1 Neuroprotection via Inhibition of Microglial Activation in a Rat Model of Parkinson’s Disease
Chen, X., Liu, Z., Cao, B., Qiu, Y., & Peng, Y.-P. (2017) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-017-9732-y · Cited by 77
Astrocytes and Microglia: Responses to Neuropathological Conditions
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“[(3)H]DA uptake assay was performed as described previously (12).”
MethodSelf-citationResveratrol Protects Cortical Neurons against Microglia‐mediated Neuroinflammation
Zhang, F., Wang, H., Wu, Q., Lu, Y., Nie, J., Xie, X., & Shi, J. (2012) · Phytotherapy Research · doi:10.1002/ptr.4734 · Cited by 77
“Cells were incubated with biotinylated secondary antibody followed by incubation with Vectastain ABC reagents, and then color was developed with 3, 3’-diaminobenzidine (Liu et al., 2000).”
MethodChen, S.-H., Oyarzabal, E. A., & Hong, J.-S. (2016) · Current Opinion in Pharmacology · doi:10.1016/j.coph.2015.10.001 · Cited by 76
Self-citationGordon, R., Anantharam, V., Kanthasamy, A. G., & Kanthasamy, A. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-82 · Cited by 77
“Uptake assays for tritiated dopamine on primary EVM cultures were performed according to previously published protocols [17,33,34].”
MethodCellular mechanisms of peroxynitrite-induced neuronal death
Ramdial, K., Franco, M. C., & Estévez, Á. G. (2017) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2017.05.008 · Cited by 77
Peripheral Immunity, Immunoaging and Neuroinflammation in Parkinson’s Disease
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“A substantial amount of literature indicates that LPS activates microglial cells in the brain and that microglia produce RONS, contributing to neurodegeneration [30,31].”
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“DA uptake assays were performed as previously described (Liu et al., 2000b).”
MethodSelf-citationZhang, P., Lokuta, K. M., Turner, D. E., & Liu, B. (2009) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2009.06477.x · Cited by 73
Self-citationChen, S., Wu, H., Ossola, B., Schendzielorz, N., Wilson, B., Chu, C., Chen, S., Wang, Q., Zhang, D., Li, Q., et al. (2011) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2011.01575.x · Cited by 72
“We next treated the neuron–glia cultures with LPS, which has been previously shown to cause dopaminergic neuron degeneration both in vitro and in vivo (Liu et al., 2000; Qin et al., 2007).”
MethodSelf-citationCD200–CD200R Regulation of Microglia Activation in the Pathogenesis of Parkinson’s Disease
Wang, X., Ye, M., Zhang, Y., & Chen, S. (2007) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-007-9075-1 · Cited by 71
“…Hong 2003b; Kim and Joh 2004; Purisai et al. 2007) have indicated that microglia may play important roles in the pathogenesis and progression of PD. Liu et al. (2000b) injected lipopolysaccharide into the substantia nigra of rats and found microglia activation and dopaminergic neurodegeneration.”
InfluentialVaccarino, A. L., & Kastin, A. J. (2001) · Peptides · doi:10.1016/s0196-9781(01)00566-6 · Cited by 72
Zhang, W., Qin, L., Wang, T., Wei, S., Gao, H., Liu, J., Wilson, B. C., Liu, B., Zhang, W., Kim, H., et al. (2004) · The FASEB Journal · doi:10.1096/fj.04-1586fje · Cited by 70
“The production of extracellular superoxide in microglia-enriched cultures was determined by measuring the superoxide dismutase (SOD)-inhibitable reduction of tetrazolium salt WST-1 (15, 41).”
BackgroundMethodSelf-citationOpioid receptor agonists reduce brain edema in stroke
Yang, L., Wang, H., Shah, K. K., Karamyan, V. T., & Abbruscato, T. J. (2011) · Brain Research · doi:10.1016/j.brainres.2011.01.083 · Cited by 69
Mitochondrial toxins and neurodegenerative diseases
Ayala, A. (2006) · Frontiers in bioscience · doi:10.2741/2119 · Cited by 68
“A single intranigral injection of LPS induces loss of nigral tyrosine hydroxylase (TH)-immunopositive neurons with concomitant decreases of DA and its metabolites in the nigrostriatal system (106).”
BackgroundZhang, P., Wong, T. A., Lokuta, K. M., Turner, D. E., Vujisic, K., & Liu, B. (2009) · Experimental Neurology · doi:10.1016/j.expneurol.2009.02.013 · Cited by 68
“The production of NO was determined by measuring the accumulated level of its stable metabolite, nitrite, in the supernatant with the Griess reagent as previously described (Liu et al., 2000a).”
BackgroundMethodResultInfluentialSelf-citationLi, F., Lu, X.-Z., Liang, X., Zhou, H.-F., Xue, B., Liu, X., Niu, D.-B., Han, J., & Wang, X. (2004) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2003.10.054 · Cited by 68
“Especially for microglia, NF-nB activation is ultimately important for strong induction of TNFa (Jana et al., 2002).”
BackgroundMethodInfluentialRingheim, G. E., & Conant, K. E. (2003) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2003.10.013 · Cited by 67
Ni, Y., Xu, G., Hu, W., Shi, L., Qin, Y., & Da, C. (2008) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.07-1173 · Cited by 67
“The neuroprotective effects of naloxone appear to be unrelated to the opioid system because this ineffective opioid receptor antagonist, ( )-naloxone, is also equally effective in the attenuation of LPS-induced nigral dopaminergic neurodegeneration.(23,24,56,57) Furthermore, the effects of naloxone isomers are not lim…”
BackgroundStromelysin-1 and gelatinase A are upregulated before TNF-α in LPS-stimulated neuroinflammation
Mun-Bryce, S., Lukes, A., Wallace, J. A., Lukes-Marx, M., & Rosenberg, G. A. (2002) · Brain Research · doi:10.1016/s0006-8993(02)02303-x · Cited by 67
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“Primary mixed glia cultures are composed of astrocytes (~80 % GFAP immunopositive cells) and microglia (~20 % OX-42 immunopositive cells) [ 8 ] and are commonly used to study the interaction between microglia and astrocytes.”
BackgroundInfluentialSelf-citationWang, Q., Zhou, H., Gao, H., Chen, S., Chu, C., Wilson, B. C., & Hong, J. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-32 · Cited by 65
“Our previous reports indicate that naloxone in these micromolar concentrations was not toxic to cell cultures and no obvious toxic signs were observed in animal studies with a 10 mg/kg/day dosage [3-6].”
BackgroundInfluentialSelf-citationLiu, B., Qin, L., Yang, S., Wilson, B. C., Liu, Y., & Hong, J. (2001) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/s0022-3565(24)29483-0 · Cited by 65
Self-citationZhang, R., Xu, S., Cai, Y., Zhou, M., Zuo, X., & Chan, P. (2009) · Evidence-based Complementary and Alternative Medicine · doi:10.1093/ecam/nep075 · Cited by 64
“RNA was primed with random 9-mers and converted into cDNA by reverse transcription (RT) using AMV reverse transcriptase by following the manufacturer’s recommended protocol [17, 18].”
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“[3H]DA Uptake Assay [3H]dopamine (DA) uptake assays were performed as described previously (Liu et al., 2000).”
MethodSelf-citationProtective effect of dextromethorphan against endotoxic shock in mice
Li, G., Liu, Y., Tzeng, N., Cui, G., Block, M. L., Wilson, B. C., Qin, L., Wang, T., Liu, B., Liu, J., et al. (2004) · Biochemical Pharmacology · doi:10.1016/j.bcp.2004.10.003 · Cited by 63
Self-citationProtective effect of isoflavones from Trifolium pratense on dopaminergic neurons
Chen, H.-Q., Wang, X., Jin, Z., Xu, X., Zhao, J.-W., & Xie, Z. (2008) · Neuroscience Research · doi:10.1016/j.neures.2008.07.001 · Cited by 63
“Many studies have demonstrated that the accumulation of these proinflammatory factors contributes to the degeneration of dopaminergic neurons (Gao et al., 2002a; Gayle et al., 2002; Kim et al., 2000; Liu et al., 2000a, 2002a).”
BackgroundThomas, M., Le, W. D., & Jankovic, J. (2003) · Clinical Neuropharmacology · doi:10.1097/00002826-200301000-00005 · Cited by 62
“dopaminergic cell degeneration in the SN (42).”
Liu, Y., Lo, Y., Li, Q., Crews, F. T., Wilson, B. C., Chen, H.-L., Wu, H.-M., Chen, S., Wei, K., Lu, R., et al. (2010) · Neuropharmacology · doi:10.1016/j.neuropharm.2010.10.002 · Cited by 61
“2.3.2 Microglia-enriched cultures—Primary enriched-microglia cultures were prepared from whole brains of 1-day-old Fisher 344 rat pups, using the previously described procedure (Liu et al., 2000a).”
InfluentialSelf-citationTreatment of Complex Regional Pain Syndrome (CRPS) Using Low Dose Naltrexone (LDN)
Chopra, P., & Cooper, M. S. (2013) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-013-9451-y · Cited by 62
“…production of pro-inflammatory cytokines and neurotoxic superoxides (Milligan and Watkins 2009; Leow-Dyke et al. 2012; Fellner et al. 2013), which act as mediators for neuropathic pain, as well as other neurological dysfunctions (Liu et al. 2000; Barbosa et al. 2012; Besedovsky and del Rey 2011).”
BackgroundJeohn, G., Cooper, C. L., Wilson, B. C., Chang, R. C., Jang, K., Kim, H.-C., Liu, B., & Hong, J. (2002) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2002.tb04078.x · Cited by 60
Self-citationNeuroinflammation and Parkinson's disease
Przedborski, S. (2007) · Handbook of clinical neurology · doi:10.1016/s0072-9752(07)83026-0 · Cited by 60
“…of bacterial endotoxin lipopolysaccharide (LPS) into the substantia nigra pars compacta of adult rats is associated with a local activation of microglia and an ensuing degeneration of dopaminergic neurons (Liu et al., 2000b), presumably mediated by IL-1b and caspase-11 (Arai et al., 2004).”
BackgroundChoi, M., Kim, E.-A., Hahn, H., Nam, K. D., Yang, S.-J., Choi, S. Y., Kim, T. U., Cho, S. W., & Huh, J. (2007) · Toxicology · doi:10.1016/j.tox.2007.07.010 · Cited by 58
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“Previous reports from our laboratory have shown that inhibition of microglial production of extracellular superoxide was a primary target in protecting DA neurons from inflammation-induced cell death [7].”
BackgroundSelf-citationZhu, Y., Chen, X., Liu, Z., Peng, Y.-P., & Qiu, Y. (2015) · International Journal of Molecular Sciences · doi:10.3390/ijms17010025 · Cited by 55
“Primary microglia were isolated from newborn Sprague-Dawley rats according to a previous study [49], with some modifications.”
MethodTetrandrine suppresses lipopolysaccharide-induced microglial activation by inhibiting NF-κB pathway
Yang, X., Wang, Y., Feng, D., Xiao, B., & Xu, L. (2008) · Acta Pharmacologica Sinica · doi:10.1111/j.1745-7254.2008.00734.x · Cited by 54
Addiction, Adolescence, and Innate Immune Gene Induction
Crews, F. T., & Vetreno, R. P. (2011) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2011.00019 · Cited by 52
“Indeed, studies have found that opiate antagonists blunt LPS inherent immune responses (Liu et al., 2000b) and protect dopaminergic neurons via inhibition of microglial activation and reduced NOX formation of reactive oxygen species (Liu et al., 2000a; Qin et al., 2005).”
Effects of chronic low dose rotenone treatment on human microglial cells
Shaikh, S. B., & Nicholson, L. F. B. (2009) · Molecular Neurodegeneration · doi:10.1186/1750-1326-4-55 · Cited by 54
“However Gao et al, [22,23] and others [43] have attributed rotenone induced neurotoxicity to the release of NADPH oxidase derived superoxide.”
Wang, J., Bi, M., Liu, H., Song, N., & Xie, J. (2015) · Scientific Reports · doi:10.1038/srep10729 · Cited by 52
Wang, J., Wu, W., Huang, H., Li, W., Chen, H.-Q., & Yin, Y. (2016) · Neurotoxicity Research · doi:10.1007/s12640-016-9648-y · Cited by 52
Neuroprotection of naloxone against ischemic injury in rats: role of mu receptor antagonism
Liao, S., Chen, W., Raung, S., & Chen, C. (2003) · Neuroscience Letters · doi:10.1016/s0304-3940(03)00540-8 · Cited by 52
Parkinson disease IgG and C5a-induced synergistic dopaminergic neurotoxicity: Role of microglia
Wang, X., Yan, Z.-Q., Lü, G., Stuart, S., & Chen, S. (2006) · Neurochemistry International · doi:10.1016/j.neuint.2006.07.014 · Cited by 52
Rotenone and paraquat do not directly activate microglia or induce inflammatory cytokine release
Klintworth, H. M., Garden, G. A., & Xia, Z. (2009) · Neuroscience Letters · doi:10.1016/j.neulet.2009.06.065 · Cited by 53
“We cultured cortices from 3–4 day old mice under conditions selective for glia proliferation followed by isolation of microglia to be used for microglia-enriched experiments [22,23].”
Wang, T., Liu, B., Qin, L., Wilson, B. C., & Hong, J. (2004) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2003.10.040 · Cited by 51
“In previous studies, we have found that ROS, generated by activated microglia, play a major role in lipopolysaccharide (LPS)-induced neurotoxicity (Liu et al., 2000; Gao et al., 2002).”
BackgroundSelf-citationChechneva, O. V., Mayrhofer, F., Daugherty, D. J., Pleasure, D., Hong, J., & Deng, W. (2011) · Neurobiology of Disease · doi:10.1016/j.nbd.2011.06.004 · Cited by 49
“…both dextra- and levorotary morphinans, was not associated with opioid receptor modulation, and was due to the inhibition of superoxide production by phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidase NOX2 (Li et al., 2005; Liu et al., 2000; Liu et al., 2003; Qin et al., 2005).”
BackgroundSelf-citationLiu, B., & Hong, J. (2003) · Humana Press eBooks · doi:10.1385/1-59259-358-5:387 · Cited by 50
Self-citationInteraction of Opioids with TLR4—Mechanisms and Ramifications
Gabr, M. M., Saeed, I., Miles, J. A., Ross, B. P., Shaw, P. N., Hollmann, M. W., & Parat, M. (2021) · Cancers · doi:10.3390/cancers13215274 · Cited by 49
“The inhibitory effects of naloxone isomers on microglial activation, and the inflammatory damage of dopaminergic neurons induced by LPS, have been reported [23].”
BackgroundQian, L., Hu, X., Zhang, D., Snyder, A., Wu, H. M., Li, Y., Wilson, B. C., Lu, R., Hong, J., & Flood, P. M. (2009) · Glia · doi:10.1002/glia.20873 · Cited by 50
“GLIA described previously (Liu et al., 2000a).”
MethodSelf-citationClozapine metabolites protect dopaminergic neurons through inhibition of microglial NADPH oxidase
Jiang, L., Wu, X., Wang, S., Chen, S., Zhou, H., Wilson, B. C., Jin, C., Lu, R., Xie, K., Wang, Q., et al. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0573-z · Cited by 48
“[(3)H]DA uptake assay [(3)H]DA uptake assays were performed as described previously [35].”
MethodSelf-citationGao, X., Hu, X., Li, Q., Yang, S., Zhang, W., Zhang, D., Wu, X., Fraser, A., Wilson, B. C., Flood, P. M., et al. (2008) · Environmental Health Perspectives · doi:10.1289/ehp.11031 · Cited by 49
“We prepared N/G cultures from the ventral mesencephalic tissues of embryonic day 13–14 rats or day 12–13 mice as described previously (Liu et al. 2000).”
MethodSelf-citationOpioids modulate post-ischemic progression in a rat model of stroke
Kao, T.-K., Ou, Y., Liao, S., Chen, W., Wang, C.-C., Chen, S., Chiang, A., & Chen, C. (2008) · Neurochemistry International · doi:10.1016/j.neuint.2008.01.007 · Cited by 49
Ruano, D., Revilla, E., Gavilán, M. P., Vizuete, M., Pintado, C., Vitórica, J., & Castaño, A. (2006) · Neuroscience · doi:10.1016/j.neuroscience.2006.02.073 · Cited by 50
Central and peripheral anti-hyperalgesic effects of diosmin in a neuropathic pain model in rats
Carballo‐Villalobos, A. I., González-Trujano, M. E., Pellicer, F., Alvarado‐Vásquez, N., & López‐Muñoz, F. J. (2017) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2017.10.077 · Cited by 48
Mao, H., Fang, X., Floyd, K. M., Polcz, J. E., Zhang, P., & Liu, B. (2007) · Brain Research · doi:10.1016/j.brainres.2007.10.020 · Cited by 49
Self-citationDutta, G., Barber, D. S., Zhang, P., Doperalski, N. J., & Liu, B. (2012) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2012.07826.x · Cited by 45
“Nitrite assay and cytokine measurement Levels of nitrite, a stable metabolite of NO were determined using the Griess reagent as previously described (Liu et al. 2000; Zhang et al. 2010).”
MethodSelf-citationMorphine promotes apoptosis via TLR2, and this is negatively regulated by β-arrestin 2
Li, Y., Sun, X., Zhang, Y., Huang, J., Hanley, G., Ferslew, K. E., Peng, Y., & Yin, D. (2008) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2008.12.001 · Cited by 47
Li, S., Bi, G., Han, S., & Huang, R. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2021.744942 · Cited by 45
Su, W.-P., Lo, Y.-C., Yan, J., Liao, I., Tsai, P.-J., Wang, H., Yeh, H.-H., Lin, C., Chen, H. H. W., Lai, W., et al. (2012) · Carcinogenesis · doi:10.1093/carcin/bgs253 · Cited by 45
“Pretreatments with other antioxidants, such as naloxone (a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (Nox) inhibitor) (34), catalase, N-acetylcysteine (NAC) and tiron (an O2 - inhibitor) did not suppress paclitaxel-induced Stat3 phosphorylation at conventional doses (Supplementary Figure 2A is availa…”
BackgroundZhang, F., Wang, Y., Liu, H., Lu, Y., Wu, Q., Liu, J., & Shi, J. (2012) · Evidence-based Complementary and Alternative Medicine · doi:10.1155/2012/937605 · Cited by 45
“At the time of treatment, cultures were composed of 10% microglia, 50% astrocytes, 40% neurons, and 1% TH-immunopositive neurons [16].”
MethodAnttila, J. E., Albert, K., Wires, E. S., Mätlik, K., Loram, L. C., Watkins, L. R., Rice, K. C., Wang, Y., Harvey, B. K., & Airavaara, M. (2018) · eNeuro · doi:10.1523/eneuro.0395-17.2018 · Cited by 44
“Also, both naloxone enantiomers reduce lipopolysaccharide (LPS)-induced microglial activation and protect neurons from LPS-induced neurodegeneration (Liu et al., 2000a, b, c).”
BackgroundAhn, S. K., Hong, S., Park, Y. M., Choi, J. Y., Lee, W. T., Park, K. A., & Lee, J. E. (2012) · Life Sciences · doi:10.1016/j.lfs.2012.10.010 · Cited by 44
“Because LPS is a potent microglial activator (Kim et al., 2000; Liu et al., 2000) and triggers iNOS in microglia (Boje and Arora, 1992; Kitamura et al.”
Gö6976 inhibits LPS-induced microglial TNFα release by suppressing p38 MAP kinase activation
Jeohn, G., Cooper, C. L., Jang, K., Liu, B., Lee, D.-S., Kim, H.-C., & Hong, J. (2002) · Neuroscience · doi:10.1016/s0306-4522(02)00356-1 · Cited by 44
Self-citationEndomorphin 1 effectively protects cadmium chloride-induced hepatic damage in mice
Gong, P., Chen, F. X., Ma, G. F., Feng, Y., Zhao, Q., & Wang, R. (2008) · Toxicology · doi:10.1016/j.tox.2008.07.051 · Cited by 41
Zhang, D., Hu, X., Wei, S., Liu, J., Gao, H., Li, Q., Wilson, B. C., Liu, G.-T., & Hong, J. (2008) · Journal of Neuroinflammation · doi:10.1186/1742-2094-5-21 · Cited by 40
“In this study, LPS-induced degeneration of dopaminergic (DA) neurons in mesencephalic neuronal-glial cultures was used as an in vitro model for studying the role of microglia in the therapeutic effect of FLZ [15-17].”
Self-citationThe Dichotomous Role of Inflammation in the CNS: A Mitochondrial Point of View
Vezzani, B., Carinci, M., Patergnani, S., Pasquin, M., Guarino, A., Aziz, N., Pinton, P., Simonato, M., & Giorgi, C. (2020) · Biomolecules · doi:10.3390/biom10101437 · Cited by 40
“For instance, the synthetic steroid dexamathasone prevents dopaminergic neurons degeneration in a mouse PD model [282], and the synthetic compound naloxone blocks microglia activation thus reducing the inflammatory damage [283].”
BackgroundVela, J. M., Yáñez, Á., González, B., & Castellano, B. (2002) · Journal of Neurotrauma · doi:10.1089/089771502320914723 · Cited by 38
“In turn, this response may exacerbate the degeneration process since microglia/macrophages are the main source of cytokines in the CNS (Giulian, 1993; Banati et al., 1993; Minghetti and Levi, 1998; Liu et al., 2000).”
Wang, J., Yang, Z.-T., Liu, C., Zhao, Y., & Chen, Y. (2012) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2012.1179 · Cited by 38
“Previous data derived from in vitro or chronic neurodegenerative disease have shown that activation of microglia contributes to neuroinflammation (2) and to exacerbation of neuronal injury (3).”
BackgroundMicroglial NADPH Oxidase Mediates Leucine Enkephalin Dopaminergic Neuroprotection
Qin, L., Liu, Y., Qian, X., HONG, J., & Block, M. L. (2005) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1344.009 · Cited by 43
Self-citation
Metadata
- Authors
- Liu, B., Du, L., & Hong, J.-S.
- Affiliations
- National Institutes of Health (US)
- National Institute of Environmental Health Sciences (US)
- Corresponding author
- Liu, Bin
- Venue
- The Journal of Pharmacology and Experimental Therapeutics
- Publisher
- Elsevier BV
- Published
- 2000-04
- Volume
- 293
- Issue
- 2
- Pages
- 607-617
- ISSN
- 0022-3565 (ISSN-L)
- OpenAlex
- W1891696008
- Cited by
- 347
- References
- 43
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 4 · 2023: 11 · 2022: 11 · 2021: 10 · 2020: 5 · 2019: 2 · 2018: 7 · 2017: 12 · 2016: 10 · 2015: 16 · 2014: 11 · 2013: 13 · 2012: 26
- FWCI
- 8.42
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Pharmacology and Experimental Therapeutics (publishedVersion)
- PubMed (publishedVersion)
- PubMed
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- naloxone, dopaminergic neurons, Parkinson's disease, microglial activation, lipopolysaccharide, neuroinflammation, oxidative stress, superoxide, neuroprotection, substantia nigra, opioid antagonists, peroxynitrite, nitric oxide, inflammatory cytokines
- MeSH terms
- Animals, Cells, Cultured, Dopamine, Immunohistochemistry, Inflammation, Interleukin-1, Lipopolysaccharides, Mesencephalon, Naloxone, Narcotic Antagonists, Neurons, Nitrates, Nitrites, Rats, Inbred F344, Stereoisomerism, Substantia Nigra, Superoxides, Tumor Necrosis Factor-alpha, Tyrosine 3-Monooxygenase, Oxidants, Microglia, Mitogen-Activated Protein Kinases, Mitogen-Activated Protein Kinase 3, Rats
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