本文選題：神經(jīng)痛 + 氫　； 參考：《天津醫(yī)科大學(xué)》2017年博士論文

【摘要】：神經(jīng)病理性疼痛是由于軀體感覺(jué)神經(jīng)系統(tǒng)的損傷或疾病引起的一種長(zhǎng)期慢性疼痛。其形成的機(jī)制復(fù)雜,是當(dāng)今醫(yī)學(xué)界較難治療的一類疾病,常常遷延不愈,給患者造成極大痛苦,生活質(zhì)量極其低下。大量研究表明,細(xì)胞自噬功能障礙參與神經(jīng)病理性疼痛形成和發(fā)展,適當(dāng)?shù)恼T導(dǎo)細(xì)胞自噬功能成為神經(jīng)病理性疼痛治療突破口。近年眾多研究表明,低濃度氫分子(4%)和富氫液具有選擇性抗氧化、抗炎、抗凋亡作用,可應(yīng)用于多種疾病的研究和治療。因此,越來(lái)越多的學(xué)者認(rèn)為氫氣與富氫液是一種新型的醫(yī)學(xué)氣體分子。一些研究已發(fā)現(xiàn)腹腔注射富氫液可改善作用神經(jīng)病理性疼痛大鼠行為學(xué),對(duì)神經(jīng)病理性疼痛有治療作用,具體的機(jī)制仍在探討中。缺氧誘導(dǎo)因子-1(HIF-1)是缺氧條件下調(diào)節(jié)細(xì)胞自噬的關(guān)鍵因子,也是細(xì)胞適應(yīng)低氧環(huán)境的關(guān)鍵調(diào)節(jié)因子,研究證實(shí)其在神經(jīng)病理性疼痛的模型初級(jí)傳導(dǎo)通路中表達(dá)增多。本課題通過(guò)建立神經(jīng)病理性疼痛大鼠模型腹腔注射富氫液和帶狀皰疹神經(jīng)痛患者霧化吸入氫氣,探討氫氣對(duì)神經(jīng)病理性疼痛變保護(hù)作用的可能機(jī)制,為臨床治療奠定基礎(chǔ)。實(shí)驗(yàn)一、富氫液激活脊髓神經(jīng)細(xì)胞自噬在神經(jīng)病理性疼痛中作用目的:細(xì)胞自噬功能障礙是神經(jīng)病理性疼痛形成機(jī)制之一,通過(guò)誘導(dǎo)細(xì)胞自噬反應(yīng),成為目前治療神經(jīng)病理性疼痛的新靶點(diǎn)。富氫液對(duì)神經(jīng)病理性疼痛有一定的治療作用,具體的機(jī)制尚不明確。本實(shí)驗(yàn)擬利用建立神經(jīng)病理性疼痛大鼠模型(CCI),探討富氫液對(duì)神經(jīng)病理性疼痛大鼠脊髓細(xì)胞自噬的影響。方法:鞘內(nèi)置管成功的雄性SD大鼠60只,采用隨機(jī)數(shù)字表法共分為5組(n=12):假手術(shù)組(S組),神經(jīng)病理性疼痛模型組(C組),神經(jīng)病理性疼痛模型組+富氫液組(C+H組),神經(jīng)病理性疼痛模型組+3-甲基腺嘌呤組(C+M組),神經(jīng)病理性疼痛模型+3-甲基腺嘌呤+富氫液組(C+H+M組),神經(jīng)病理性疼痛模型采用慢性坐骨神經(jīng)結(jié)扎模型CCI。C+H組和C+H+M組于術(shù)后1h開(kāi)始腹腔注射富氫液(0.6 mmol/L)5ml/kg Bid,C+M組和C+H+M組術(shù)后1h開(kāi)始鞘內(nèi)注射自噬抑制劑3-甲基腺嘌呤10μl/kg Bid,其他組腹腔/鞘內(nèi)給予等量生理鹽水Bid。分別于術(shù)前1天(-1d),術(shù)后1天(1d),3天(3d),7天(7d),10天(10d),14天(14d)測(cè)大鼠機(jī)械刺激縮足閾值和冷、熱刺激縮足潛伏期,術(shù)后第14天測(cè)定痛閾后心臟灌注取脊髓L4-6節(jié)段,采用Western blot和Real-time PCR法測(cè)定脊髓的自噬相關(guān)基因和蛋白LC3Ⅱ,Beclin-1,P62的表達(dá);采用電鏡觀察各組大鼠脊髓背角自噬小體的形態(tài)和數(shù)量;應(yīng)用酶聯(lián)免疫法測(cè)定各組大鼠血清炎癥因子(IL-6,TNF-α)表達(dá),脊髓超氧化物歧化酶(SOD)和丙二醛(MDA)。結(jié)果:與S組比較,C組3d后MWT降低,TWL縮短,冷痛閾降低,大鼠脊髓組織Beclin-1、LC3-II基因及蛋白表達(dá)上調(diào),p62表達(dá)下調(diào),自噬小體數(shù)量增多,SOD活力降低,MDA、IL-6和TNF-α表達(dá)水平上調(diào)(P0.05);與C組比較,富氫液注射逆轉(zhuǎn)了這些變化C+H組的MWT升高,TWL延長(zhǎng),冷痛閾升高,大鼠脊髓組織Beclin-1、LC3-II表達(dá)上調(diào),p62基因及蛋白下調(diào),自噬小體增多,SOD活力增高,MDA,IL-6和TNF-α表達(dá)水平水平下調(diào)(P0.05);與C組比較,應(yīng)用3-MA的C+M組3d后MWT降低,TWL縮短,冷痛閾降低,痛覺(jué)過(guò)敏行為加劇,Beclin-1、LC3-II表達(dá)下調(diào),p62基因及蛋白上調(diào),自噬小體減少,SOD活力下降,MDA,IL-6和TNF-α表達(dá)水平上調(diào)(P0.05)。結(jié)論:富氫液減輕大鼠神經(jīng)病理性痛的機(jī)制與誘導(dǎo)脊髓神經(jīng)細(xì)胞自噬,降低氧化應(yīng)激,抑制炎癥反應(yīng)有關(guān)。實(shí)驗(yàn)二HIF-1α介導(dǎo)細(xì)胞自噬在富氫液治療神經(jīng)病理性疼痛中的作用目的:缺血缺氧的微環(huán)境是神經(jīng)病理性疼痛的重要形成因素,在缺氧條件下激活一系列適應(yīng)性反應(yīng),低氧誘導(dǎo)因子HIF-1α在其中發(fā)揮中心作用,通過(guò)轉(zhuǎn)錄各種幫助細(xì)胞因子適應(yīng)低氧環(huán)境,研究證實(shí)它及下游通路是低氧環(huán)境下調(diào)節(jié)自噬經(jīng)典通路。本實(shí)驗(yàn)擬利用HIF-1α激動(dòng)劑和抑制劑,探討HIF-1α在富氫液對(duì)神經(jīng)病理性疼痛大鼠脊髓細(xì)胞自噬的作用。方法:健康雄性SD大鼠96只,采用隨機(jī)數(shù)字表法分為8組(n=12):假手術(shù)組(S組),假手術(shù)+富氫液組(S+H組),神經(jīng)病理性疼痛模型組(C組),神經(jīng)病理性疼痛+富氫液組(C+H組),神經(jīng)病理性疼痛+2-甲氧基雌二醇組(C+2Me2組),CCI+H2組+2-甲氧基雌二醇(C+H+2Me2組),CCI+二羥基苯甲酸乙酯組(C+EDHB組),CCI+H2+二羥基苯甲酸乙酯組(C+H+EDHB組)。富氫液給藥方式同實(shí)驗(yàn)一。HIF-1α抑制劑2ME2溶解在0.5%的二甲基亞砜,于術(shù)后30分鐘(10mg/kg)腹腔注射Qd,HIF-1α拮抗劑EDHB在CCI術(shù)后30分鐘以100 mg/kg腹腔注射Qd。分別于術(shù)前1天(-1d),術(shù)后1天(1d),3天(3d),7天(7d),10天(10d),14天(14d)測(cè)大鼠行為學(xué)變化,術(shù)后第14天(T5)測(cè)定痛閾后心臟灌注取脊髓L4-6節(jié)段,采用Western blot和Real-time PCR法測(cè)定脊髓的自噬相關(guān)蛋白和基因Beclin-1,HIF-1α,BNIP3的表達(dá);應(yīng)用酶聯(lián)免疫法測(cè)定各組大鼠血清IL-6,TNF-α,脊髓SOD和MDA的表達(dá)水平。結(jié)果:在術(shù)后14天,與S組相比,Beclin-1,HIF-1α,BNIP3在C組,C+H組,C+H+2Me2組,C+EDHB組和C+H+EDHB組表達(dá)是顯著增多,MWT降低,TWL縮短,SOD活力降低,MDA、IL-6和TNF-α表達(dá)水平上調(diào)(P0.05);與C組相比,在C+H組、C+EDHB及C+H+EDHB組的Beclin-1,HIF-1α,和BNIP3在脊髓表達(dá)上調(diào),逆轉(zhuǎn)了患肢的痛覺(jué)過(guò)敏現(xiàn)象MWT升高,TWL延長(zhǎng),SOD活力降低,MDA、炎性因子IL-6和TNF-α表達(dá)水平下調(diào);在C+2Me2組Beclin-1,HIF-1α和BNIP3在脊髓表達(dá)下調(diào),患肢的痛覺(jué)過(guò)敏加劇,MWT降低,TWL縮短,SOD活力降低,MDA、IL-6和TNF-α表達(dá)水平上調(diào)(P0.05);與C+H組相比,C+H+EDHB組的Beclin-1,HIF-1α和BNIP3在脊髓表達(dá)上調(diào),MWT降低,TWL縮短,SOD活力升高,MDA、IL-6和TNF-α表達(dá)水平下調(diào);在C+H+2Me2組Beclin-1,HIF-1α和BNIP3在脊髓表達(dá)下調(diào),MWT降低,TWL縮短,SOD活力降低,MDA、IL-6和TNF-α含量上調(diào)(P0.05)。結(jié)論:富氫液通過(guò)HIF-1α介導(dǎo)的細(xì)胞自噬對(duì)神經(jīng)病理性疼痛大鼠起到治療作用。實(shí)驗(yàn)三、氫氣霧化吸入對(duì)帶狀皰疹后神經(jīng)痛患者的隨機(jī)對(duì)照臨床研究目的:帶狀皰疹后神經(jīng)痛(PHN)為由水痘-帶狀皰疹病毒(varicella zoster virus,VZV)引起的帶狀皰疹的皮疹治愈后3月仍遺留的持續(xù)性疼痛。它屬于神經(jīng)病理性疼痛,PHN的治療可謂世界性難題,尋找安全有效的治療方法至關(guān)重要。本研究擬采用隨機(jī)對(duì)照研究方法,明確霧化吸入氫氣對(duì)PHN的治療安全性及有效性,探討氫氣對(duì)神經(jīng)病理性疼痛的治療機(jī)制。方法:2016年01月-2016年06月在天津醫(yī)科大學(xué)第二醫(yī)院連續(xù)就診的帶狀皰疹后遺神經(jīng)痛患者60例,男31例,女29例,年齡45~79歲。采用隨機(jī)數(shù)字法分為3組(n=20):對(duì)照組(S組),低頻率組(H1組),高頻率組(H2組)。S組為基礎(chǔ)藥物+100%氧氣以3L/min速度吸入30分鐘,Qd,H1組為基礎(chǔ)藥物+混合氣體(67%H2+33%O2)吸入30分鐘Qd,H2組基礎(chǔ)藥物+混合氣體(67%H2+33%O2)吸入30分鐘Bid,均連續(xù)治療7天。分別于治療前1天(0d),治療后1天(1d),3天(3d),5天(5d),7天(7d),1月(1M),3月(3M),6月(6M)進(jìn)行門診評(píng)估疼痛程度和靜脈采血。主要評(píng)價(jià)指標(biāo):視覺(jué)模擬評(píng)分(visual analogue scale,VAS)和次要評(píng)價(jià)指標(biāo):1)簡(jiǎn)化的Mc Gill疼痛問(wèn)卷評(píng)分;2)睡眠評(píng)分;3)鎮(zhèn)痛和抗癲癇藥物用量。治療過(guò)程每日晨起8點(diǎn)檢測(cè)生命體征。靜脈采實(shí)驗(yàn)室檢測(cè)血常規(guī)、肝腎功能評(píng)估其安全性。治療后7天采用酶聯(lián)免疫吸附法(ELISA)測(cè)定IL-6,TNF-α,LC3Ⅱ,Beclin-1。結(jié)果:三組患者生命體征平穩(wěn),血常規(guī),肝腎功能未見(jiàn)異常。與0d比較,S組各時(shí)間點(diǎn)差異無(wú)統(tǒng)計(jì)學(xué)意義(P0.05),H1組,H2組的VAS、SF-MPQ、SIS評(píng)分、曲馬多和加巴噴丁用量在治療后3d后開(kāi)始時(shí)明顯降低,差異有統(tǒng)計(jì)學(xué)意義(P0.05);與S組比較,H1組在5d后VAS、SF-MPQ、SIS評(píng)分、曲馬多和加巴噴丁用量明顯降低,H2組在3d后VAS、SF-MPQ、SIS評(píng)分、曲馬多和加巴噴丁用量明顯降低差異有統(tǒng)計(jì)學(xué)意義(P0.05);與H1組比較,H2組VAS、SF-MPQ、SIS評(píng)分、曲馬多和加巴噴丁用量在5d后明顯降低,差異有統(tǒng)計(jì)學(xué)意義(P0.05)。在治療后7d,與S組比較,H1和H2組SOD,LC3Ⅱ,Beclin-1水平升高,MDA,IL-6,TNF-α表達(dá)減少(P0.05),與H1組比較,H2組患者SOD、LC3Ⅱ、Beclin-1水平升高,MDA,IL-6,TNF-α表達(dá)減少(P0.05)。結(jié)論:吸入氫氣對(duì)帶狀皰疹神經(jīng)痛患者起到治療作用,可能與減少氧化應(yīng)激,降低炎性反應(yīng),激活細(xì)胞自噬有關(guān)。
[Abstract]:Neuropathic pain is a chronic and chronic pain caused by the injury or disease of the somatosensory nervous system. The mechanism of its formation is complex. It is a kind of disease which is difficult to treat in the medical field today. It often causes great pain and low quality of life for the patients. A large number of studies show that the cell autophagy dysfunction is involved. Neuropathic pain is formed and developed, and proper induction of autophagic function has become a breakthrough in the treatment of neuropathic pain. In recent years, a number of studies have shown that low concentration hydrogen molecules (4%) and hydrogen rich fluids have selective antioxidant, anti-inflammatory and anti apoptosis effects, which can be applied to the research and treatment of various diseases. Hydrogen and hydrogen rich liquid are a new kind of medical gas molecules. Some studies have found that intraperitoneal injection of hydrogen rich liquid can improve the behavior of neuropathic pain rats, and it has a therapeutic effect on neuropathic pain. The specific mechanism is still discussed. Hypoxia inducible factor -1 (HIF-1) is the key factor to regulate autophagy in the condition of hypoxia. It is also the key regulator of the cell adaptation to the hypoxic environment. The study confirms that it is more expressed in the primary pathway of neuropathic pain. This topic is to explore the neuropathic pain of the neuropathic pain in the neuropathic pain rat model by intraperitoneal injection of hydrogen rich fluid and herpes zoster neuralgia. The possible mechanism of protective action is the basis for clinical treatment. Experiment 1, hydrogen rich fluid activates the role of autophagy in neuropathic pain of spinal nerve cells: autophagic dysfunction is one of the mechanisms of neuropathic pain formation. By inducing autophagy reaction, it is a new target for the treatment of neuropathic pain. The hydrogen solution has a certain therapeutic effect on neuropathic pain. The specific mechanism is not clear. This experiment is to establish a neuropathic pain rat model (CCI) to explore the effect of hydrogen rich solution on the autophagy of spinal cord cells in neuropathic pain rats. Methods: 60 male SD rats with a successful sheath in the sheath were divided into a random digital table. 5 groups (n=12): sham operation group (group S), neuropathic pain model group (group C), neuropathic pain model group + rich hydrogen group (group C+H), neuropathic pain model group +3- methyl adenine group (C+M group), neuropathic pain model +3- methyladenopurinopterin + rich hydrogen group (C+H+M group), neuropathic pain model using chronic sciatic God After the ligation of the CCI.C+H group and the C+H+M group, the peritoneal injection of hydrogen rich liquid (0.6 mmol/L) 5ml/kg Bid was injected into the abdominal cavity after the operation, and the C+M group and the C+H+M group were injected with the autophagic inhibitor, 3- methyl adenine 3-, 3- methyl adenine l/kg Bid. The other groups were given equal amount of saline in the abdominal cavity / sheath for 1 days before the operation, 1 days after the operation, 3 days, 7 days, 10 days. 10d), 14 days (14d) measured the threshold of mechanical stimulation of the foot and cold, the incubation period of heat stimulation, and the L4-6 segment of the spinal cord after the fourteenth day after the operation. The autophagy related genes and LC3 II, Beclin-1, P62 expression of the spinal cord were measured by Western blot and Real-time PCR, and the autophagy of the spinal dorsal horn of the rats was observed by electron microscopy. The expression of serum inflammatory factors (IL-6, TNF- a), superoxide dismutase (SOD) and malondialdehyde (MDA) in spinal cord of rats were measured by enzyme linked immunosorbent assay. Results: compared with group S, MWT decreased, TWL shortened, cold pain threshold decreased, Beclin-1, LC3-II gene and protein expression of rat spinal cord was up, p62 expression was down, down regulation of p62 expression, and down regulation of p62 expression. The number of phagocytic bodies increased, the activity of SOD decreased, and the expression level of MDA, IL-6 and TNF- alpha was up (P0.05). Compared with the C group, the injection of hydrogen rich solution reversed these changes in the MWT of the C+H group, the TWL lengthening, the increase of the cold pain threshold, the Beclin-1 of the spinal cord and the LC3-II expression in the rat spinal cord, the downregulation of the p62 genes and proteins, the increase of autophagic bodies and the increase of vitality. Expression level decreased (P0.05); compared with group C, MWT decreased after 3D in group C+M of 3-MA, TWL shortened, cold pain threshold decreased, hyperalgesia increased, Beclin-1, LC3-II downregulation, p62 gene and protein up-regulated, autophagic corpuscle decreased, SOD vitality decreased. Conclusion: rich hydrogen solution alleviated neuropathy in rats. The mechanism of rational pain is associated with the induction of autophagy in the spinal cord, reducing oxidative stress and inhibiting the inflammatory response. Experiment two HIF-1 alpha mediates the role of autophagy in the treatment of neuropathic pain in the hydrogen rich solution. The microenvironment of ischemic anoxia is an important form of neuropathic pain and activates a series of adaptations under the condition of hypoxia. Hypoxic inducible factor HIF-1 alpha plays a central role in it. By transcription of various help cytokines to adapt to the hypoxic environment, the study confirms that the downstream pathway is a classical pathway to regulate autophagy in low oxygen environments. This experiment is to use HIF-1 alpha agonists and inhibitors to explore the spinal cord of HIF-1 alpha in the neuropathic pain rats with hydrogen rich fluid Methods: the function of autophagy. Methods: 96 healthy male SD rats were divided into 8 groups (n=12): sham operation group (group S), sham operation + hydrogen rich group (group S+H), neuropathic pain model group (group C), neuropathic pain + hydrogen rich group (C+H group), neuropathic pain +2- methoxy estradiol group (C+2Me2 group), CCI+H2 group +2- a Oxygen based estradiol (group C+H+2Me2), CCI+ two hydroxy benzoate group (group C+EDHB), CCI+H2+ two hydroxy benzoate group (C+H+EDHB group). The way of hydrogen rich solution was dissolved in 0.5% of two methyl sulfoxide with experimental one.HIF-1 alpha inhibitor 2ME2, Qd in 30 minutes after operation (10mg/kg), HIF-1 alpha antagonist EDHB in 30 minutes after CCI. Intraperitoneal injection of Qd. was performed 1 days (-1d), 1 days (1D), 3 days (3D), 7 days (7D), 10 days (10d), 14 days (14d) to measure the behavioral changes of rats, and the L4-6 segment of the spinal cord was perfused after fourteenth days (T5) for the determination of the pain threshold. The expression of autophagy related protein and gene of spinal cord was measured by Western blot and Real-time. The expression level of serum IL-6, TNF- alpha and spinal cord SOD and MDA were measured by ELISA. Results: at the 14 day after the operation, the expression of Beclin-1, HIF-1 a, BNIP3 in C, C+H, C+H+2Me2, C+EDHB and other groups were increased significantly. In group C+H, in group C+H, Beclin-1, HIF-1 a, and BNIP3 in the group of C+EDHB and C+H+EDHB were up-regulated in the spinal cord, reversing the hyperalgesia phenomenon of the affected limbs, MWT increased, TWL prolonged, SOD activity decreased, MDA, inflammatory factor IL-6 and TNF- alpha expression down regulated. Decreased TWL, decreased SOD activity, MDA, IL-6 and TNF- alpha expression level up up (P0.05). Compared with group C+H, Beclin-1, HIF-1 A and BNIP3 were up regulation of the spinal cord expression, MWT decreased, decreased activity and decreased expression level. Shorten the activity of SOD and increase the content of MDA, IL-6 and TNF- alpha (P0.05). Conclusion: hydrogen rich solution can play a therapeutic role in neuropathic pain rats through HIF-1 alpha mediated autophagy. Experiment three, a randomized controlled clinical study of hydrogen atomization inhalation for patients with post herpetic neuralgia: postherpetic neuralgia (PHN) from varicella to band The rash of herpes zoster caused by herpes zoster virus (varicella zoster virus, VZV) remains persistent pain in March. It belongs to neuropathic pain. The treatment of PHN is a worldwide problem. It is very important to find a safe and effective treatment method. This study is to use a randomized controlled study to clarify the atomization inhalation of hydrogen to PHN The therapeutic mechanism of hydrogen on neuropathic pain was discussed. Methods: 60 cases of herpes zoster sequela neuralgia in Second Hospital Affiliated to Tianjin Medical University in 01 months of 2016 -2016, 31 men, 29 women, age 45~79 years, were divided into 3 groups (n=20): the control group (group S), low frequency rate. Group (group H1), group.S of high frequency (group H2) group.S as base drug +100% oxygen inhaled at 3L/min rate for 30 minutes, Qd, H1 group as basic drug + gas mixture (67%H2+33%O2) inhaled Qd, H2 group basic drugs + mixture gas (67%H2+33%O2) inhalation 30 minutes Bid, 7 days, respectively, 1 days before treatment, 1 days after treatment, 3 days 3 days, 5 days ), 7 days (7D), January (1M), March (3M), June (6M) to evaluate the degree of pain and venous blood collection. Major evaluation indexes: visual analogue scale (visual analogue scale, VAS) and secondary evaluation index: 1) simplified Mc Gill pain questionnaire score; 2) sleep and sleep score; 3) dosage of analgesic and antiepileptic drugs. The treatment process was tested at 8 points of life on the morning of the morning. Test blood routine, liver and kidney function to assess the safety of the blood routine test. 7 days after treatment, IL-6, TNF- a, LC3 II, Beclin-1. results were measured by enzyme linked immunosorbent assay (ELISA). The results of the three groups were stable, blood routine, liver and kidney function was not abnormal. Compared with 0d, there was no statistical significance (P0.05), H1 group, H2 group VA, compared with 0d. S, SF-MPQ, SIS score, the dosage of tramadol and gabapentin decreased significantly after the treatment after 3D, and the difference was statistically significant (P0.05). Compared with the S group, the H1 group was significantly reduced in VAS, SF-MPQ, SIS score after 5D, and the dosage of tramadol and gabapentin significantly decreased after the H2 group, and the dosage of tramadol and gabapentin significantly decreased the difference. Compared with group H1, H2 group VAS, SF-MPQ, SIS score, the dosage of tramadol and Gaba Martin decreased significantly after 5D, and the difference was statistically significant (P0.05). Flat MDA, IL-6, TNF- increased and decreased expression of alpha (P0.05). Conclusion: hydrogen inhalation on patients with herpes zoster neuralgia plays a role in the treatment, and may reduce oxidative stress, reduce inflammatory reaction, activation of autophagy.
【學(xué)位授予單位】：天津醫(yī)科大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2017
【分類號(hào)】：R402

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