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当代阿耳茨海默病研究

Editor-in-Chief

ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

Research Article

七氟醚而不是异丙酚在人神经母细胞瘤SH-SY5Y细胞中提供细胞存活的双重作用

卷 17, 期 14, 2020

页: [1311 - 1319] 页: 9

弟呕挨: 10.2174/1567205018666210218162856

价格: $65

摘要

背景:我们假设最常用的静脉(丙泊酚)和吸入(七氟醚)全身麻醉药会影响细胞存活浓度和持续时间,并依赖于其影响细胞内Ca + 2稳态的不同潜能而具有不同的潜能。 方法:用野生型或M146L突变型人早老素1稳定转染的人神经母细胞瘤SH-SY5Y细胞进行培养,并使其与异丙酚或七氟醚等效。测量细胞活力,细胞溶质和线粒体钙。 结果:在临床相关浓度和持续时间下,七氟醚而非丙泊酚可促进细胞存活。 1%七氟醚的长时间暴露(24小时)导致两种类型的细胞均受到明显的细胞损害。在细胞外钙存在的情况下,七氟醚和异丙酚对细胞质Ca + 2或线粒体Ca + 2升高的细胞反应率均显着较高。由于Ca + 2的流入,七氟醚而不是等价的1 MAC丙泊酚导致阿尔茨海默氏病突变细胞的峰和总Ca + 2的增加明显大于野生型细胞,但线粒体Ca + 2的总浓度增加更多在野生型中比突变细胞。在不存在细胞外Ca + 2流入的情况下,七氟醚而非丙泊酚引起突变细胞中线粒体Ca + 2总体浓度的升高比对照细胞更为明显。 结论:钙的大量流入介导了全身麻醉药介导的细胞质或线粒体Ca + 2的升高,尤其是异丙酚。七氟醚比丙泊酚具有更高的促进或抑制细胞存活的能力,这可能与其影响细胞溶质或线粒体Ca + 2浓度的能力有关。

关键词: 麻醉药,阿尔茨海默氏病,钙,神经退行性疾病,细胞凋亡,细胞死亡。

[1]
Twaroski DM, Yan Y, Zaja I, Clark E, Bosnjak ZJ, Bai X. Altered mitochondrial dynamics contributes to propofol-induced cell death in human stem cell-derived neurons. Anesthesiology 2015; 123(5): 1067-83.
[http://dx.doi.org/10.1097/ALN.0000000000000857] [PMID: 26352374]
[2]
Ren G, Zhou Y, Liang G, et al. General anesthetics regulate autophagy via modulating the inositol 1,4,5-trisphosphate receptor: Implications for dual effects of cytoprotection and cytotoxicity. Sci Rep 2017; 7(1): 12378.
[http://dx.doi.org/10.1038/s41598-017-11607-0] [PMID: 28959036]
[3]
Sohn H-M, Kim HY, Park S, Han S-H, Kim J-H. Isoflurane decreases proliferation and differentiation, but none of the effects persist in human embryonic stem cell-derived neural progenitor cells. J Anesth 2017; 31(1): 36-43.
[http://dx.doi.org/10.1007/s00540-016-2277-z] [PMID: 27817157]
[4]
Liang G, Ward C, Peng J, Zhao Y, Huang B, Wei H. Isoflurane causes greater neurodegeneration than an equivalent exposure of sevoflurane in the developing brain of neonatal mice. Anesthesiology 2010; 112(6): 1325-34.
[http://dx.doi.org/10.1097/ALN.0b013e3181d94da5] [PMID: 20460994]
[5]
Huang B-Y, Huang H-B, Zhang Z-J, et al. Cell cycle activation contributes to isoflurane-induced neurotoxicity in the developing brain and the protective effect of CR8. CNS Neurosci Ther 2019; 25(5): 612-20.
[http://dx.doi.org/10.1111/cns.13090] [PMID: 30676695]
[6]
Liu F, Rainosek SW, Frisch-Daiello JL, et al. Potential adverse effects of prolonged sevoflurane exposure on developing monkey brain: From abnormal lipid metabolism to neuronal damage. Toxicol Sci 2015; 147(2): 562-72.
[http://dx.doi.org/10.1093/toxsci/kfv150] [PMID: 26206149]
[7]
Tao KM, Yang LQ, Liu YT, et al. Volatile anesthetics might be more beneficial than propofol for postoperative liver function in cirrhotic patients receiving hepatectomy. Med Hypotheses 2010; 75(6): 555-7.
[http://dx.doi.org/10.1016/j.mehy.2010.07.028] [PMID: 20709457]
[8]
Yang M, Wang Y, Liang G, Xu Z, Chu CT, Wei H. Alzheimer’s Disease Presenilin-1 Mutation Sensitizes Neurons to Impaired Autophagy Flux and Propofol Neurotoxicity: Role of Calcium Dysregulation. J Alzheimers Dis 2019; 67(1): 137-47.
[http://dx.doi.org/10.3233/JAD-180858] [PMID: 30636740]
[9]
Bianchi SL, Tran T, Liu C, et al. Brain and behavior changes in 12-month-old Tg2576 and nontransgenic mice exposed to anesthetics. Neurobiol Aging 2008; 29(7): 1002-10.
[http://dx.doi.org/10.1016/j.neurobiolaging.2007.02.009] [PMID: 17346857]
[10]
Perucho J, Rubio I, Casarejos MJ, et al. Anesthesia with isoflurane increases amyloid pathology in mice models of Alzheimer’s disease. J Alzheimers Dis 2010; 19(4): 1245-57.
[http://dx.doi.org/10.3233/JAD-2010-1318] [PMID: 20308791]
[11]
Yang H, Liang G, Hawkins BJ, Madesh M, Pierwola A, Wei H. Inhalational anesthetics induce cell damage by disruption of intracellular calcium homeostasis with different potencies. Anesthesiology 2008; 109(2): 243-50.
[http://dx.doi.org/10.1097/ALN.0b013e31817f5c47] [PMID: 18648233]
[12]
Wei H, Liang G, Yang H, et al. The common inhalational anesthetic isoflurane induces apoptosis via activation of inositol 1,4,5-trisphosphate receptors. Anesthesiology 2008; 108(2): 251-60.
[http://dx.doi.org/10.1097/01.anes.0000299435.59242.0e] [PMID: 18212570]
[13]
Joseph JD, Peng Y, Mak DO, et al. General anesthetic isoflurane modulates inositol 1,4,5-trisphosphate receptor calcium channel opening. Anesthesiology 2014; 121(3): 528-37.
[http://dx.doi.org/10.1097/ALN.0000000000000316] [PMID: 24878495]
[14]
Wang H, Dong Y, Zhang J, et al. Isoflurane induces endoplasmic reticulum stress and caspase activation through ryanodine receptors. Br J Anaesth 2014; 113(4): 695-707.
[http://dx.doi.org/10.1093/bja/aeu053] [PMID: 24699520]
[15]
Kelliher M, Fastbom J, Cowburn RF, et al. Alterations in the ryanodine receptor calcium release channel correlate with Alzheimer’s disease neurofibrillary and beta-amyloid pathologies. Neuroscience 1999; 92(2): 499-513.
[http://dx.doi.org/10.1016/S0306-4522(99)00042-1] [PMID: 10408600]
[16]
Cheung KH, Shineman D, Müller M, et al. Mechanism of Ca2+ disruption in Alzheimer’s disease by presenilin regulation of InsP3 receptor channel gating. Neuron 2008; 58(6): 871-83.
[http://dx.doi.org/10.1016/j.neuron.2008.04.015] [PMID: 18579078]
[17]
Hitomi J, Katayama T, Taniguchi M, Honda A, Imaizumi K, Tohyama M. Apoptosis induced by endoplasmic reticulum stress depends on activation of caspase-3 via caspase-12. Neurosci Lett 2004; 357(2): 127-30.
[http://dx.doi.org/10.1016/j.neulet.2003.12.080] [PMID: 15036591]
[18]
Zhang Y, Zhen Y, Dong Y, et al. Anesthetic propofol attenuates the isoflurane-induced caspase-3 activation and Aβ oligomerization. PLoS One 2011; 6(11)e27019
[http://dx.doi.org/10.1371/journal.pone.0027019] [PMID: 22069482]
[19]
Berridge MJ. Calcium signalling and cell proliferation. BioEssays 1995; 17(6): 491-500.
[http://dx.doi.org/10.1002/bies.950170605] [PMID: 7575490]
[20]
Waldron RT, Short AD, Meadows JJ, Ghosh TK, Gill DL. Endoplasmic reticulum calcium pump expression and control of cell growth. J Biol Chem 1994; 269(16): 11927-33.
[http://dx.doi.org/10.1016/S0021-9258(17)32661-3] [PMID: 8163492]
[21]
Yang M, Wei H. Anesthetic neurotoxicity: Apoptosis and autophagic cell death mediated by calcium dysregulation. Neurotoxicol Teratol 2017; 60: 59-62.
[http://dx.doi.org/10.1016/j.ntt.2016.11.004] [PMID: 27856359]
[22]
Ureshino RP, Rocha KK, Lopes GS, Bincoletto C, Smaili SS. Calcium signaling alterations, oxidative stress, and autophagy in aging. Antioxid Redox Signal 2014; 21(1): 123-37.
[http://dx.doi.org/10.1089/ars.2013.5777] [PMID: 24512092]
[23]
Klein GL, Castro SM, Garofalo RP. The calcium-sensing receptor as a mediator of inflammation. Semin Cell Dev Biol 2016; 49: 52-6.
[http://dx.doi.org/10.1016/j.semcdb.2015.08.006] [PMID: 26303192]
[24]
Müller M, Cárdenas C, Mei L, Cheung KH, Foskett JK. Constitutive cAMP response element binding protein (CREB) activation by Alzheimer’s disease presenilin-driven inositol trisphosphate receptor (InsP3R) Ca2+ signaling. Proc Natl Acad Sci USA 2011; 108(32): 13293-8.
[http://dx.doi.org/10.1073/pnas.1109297108] [PMID: 21784978]
[25]
Filadi R, Greotti E, Turacchio G, Luini A, Pozzan T, Pizzo P. Mitofusin 2 ablation increases endoplasmic reticulum-mitochondria coupling. Proc Natl Acad Sci USA 2015; 112(17): E2174-81.
[http://dx.doi.org/10.1073/pnas.1504880112] [PMID: 25870285]
[26]
Bonora M, Giorgi C, Bononi A, et al. Subcellular calcium measurements in mammalian cells using jellyfish photoprotein aequorin-based probes. Nat Protoc 2013; 8(11): 2105-18.
[http://dx.doi.org/10.1038/nprot.2013.127] [PMID: 24113784]
[27]
Bellanti F, Mirabella L, Mitarotonda D, et al. Propofol but not sevoflurane prevents mitochondrial dysfunction and oxidative stress by limiting HIF-1α activation in hepatic ischemia/reperfusion injury. Free Radic Biol Med 2016; 96: 323-33.
[http://dx.doi.org/10.1016/j.freeradbiomed.2016.05.002] [PMID: 27154980]
[28]
Humeau J, Bravo-San Pedro JM, Vitale I, et al. Calcium signaling and cell cycle: Progression or death. Cell Calcium 2018; 70: 3-15.
[http://dx.doi.org/10.1016/j.ceca.2017.07.006] [PMID: 28801101]
[29]
Andropoulos DB, Greene MF. Anesthesia and developing brains - implications of the FDA warning. N Engl J Med 2017; 376(10): 905-7.
[http://dx.doi.org/10.1056/NEJMp1700196] [PMID: 28177852]
[30]
Grover LA, Mitchell RB, Szmuk P. Anesthesia Exposure and neurotoxicity in children-understanding the FDA warning and implications for the otolaryngologist. JAMA Otolaryngol Head Neck Surg 2017; 143(11): 1071-2.
[http://dx.doi.org/10.1001/jamaoto.2017.1570] [PMID: 28910434]
[31]
Luo T, Wu J, Kabadi SV, et al. Propofol limits microglial activation after experimental brain trauma through inhibition of nicotinamide adenine dinucleotide phosphate oxidase. Anesthesiology 2013; 119(6): 1370-88.
[http://dx.doi.org/10.1097/ALN.0000000000000020] [PMID: 24121215]
[32]
Davidson AJ, Disma N, de Graaff JC, et al. Neurodevelopmental outcome at 2 years of age after general anaesthesia and awake-regional anaesthesia in infancy (GAS): An international multicentre, randomised controlled trial. Lancet 2016; 387(10015): 239-50.
[http://dx.doi.org/10.1016/S0140-6736(15)00608-X] [PMID: 26507180]
[33]
Sun LS, Li G, Miller TL, et al. Association between a single general anesthesia exposure before age 36 months and neurocognitive outcomes in later childhood. JAMA 2016; 315(21): 2312-20.
[http://dx.doi.org/10.1001/jama.2016.6967] [PMID: 27272582]
[34]
Xu Z, Dong Y, Wu X, et al. The potential dual effects of anesthetic isoflurane on Aβ-induced apoptosis. Curr Alzheimer Res 2011; 8(7): 741-52.
[http://dx.doi.org/10.2174/156720511797633223] [PMID: 21244349]
[35]
Swyers T, Redford D, Larson DF. Volatile anesthetic-induced preconditioning. Perfusion 2014; 29(1): 10-5.
[http://dx.doi.org/10.1177/0267659113503975] [PMID: 24002781]
[36]
Kato R, Foëx P. Myocardial protection by anesthetic agents against ischemia-reperfusion injury: an update for anesthesiologists. Can J Anaesth 2002; 49(8): 777-91.
[http://dx.doi.org/10.1007/BF03017409] [PMID: 12374705]
[37]
Wilder RT, Flick RP, Sprung J, et al. Early exposure to anesthesia and learning disabilities in a population-based birth cohort. Anesthesiology 2009; 110(4): 796-804.
[http://dx.doi.org/10.1097/01.anes.0000344728.34332.5d] [PMID: 19293700]

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