姜黄素在调节TNF-α介导的大脑炎症反应中的作用
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摘要
炎症是人体对外界伤害性刺激的保护性反应,然而,过度炎症能够引起机体伤害性反应,导致慢性疾病。炎症在神经系统疾病的发展过程中起重要作用,细胞因子在很多神经退行性疾病中表达上调,最终引发脑内炎症反应。在脑内细胞因子中,肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)介导了许多疾病的炎症过程,在阿尔茨海默病、帕金森病、多发性硬化症、肌萎缩侧索硬化症等疾病的发展中起重要作用,其功能受转录因子核因子κB(nuclear factor-kappa B,NF-κB)活化的调节。最近有研究表明,姜黄素具有抗炎和抗氧化的特性,能有效抑制炎症反应,因此具有治疗神经炎症疾病的潜力,当前已被尝试用于治疗与大脑相关的各种慢性疾病。本文旨在阐明姜黄素在TNF-α和NF-κB介导的神经炎症反应中的作用,为今后治疗神经炎症相关疾病提供新的思路。
Inflammation is a protective response of the body system to various kinds of external and internal stimuli. However, it has been found that excessive inflammation can cause nociceptive reactions and lead to chronic diseases. Inflammation plays a major role in developing neurological diseases. The expression of cytokines is up-regulated in many neurodegenerative diseases, which eventually leads to inflammatory reactions in the brain. In the brain cytokines, tumor necrosis factor-α(TNF-α) is known to mediate inflammation in many diseases. It plays an important role in the development of Alzheimer's disease, Parkinson's disease, multiple sclerosis and amyotrophic lateral sclerosis. The functions of these cytokines are regulated by the activation of transcription factor nuclear factor-kappa B(NF-κb). Recent evidence suggested that curcumin had an immense therapeutic potential for neuroinflammatory diseases because of its anti-inflammatory and anti-oxidant properties. It has been tested for treating various chronic illnesses associated with the brain. This article reviewed the role of curcumin in the neuroinflammatory responses mediated by TNF-α and NF-κB, and provided a new thought for the treatment of neuroinflammatory related diseases in the future.
Inflammation is a protective response of the body system to various kinds of external and internal stimuli. However, it has been found that excessive inflammation can cause nociceptive reactions and lead to chronic diseases. Inflammation plays a major role in developing neurological diseases. The expression of cytokines is up-regulated in many neurodegenerative diseases, which eventually leads to inflammatory reactions in the brain. In the brain cytokines, tumor necrosis factor-α(TNF-α) is known to mediate inflammation in many diseases. It plays an important role in the development of Alzheimer's disease, Parkinson's disease, multiple sclerosis and amyotrophic lateral sclerosis. The functions of these cytokines are regulated by the activation of transcription factor nuclear factor-kappa B(NF-κb). Recent evidence suggested that curcumin had an immense therapeutic potential for neuroinflammatory diseases because of its anti-inflammatory and anti-oxidant properties. It has been tested for treating various chronic illnesses associated with the brain. This article reviewed the role of curcumin in the neuroinflammatory responses mediated by TNF-α and NF-κB, and provided a new thought for the treatment of neuroinflammatory related diseases in the future.
引文
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[7] Shang WQ, Li H, Liu LB, et al. RANKL/RANK interaction promotes the growth of cervical cancer cells by strengthening the dialogue between cervical cancer cells and regulation of IL-8 secretion[J]. Oncol Rep, 2015, 34(6):3007-3016.
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[11] Shamim D, Laskowski M. Inhibition of inflammation mediated through the tumor necrosis factorαbiochemical pathway can lead to favorable outcomes in alzheimer disease[J]. J Cent Nerv Syst Dis, 2017, 9(11):72-79.
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[13] Qin JL, Zhang XY, Wang ZQ, et al. Presenilin 2 deficiency facilitates Aβ-induced neuroinflammation and injury by upregulating P2X7 expression[J]. Sci China Life Sci, 2017, 60(2):189-201.
[14]Kempuraj D, Thangavel R, Natteru PA, et al. Neuroinflammation induces neurodegeneration[J]. J Neurol Neurosurg Spine, 2016, 1(1):1003-1023.
[15]Wang XL, Wang WZ, Li L, et al. Oxidative stress and mitochondrial dysfunction in Alzheimer's disease[J]. Biochimica et Biophysica Acta(BBA)-Molecular Basis of Disease,2014, 1842(8):1240-1247.
[16] Ye JL, Jiang ZX, Chen XH, et al. The role of autophagy in pro-inflammatory responses of microglia activation via mitochondrial reactive oxygen species in vitro[J]. J Neurochem,2017, 142(2):215-230.
[17] Guo LY, Xing YY, Pan R, et al. Curcumin protects microglia and primary rat cortical neurons against HIV-1 gp120-mediated inflammation and apoptosis[J]. PLoS One, 2013, 8(8):e70565.
[18] Mehta SL, Kumari S, Mendelev N, et al. Selenium preserves mitochondrial function, stimulates mitochondrial biogenesis,and reduces infarct volume after focal cerebral ischemia[J].BMC Neurosci, 2012, 13(8):73-79.
[19] Zhong WH, Qian KJ, Xiong JB, et al. Curcumin alleviates lipopolysaccharide induced sepsis and liver failure by suppression of oxidative stress-related inflammation via PI3K/AKT and NF-κB related signaling[J]. Biomed Pharmacother,2016, 83:302-313.
[20] Parada E, Buendia I, Navarro E, et al. Microglial HO-1 induction by curcumin provides antioxidant, antineuroinflammatory, and glioprotective effects[J]. Mol Nutr Food Res,2015, 59(9):1690-1700.
[21] Miao YP, Zhao S, Gao Y, et al. Curcumin pretreatment attenuates inflammation and mitochondrial dysfunction in experimental stroke:The possible role of Sirt1 signaling[J].Brain Res Bull, 2016, 5(121), 9-15.
[22] Xiao L, Ding M, Fernandez A, et al. Curcumin alleviates lumbar radiculopathy by reducing neuroinflammation, oxidative stress and nociceptive factors[J]. Eur Cell Mater, 2017,33:279-293.
[23] Aggarwal BB. Signalling pathways of the TNF superfamily:a double-edged sword[J]. Nat Rev Immunol, 2003, 3(9):745-756.
[24] Jagetia GC, Aggarwal BB.“Spicing up”of the immune system by curcumin[J]. J Clin Immunol, 2007, 27(1):19-35.
[25] Mrak RE, Griffin WST. Glia and their cytokines in progression of neurodegeneration[J]. Neurobiology of Aging, 2005,26(3):349-354.
[26] Lim GP, Chu T, Yang F, et al. The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse[J]. J Neurosci, 2001, 21(21):8370-8377.
[27]Billings LM, Oddo S, Green KN, et al. Intraneuronal Abeta causes the onset of early Alzheimer's disease-related cognitive deficits in transgenic mice[J]. Neuron, 2005, 45(5):675-688.
[28]Douglass BJ, Clouatre DL. Beyond yellow curry:assessing commercial curcumin absorption technologies[J]. J Am Coll Nutr, 2015, 34(4):347-358.
[29]Bisht S, Feldmann G, Soni S, et al. Polymeric nanoparticleencapsulated curcumin(“nanocurcumin”):a novel strategy for human cancer therapy[J]. J Nanobiotechnology, 2013, 10(5):1977-1987.
[30]Schiborr C, Kocher A, Behnam D, et al. The oral bioavailability of curcumin from micronized powder and liquid micelles is significantly increased in healthy humans and differs between sexes[J]. Mol Nutr Food Res, 2014, 58(3):516-527.
[31]Frank J, Schiborr C, Kocher A, et al. Transepithelial transport of curcumin in caco-2 cells is significantly enhanced by micellar solubilisation[J]. Plant Foods Hum Nutr, 2017, 72(1):48-53.
[2] Pickering M, Cumiskey D, O'Connor JJ. Actions of TNF-alpha on glutamatergic synaptic transmission in the central nervous system[J]. Exp Physiol, 2005, 90(5):663-670.
[3] Belarbi K, Jopson T, Tweedie D, et al. TNF-αprotein synthesis inhibitor restores neuronal function and reverses cognitive deficits induced by chronic neuroinflammation[J]. J Neuroinflammation, 2012, 1(25):9-23.
[4] Locksley RM, Killeen N, Lenardo MJ. The TNF and TNF receptor superfamilies:integrating mammalian biology[J]. Cell,2001, 104(4):487-501.
[5] Wilhelm A, Shepherd EL, Amatucci A, et al. Interaction of TWEAK with Fn14 leads to the progression of fibrotic liver disease by directly modulating hepatic stellate cell proliferation[J]. J Pathol, 2016, 239(1):109-121.
[6] Cassol E, Rossouw T, Malfeld S, et al. CD14(+)macrophages that accumulate in the colon of African AIDS patients express pro-inflammatory cytokines and are responsive to lipopolysaccharide[J]. BMC Infect Dis, 2015, 10(15):430-440.
[7] Shang WQ, Li H, Liu LB, et al. RANKL/RANK interaction promotes the growth of cervical cancer cells by strengthening the dialogue between cervical cancer cells and regulation of IL-8 secretion[J]. Oncol Rep, 2015, 34(6):3007-3016.
[8] Guerrini MM, Okamoto K, Komatsu N, et al. Inhibition of the TNF family cytokine RANKL prevents autoimmune inflammation in the central nervous system[J]. Immunity, 2015, 43(6):1174-1185.
[9] Lokensgard JR, Hu S, Sheng W, et al. Robust expression of TNF-alpha, IL-1beta, RANTES, and IP-10 by human microglial cells during nonproductive infection with herpes simplex virus[J]. J Neurovirol, 2001, 7(3):208-219.
[10] Olmos G, LladóJ. Tumor necrosis factor alpha:a link between neuroinflammation and excitotoxicity[J]. Mediators Inflamm, 2014, 8(6):13-26.
[11] Shamim D, Laskowski M. Inhibition of inflammation mediated through the tumor necrosis factorαbiochemical pathway can lead to favorable outcomes in alzheimer disease[J]. J Cent Nerv Syst Dis, 2017, 9(11):72-79.
[12] Yamamoto M, Kiyota T, Horiba M, et al. Interferon-gamma and tumor necrosis factor-alpha regulate amyloid-beta plaque deposition and beta-secretase expression in Swedish mutant APP transgenic mice[J]. Am J Pathol, 2007, 170(2):680-692.
[13] Qin JL, Zhang XY, Wang ZQ, et al. Presenilin 2 deficiency facilitates Aβ-induced neuroinflammation and injury by upregulating P2X7 expression[J]. Sci China Life Sci, 2017, 60(2):189-201.
[14]Kempuraj D, Thangavel R, Natteru PA, et al. Neuroinflammation induces neurodegeneration[J]. J Neurol Neurosurg Spine, 2016, 1(1):1003-1023.
[15]Wang XL, Wang WZ, Li L, et al. Oxidative stress and mitochondrial dysfunction in Alzheimer's disease[J]. Biochimica et Biophysica Acta(BBA)-Molecular Basis of Disease,2014, 1842(8):1240-1247.
[16] Ye JL, Jiang ZX, Chen XH, et al. The role of autophagy in pro-inflammatory responses of microglia activation via mitochondrial reactive oxygen species in vitro[J]. J Neurochem,2017, 142(2):215-230.
[17] Guo LY, Xing YY, Pan R, et al. Curcumin protects microglia and primary rat cortical neurons against HIV-1 gp120-mediated inflammation and apoptosis[J]. PLoS One, 2013, 8(8):e70565.
[18] Mehta SL, Kumari S, Mendelev N, et al. Selenium preserves mitochondrial function, stimulates mitochondrial biogenesis,and reduces infarct volume after focal cerebral ischemia[J].BMC Neurosci, 2012, 13(8):73-79.
[19] Zhong WH, Qian KJ, Xiong JB, et al. Curcumin alleviates lipopolysaccharide induced sepsis and liver failure by suppression of oxidative stress-related inflammation via PI3K/AKT and NF-κB related signaling[J]. Biomed Pharmacother,2016, 83:302-313.
[20] Parada E, Buendia I, Navarro E, et al. Microglial HO-1 induction by curcumin provides antioxidant, antineuroinflammatory, and glioprotective effects[J]. Mol Nutr Food Res,2015, 59(9):1690-1700.
[21] Miao YP, Zhao S, Gao Y, et al. Curcumin pretreatment attenuates inflammation and mitochondrial dysfunction in experimental stroke:The possible role of Sirt1 signaling[J].Brain Res Bull, 2016, 5(121), 9-15.
[22] Xiao L, Ding M, Fernandez A, et al. Curcumin alleviates lumbar radiculopathy by reducing neuroinflammation, oxidative stress and nociceptive factors[J]. Eur Cell Mater, 2017,33:279-293.
[23] Aggarwal BB. Signalling pathways of the TNF superfamily:a double-edged sword[J]. Nat Rev Immunol, 2003, 3(9):745-756.
[24] Jagetia GC, Aggarwal BB.“Spicing up”of the immune system by curcumin[J]. J Clin Immunol, 2007, 27(1):19-35.
[25] Mrak RE, Griffin WST. Glia and their cytokines in progression of neurodegeneration[J]. Neurobiology of Aging, 2005,26(3):349-354.
[26] Lim GP, Chu T, Yang F, et al. The curry spice curcumin reduces oxidative damage and amyloid pathology in an Alzheimer transgenic mouse[J]. J Neurosci, 2001, 21(21):8370-8377.
[27]Billings LM, Oddo S, Green KN, et al. Intraneuronal Abeta causes the onset of early Alzheimer's disease-related cognitive deficits in transgenic mice[J]. Neuron, 2005, 45(5):675-688.
[28]Douglass BJ, Clouatre DL. Beyond yellow curry:assessing commercial curcumin absorption technologies[J]. J Am Coll Nutr, 2015, 34(4):347-358.
[29]Bisht S, Feldmann G, Soni S, et al. Polymeric nanoparticleencapsulated curcumin(“nanocurcumin”):a novel strategy for human cancer therapy[J]. J Nanobiotechnology, 2013, 10(5):1977-1987.
[30]Schiborr C, Kocher A, Behnam D, et al. The oral bioavailability of curcumin from micronized powder and liquid micelles is significantly increased in healthy humans and differs between sexes[J]. Mol Nutr Food Res, 2014, 58(3):516-527.
[31]Frank J, Schiborr C, Kocher A, et al. Transepithelial transport of curcumin in caco-2 cells is significantly enhanced by micellar solubilisation[J]. Plant Foods Hum Nutr, 2017, 72(1):48-53.