本文選題：黃芪甲甙 + 麻醉�。� 參考：《南京醫(yī)科大學(xué)》2016年博士論文

【摘要】：第一部分:黃芪甲甙對異氟醚麻醉后新生大鼠神經(jīng)元凋亡的保護(hù)作用麻醉藥在神經(jīng)元生長的突觸發(fā)生階段對大腦有損害作用,是由于麻醉藥是通過NMDA(N-甲基-D-天冬氨酸)受體和GABA(γ-氨基丁酸)受體產(chǎn)生麻醉作用的。這種神經(jīng)毒性的易損期是在突觸的發(fā)生階段,也就是大腦快速生長階段。這種損害會影響整個神經(jīng)網(wǎng)絡(luò)的生長,并且這種損害會影響到以后的行為和認(rèn)知能力。這些研究結(jié)果使人們對全身麻醉藥的神經(jīng)毒性作用更加關(guān)注,特別是對小兒來說,他們的大腦正處于麻醉藥的神經(jīng)毒性的易損期。神經(jīng)毒性主要是因?yàn)樯窠?jīng)元的凋亡。關(guān)于麻醉引起的神經(jīng)元的凋亡機(jī)制已經(jīng)被廣泛研究。一方面促凋亡蛋白的活化如Bax等會導(dǎo)致線粒體膜的損傷,caspases的活化會引起細(xì)胞的凋亡。另一方面,活性氧族(ROS)和活性氮族(RNS)等自由基的產(chǎn)生會導(dǎo)致脂質(zhì)過氧化反應(yīng),這種反應(yīng)會導(dǎo)致大腦的損害。這種自由基的損害也會引起炎癥反應(yīng),更進(jìn)一步放大了凋亡作用。相反,如超氧化物歧化酶這種抗氧化劑(SOD)能清除過量的自由基并且能減輕他們的毒性作用。黃芪甲甙是從傳統(tǒng)中藥黃芪中提純而來的一種皂素。它在各種類型的細(xì)胞核組織中都顯示出抗氧化應(yīng)激和抗凋亡的作用。例如,它能通過抑制絲裂原活化蛋白激酶(MAPK)的活性來抑制腎組織的纖維化,它能減輕單側(cè)輸尿管梗阻和轉(zhuǎn)化生長因子-β(TGF-β)引起的腎小管細(xì)胞的凋亡。另外,它能夠通過抑制ROS的產(chǎn)生和抑制Bax的促凋亡途徑對1-甲基-4-苯基-吡啶離子引起的神經(jīng)毒性產(chǎn)生保護(hù)作用。黃芪甲甙還能通過抑制線粒體通透性轉(zhuǎn)換孔的開放來減輕1-甲基-4-苯基吡啶離子引起的神經(jīng)毒性。然而,它在麻醉藥物引起的神經(jīng)元的凋亡和神經(jīng)毒性中的作用還沒有被研究。為了明確黃芪甲甙是否對麻醉引起的發(fā)育中的大腦神經(jīng)元凋亡有保護(hù)作用,我們研究了黃芪甲甙預(yù)處理對異氟醚引起的新生大鼠海馬組織神經(jīng)元凋亡的影響。測量海馬組織和血清中氧化應(yīng)激相關(guān)的酶的活性,使用酶聯(lián)免疫吸附劑測定(ELISA)法測量血清中促炎性因子的水平。使用免疫印跡試驗(yàn)(Western blot)分析法測量NF-κB,caspase-3,BCL-2,磷酸化c-Jun氨基末端激酶(phosphorylated JNK),細(xì)胞外調(diào)節(jié)蛋白激酶(ERK),蛋白激酶B(AKT)的蛋白表達(dá)水平。我們的實(shí)驗(yàn)表明黃芪甲甙對異氟醚引起的神經(jīng)元的凋亡有保護(hù)作用,并且證明了其潛在的機(jī)制。綜上所述,我們的研究提供了新的實(shí)驗(yàn)證據(jù),證明了黃芪甲甙對麻醉相關(guān)的神經(jīng)毒性有保護(hù)作用。研究目的:探討黃芪甲甙預(yù)處理能否減少異氟醚麻醉下大鼠神經(jīng)細(xì)胞的凋亡及其可能的機(jī)制。研究方法:新生的大鼠隨機(jī)分為5組,每組6只大鼠:組1:異氟醚組;組2-4:黃芪甲甙預(yù)處理(10mg/kg,40mg/kg,100mg/kg通過灌胃法給予黃芪甲甙的溶解液預(yù)處理3天)組;對照組:未麻醉組。測量海馬組織和血清中氧化應(yīng)激相關(guān)的酶的活性,使用ELISA法測量血清中促炎性因子的水平。使用Western blot 分析法測量 NF-κB,caspase-3,BCL-2,phosphorylated JNK,ERK,and AKT 的蛋白表達(dá)水平。不同組別間的結(jié)果采用單因素方差分析。P0.05表示差異有統(tǒng)計(jì)學(xué)意義。研究結(jié)果:1、海馬CA1區(qū)神經(jīng)元凋亡在對照組海馬CA1區(qū)沒有死亡的神經(jīng)元細(xì)胞。而在異氟醚組顯示縮小的細(xì)胞質(zhì)和變性的細(xì)胞核的死亡的細(xì)胞數(shù)量明顯增多。與之相比,黃芪甲甙組神經(jīng)元細(xì)胞的死亡數(shù)量明顯減少。我們進(jìn)一步通過TUNEL分析法檢測這些凋亡細(xì)胞。在對照組,海馬CA1區(qū)的神經(jīng)元很少被TUNEL法染色,而異氟醚組則明顯增多(P0.01)。相對的,黃芪甲甙組(40和100mg/kg)神經(jīng)元細(xì)胞的凋亡明顯減少(P0.01)。2、大鼠血清和海馬中SOD,iNOS,MDA,NO測量我們分離出大鼠血清和海馬組織,測量SOD、誘導(dǎo)型一氧化氮合酶(iNOS)、一氧化氮(NO)和丙二醛(MDA)酶活性。在對照組,血清和海馬CA1的MDA水平相對較低。異氟醚組則顯著抑制SOD活性水平,但促進(jìn)凋亡的iNOS、NO和MDA的水平增高。相對的,黃芪甲甙組顯著地抑制了異氟醚引起的MDA、iNOS和NO的產(chǎn)生,而提高了 SOD的活性水平。3、血清中促炎性因子的測量我們測量一些主要的促炎性因子的水平,如腫瘤壞死因子α(TNF-α),白細(xì)胞介素6(IL-6)和白細(xì)胞介素1β(IL-1β)。在對照組,這些因子的水平相對較低。在異氟醚組,這些因子的水平明顯增高。相對的,在黃芪甲甙組(低劑量和高劑量組),顯著降低了這些促炎性因子的釋放(P0.01)。4、炎性反應(yīng)和抗凋亡信號通路的分析我們通過Western blot的方法測量了大鼠海馬組織中NF-κB的活性。在對照組的蛋白樣本中,NF-κB蛋白主要存在細(xì)胞質(zhì)中,細(xì)胞核含量很低,所以NF-κB活性很低。而異氟醚組在海馬組織中細(xì)胞核中的NF-κB水平升高。相對的,在黃芪甲甙組(低劑量和高劑量組),細(xì)胞核中NF-κB的水平降低。我們測量了不同組別中凋亡相關(guān)的蛋白表達(dá)水平。在對照組中,促凋亡標(biāo)記蛋白,Caspase-3相對較低,而抗凋亡標(biāo)記蛋白BCL-2則大量表達(dá)。異氟醚組Caspase-3則顯著升高,而BCL-2蛋白水平顯著降低。相對的,在黃芪甲甙組(低劑量和高劑量組),則明顯抑制了異氟醚引起的caspase-3上調(diào)和BCL-2下調(diào)。相似的,異氟醚組糖原合成酶激酶-3β(GSK-3β)水平升高,Klotho和磷酸化Akt蛋白水平降低。而黃芪甲甙組(低劑量和高劑量組)則顯著抑制了異氟醚引起的這些改變。我們觀察了異氟醚組中JNK和ERK的活性水平,發(fā)現(xiàn)它們的磷酸化蛋白水平都增高。然而,在黃芪甲甙組(低劑量和高劑量組)則顯著抑制了異氟醚引起的MAPK的活性水平。結(jié)論:我們的研究顯示在發(fā)育中的大腦黃芪甲甙對異氟醚麻醉導(dǎo)致的神經(jīng)元的凋亡有保護(hù)作用,這種保護(hù)作用和黃芪甲甙的抗氧化應(yīng)激和抗炎性特性有關(guān)。氧化應(yīng)激和炎癥反應(yīng)能激活NF-κB和JNK途徑導(dǎo)致神經(jīng)元細(xì)胞的凋亡,而黃芪甲甙能抑制這兩種途徑來產(chǎn)生神經(jīng)保護(hù)作用。第二部分:異氟醚麻醉對小兒腹腔鏡腹股溝斜疝修補(bǔ)術(shù)后認(rèn)知功能的影響目的比較七氟醚與異氟醚吸入全身麻醉對小兒腹腔鏡腹股溝斜疝修補(bǔ)術(shù)后認(rèn)知功能的影響。方法選取我院2013年1月至2015年1月收治的行腹腔鏡腹股溝修補(bǔ)術(shù)的患兒60例和正常兒童30例,將患兒隨機(jī)分為異氟醚組、七氟醚組和正常兒童的對照組,每組各30例。異氟醚組、七氟醚組兩組進(jìn)行誘導(dǎo)麻醉后行腹腔鏡腹股溝斜疝修補(bǔ)術(shù),觀察和記錄異氟醚組、七氟醚組兩組患兒術(shù)后蘇醒及清醒時(shí)間,術(shù)后不良反應(yīng),手術(shù)過程中不同時(shí)間的心率、平均動脈壓及3組小兒術(shù)前、術(shù)后3天和7天的韋氏智力量表評分。結(jié)果1異氟醚組患兒在手術(shù)開始、手術(shù)15min時(shí)的心率較七氟醚組低,但仍在正常心率范圍內(nèi),差異有統(tǒng)計(jì)學(xué)意義,P0.05。異氟醚組與七氟醚組患兒在麻醉前、手術(shù)時(shí)、手術(shù)過程中及手術(shù)完畢后的平均動脈壓無顯著性差異,P0.05。七氟醚組患兒總的不良反應(yīng)發(fā)生率(包括躁動)低于異氟醚組,差異有統(tǒng)計(jì)學(xué)意義(P0.05)。異氟醚組患兒的術(shù)后蘇醒時(shí)間均比七氟醚組長,差異有統(tǒng)計(jì)學(xué)意義,P0.05。2術(shù)后3天異氟醚組術(shù)后認(rèn)知功能障礙(POCD)的發(fā)生率為15%(26個兒童中有4個),異氟醚組在常識、詞匯和數(shù)字廣度項(xiàng)目評分明顯低于對照組,術(shù)后7天差異無統(tǒng)計(jì)學(xué)意義。七氟醚組術(shù)后3天POCD的發(fā)生率為12%(25個兒童中有3個),詞匯和數(shù)字廣度項(xiàng)目評分明顯低于對照組,術(shù)后7天差異無統(tǒng)計(jì)學(xué)意義。異氟醚組和七氟醚組術(shù)后3、7天比較差異無統(tǒng)計(jì)學(xué)意義。結(jié)論1吸入麻醉藥(異氟醚和七氟醚)會引起腹腔鏡腹股溝斜疝修補(bǔ)術(shù)兒童術(shù)后不同程度的POCD,這種影響是可逆性的,能在短期內(nèi)恢復(fù),影響時(shí)間是3天。2全憑吸入麻醉安全有效,七氟醚和異氟醚麻醉對術(shù)后認(rèn)知功能的影響無差異。
[Abstract]:The first part: the protective effect of astragalin on the neuronal apoptosis of neonatal rats after isoflurane anaesthesia, the anesthetic effect on the brain at the synaptogenesis stage of neuron growth is due to the anesthetic effect of the anesthetic by NMDA (N- methyl -D- aspartic acid) receptor and GABA (gamma aminobutyric acid) receptor. This neurotoxicity is easy. The damage is at the stage of synapse, the rapid growth stage of the brain. This damage affects the growth of the whole neural network, and the damage affects future behavior and cognitive ability. These results make people more concerned about the neurotoxicity of general anesthetics, especially for children, their brains. The neurotoxicity of anesthetics is in a period of vulnerability to neurotoxicity. Neurotoxicity is mainly due to neuronal apoptosis. The mechanism of apoptosis induced by anesthesia has been widely studied. On the one hand, the activation of apoptotic proteins, such as Bax, can lead to mitochondrial membrane damage, and the activation of caspases causes cell apoptosis. On the other hand, the active oxygen family The formation of free radicals such as (ROS) and active nitrogen (RNS) can lead to lipid peroxidation, which causes brain damage. This free radical damage can also cause inflammation, further amplifying the effect of apoptosis. On the contrary, the superoxide dismutase, an antioxidant (SOD), can remove excessive free radicals and reduce them. The toxic effect of astragalin is a saponin purified from the traditional Chinese medicine Astragalus membranaceus. It shows anti oxidative stress and anti apoptosis in various types of nuclear tissue. For example, it can inhibit the fibrosis of the renal tissue by inhibiting the activity of mitogen activated protein kinase (MAPK). It can reduce unilateral ureteral stem. The apoptosis of renal tubular cells caused by hindrance and transforming growth factor beta (TGF- beta). In addition, it can protect the neurotoxicity caused by the 1- methyl -4- phenyl pyridine ion by inhibiting the production of ROS and inhibiting the apoptosis pathway of Bax. Astragaloside can also reduce the 1- methyl -4- by inhibiting the opening of the permeability transition pore of the grain body. The neurotoxicity caused by benzyl pyridine ions. However, its role in neuronal apoptosis and neurotoxicity induced by narcotic drugs has not yet been studied. In order to determine whether astragalin has protective effect on the apoptosis of brain neurons in the development of anaesthesia, we have studied the new birth of Astragaloside on isoflurane. The effects of neuronal apoptosis in the hippocampus of rats. The activity of enzymes related to oxidative stress in the hippocampus and serum was measured. The levels of proinflammatory factors in serum were measured by enzyme linked immunosorbent assay (ELISA). NF- kappa B, Caspase-3, BCL-2, and phosphorylated c-Jun amino terminal kinase (NF-) were measured by the immunoblotting test (Western blot) analysis. Phosphorylated JNK) the protein expression level of extracellular regulated protein kinase (ERK) and protein kinase B (AKT). Our experiment showed that astragalin had protective effects on the apoptosis of neurons induced by isoflurane and demonstrated its potential mechanism. The study aims: To investigate whether astragalin preconditioning can reduce the apoptosis and possible mechanism of nerve cells in rats under isoflurane anesthesia. The study method: the neonatal rats were randomly divided into 5 groups, 6 rats in each group: group 1: isoflurane group, group 2-4: astragaloside pretreatment (10mg/kg, 40mg/kg, 100mg/kg pass) In the control group, the control group was given the solution of astragaloside for 3 days. The control group: the activity of oxidative stress related enzymes in the hippocampus and serum was measured in the control group. The serum levels of proinflammatory factors were measured by the ELISA method. The protein table of NF- kappa B, Caspase-3, BCL-2, phosphorylated JNK, ERK, and AKT was measured by the Western blot analysis method. The results of different groups using single factor analysis of variance.P0.05 indicated that the difference was statistically significant. 1, the neuronal apoptosis in hippocampal CA1 region was not dead in the hippocampus CA1 area of the control group, but the number of cells in the isoflurane group that showed a reduced cytoplasm and denatured nucleus increased significantly. In contrast, the number of neuronal cell deaths in the astragalin group decreased significantly. We further detected these apoptotic cells by TUNEL analysis. In the control group, the neurons in the hippocampus CA1 region were rarely stained by TUNEL, while the isoflurane group increased significantly (P0.01). Relative, the apoptosis of the astragalin group (40 and 100mg/kg) neurons was obvious. Decrease (P0.01).2, SOD, iNOS, MDA, NO in rat serum and hippocampus, measure the serum and hippocampus of rats, measure SOD, inducible nitric oxide synthase (iNOS), nitric oxide (NO) and malondialdehyde (MDA) enzyme activity. In the control group, the level of MDA in the serum and hippocampus CA1 is relatively low. The levels of apoptotic iNOS, NO and MDA increased. Relative, astragalin group significantly inhibited the production of MDA, iNOS and NO induced by isoflurane, and increased the activity level.3 of SOD, and the levels of serum proinflammatory factors in serum were measured for some of the major proinflammatory factors, such as tumor necrosis factor alpha (TNF- alpha), interleukin 6 (IL-6), and Interleukin 1 beta (IL-1 beta). In the control group, the levels of these factors were relatively low. In the isoflurane group, the levels of these factors were significantly higher. Relative, in the astragalin group (low and high dose groups), the release of these proinflammatory factors (P0.01).4 was significantly reduced, and the analysis of the inflammatory response and anti apoptosis signaling pathway was carried out through Western The blot method measured the activity of NF- kappa B in the hippocampus of rats. In the sample of the control group, the NF- kappa B protein mainly existed in the cytoplasm, and the nucleus content was very low, so the activity of NF- kappa B was very low. And the level of NF- kappa B in the nucleus of the hippocampus in the isoflurane group was higher. The level of NF- kappa B in the nucleus was reduced. We measured the expression level of apoptosis related proteins in different groups. In the control group, the apoptotic marker protein, Caspase-3 was relatively low, and the anti apoptotic marker protein BCL-2 was expressed in large numbers. The Caspase-3 in the isoflurane group increased significantly, while the BCL-2 protein level decreased significantly. Low and high dose groups significantly inhibited the up regulation of Caspase-3 and down regulation of BCL-2 induced by isoflurane. Similarly, the level of glycogen synthetase kinase -3 beta (GSK-3 beta) in isoflurane group increased and the level of Klotho and phosphorylated Akt protein decreased, while the astragalin group (low and high dose groups) significantly inhibited these changes caused by isoflurane. We observed the activity levels of JNK and ERK in isoflurane group and found that their phosphorylated protein levels increased. However, the activity level of MAPK caused by isoflurane in the astragalin group (low dose and high dose group) was significantly inhibited. Conclusion: our study showed that the development of astragaloside in the development of isoflurane induced nerve induced by isoflurane anesthesia. The apoptosis has protective effect, which is related to the antioxidant stress and anti-inflammatory properties of Astragalus membranaceus. Oxidative stress and inflammatory response can activate NF- kappa B and JNK pathway to induce neuronal cell apoptosis, and Astragalus glucoside can inhibit these two pathways to produce neuroprotective effects. The second part: isoflurane anesthesia for children's abdominal cavity The effect of cognitive function after endoscopic inguinal hernia repair. Objective to compare the effects of sevoflurane and isoflurane on the cognitive function of laparoscopic inguinal hernia repair in children. Methods 60 children with laparoscopic inguinal repair and 30 cases of normal children were selected from January 2013 to January 2015. The machine was divided into isoflurane group, sevoflurane group and normal children's control group, 30 cases in each group. Two groups of isoflurane group and sevoflurane group underwent laparoscopic inguinal hernia repair after induction anesthesia. Observe and record isoflurane group and sevoflurane group, two groups of sevoflurane group after operation recovery and waking time, postoperative adverse reaction, and the heart of different time during the operation. Rate, mean arterial pressure and 3 groups of children before operation, 3 days and 7 days after operation. Results the heart rate of the 1 isoflurane group was lower than that of the sevoflurane group at 15min, but the difference was statistically significant in the normal heart rate range. The P0.05. isoflurane group and the sevoflurane group were in the operation and the operation process before the anesthesia. There was no significant difference in the average arterial pressure between the two groups. The incidence of total adverse reactions (including agitation) in the P0.05. sevoflurane group was lower than that in the isoflurane group (P0.05). The postoperative recovery time of the isoflurane group was significantly longer than the sevoflurane group, and the difference was statistically significant. 3 days after the operation, the isoflurane group was recognized after the operation. The incidence of POCD was 15% (4 in 26 children). In the isoflurane group, the scores of the vocabulary and digital breadth were significantly lower than those in the control group. There was no significant difference at 7 days after operation. The incidence of POCD in the sevoflurane group was 12% (3 of 25 children) 3 days after operation, and the vocabulary and digital breadth scores were significantly lower than those in the control group. There was no statistical difference at 7 days after operation. There was no significant difference in the 3,7 days after operation in the isoflurane group and the sevoflurane group. Conclusion 1 inhaled anesthetics (isoflurane and sevoflurane) can cause different degrees of POCD after laparoscopic inguinal hernia repair in children. This effect is reversible, can be recovered in the short term, and the time is 3 days.2. Inhalation anesthesia is safe and effective. Sevoflurane and isoflurane anesthesia have no difference in postoperative cognitive function.
【學(xué)位授予單位】：南京醫(yī)科大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2016
【分類號】：R614

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5 周桔;雙波長薄層掃描法測定補(bǔ)陽還五丸中黃芪甲甙的含量[J];廣西醫(yī)學(xué);2000年06期

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4 譚艷芳;黃芪甲甙對大鼠骨髓間充質(zhì)干細(xì)胞表達(dá)多種造血相關(guān)因子的干預(yù)研究[D];南華大學(xué);2010年

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10 趙建軍;黃芪甲甙對急性肺損傷大鼠肺水通道蛋白1、5表達(dá)的影響[D];遵義醫(yī)學(xué)院;2009年

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