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1.
OU-YANG Ying ZENG Ai-hong ZHANG Ling-mei ZHOU Rui-yu TANG Shu-min RUAN Yang-hao LI Wu-feng 《园艺学报》2021,36(12):2182-2189
2.
Tau is the most abundant microtubule-associated protein in the brain. If tau protein lost the normal function, the toxic effect should be showed and plays an important role in various central nervous system lesions. Hypoxic-ischemic encephalopathy (HIE) is an important cause of mortality in the neonatal period and it is mainly characterized by neurological deficits such as cognitive limitations. However, the mechanism still needs further study, and the underlying relationship between tau protein and HIE lacks direct evidence. Some recent clinical study reported that tau protein expression elevated in the serum of asphyxia children and had a high correlation with behavior deficient. In this review, we focus on 3 key points to provide new insights to understand the tau protein-related pathogenesis of HIE as followed: (1) tau protein and its phosphorylation change during central nervous system development; (2) comparison of tau protein expression in developing brain and adult brain under some neurological disorders; (3) potential pathological change of tau in HIE related pathological conditions, such as dysmyelination, inflammation response and glutamate metabolism. 相似文献
3.
AIM: To study the effect of adenosine A2A receptor antagonist SCH58261 on hypoxic-ischemic brain damage (HIBD) in a mature fetal rabbit model.METHODS: Pregnant New Zealand white rabbits at gestational day 29 were selected and were randomly divided into sham-operated group, hypoxic-ischemic group, SCH58261 0.04 mg/kg group, SCH58261 0.12 mg/kg group and DMSO group. The intrauterine rabbit HIBD model was established. All pregnant rabbits were subjected to cesarean section 24 h after the sham operation or experimental procedure to induce hypoxic-ischemic injury in the fetus. The survival neonatal rabbits were kept in a neonatal incubator at 35℃. The general conditions of the newborn rabbits were recorded. The degree of neurobehavioral damage in the newborn rabbits was estimated by a neurobehavioral scoring protocol. The concentration of SCH58261 in the serum of pregnant rabbits, the serum of neonatal rabbits and the brain tissues of neonatal rabbits was measured by mass spectrometry. The mRNA expression of Bcl-2/Bax and protein levels of p-P38 mitogen-activated protein kinase (MAPK) in the cortex, hippocampus and striatum area in the brain of the neonatal rabbits were determined by real-time PCR and Western blot. RESULTS: SCH58261 was detected in the serum and brain tissues of the newborn rabbits. The SCH58261 concentration was approximately 40 μg/L in the brain tissue of the newborn rabbits. The mRNA expression of Bcl-2 in the cortex, hippocampus and striatum of brain tissues in SCH58261 0.04 mg/kg group and SCH58261 0.12 mg/kg group was higher, and the mRNA expression of Bax was lower than those in HI group (P<0.05). The protein level of p-P38 MAPK in the cortex, hippocampus and striatum of brain tissues was reduced in SCH58261 0.04 mg/kg group and SCH58261 0.12 mg/kg group compared with HI group (P<0.05). The protein level of p-P38 MAPK in SCH58261 0.12 mg/kg group was a little lower than that in SCH58261 0.04 mg/kg group (P<0.05). CONCLUSION: Adenosine A2A receptor antagonist SCH58261 attenuates hypoxia-ischemia induced neonatal brain injury by blocking adenosine A2A receptor, subsequently inhibiting p-P38 MAPK phosphorylation to reduce neuronal apoptosis. 相似文献
4.
AIM：To explore the anti-inflammatory effect of huperzine A (HupA) and its neuroprotective effect on rat neural stem cells (NSCs). METHODS：The microglia and NSCs were isolated from neonatal rat hippocampal tissues and co-cultured in a Transwell system. The cells were divided into 3 groups：control group, amyloid beta-peptide (Aβ) group and HupA group. The microglia layer in Aβ group was treated with Aβ1-42 (10 μmol/L), while that in HupA group was pretreated with HupA (1 μmol/L) before Aβ1-42 stimulation. The culture supernatant levels of inflammatory mediators, including interleukin 6 (IL-6), tumor necrosis factor α (TNF-α) and macrophage inflammatory protein 1α (MIP-1α), were detected by LiquiChip technique. The apoptosis of NSCs was determined by flow cytometry and Western blotting. RESULTS：The microglia secreted a large number of inflammatory mediators with the stimulation of Aβ. In Aβ group, the levels of IL-6, TNF-α and MIP-1α were significantly higher than those in control group at 72 h (P<0.01), and the apoptotic rate of NSCs was 25.46% (P<0.01). In HupA group, the concentrations of IL-6, TNF-α and MIP-1α decreased significantly as compared with Aβ group (P<0.01), and the apoptotic rate of NSCs was only 8.05% (P<0.01). The Bcl-2/Bax ratio in HupA group was higher than that in Aβ group (P<0.05). CONCLUSION：Huperzine A reduces the secretion of cytokines and chemokines, and attenuates microglia-mediated neuroinflammation, thus protecting NSCs against inflammation-induced apoptosis. 相似文献
5.
AIM: To investigate the protective effects of astrocyte protein phosphatase 2A(PP2A) up-regulation on APP/PS1 double transgenic mice.METHODS: An eGFP-wtPP2A lentivirus with glial fiber acidic protein promoter was constructed to specifically increase PP2A expression in the astrocytes. The mice were divided into wild -type mice+vector virus group(Con), APP/PS1 transgenic mice+vector virus group(APP/PS1) and APP/PS1 transgenic mice+eGFP-wtPP2A lentivirus group(PP2A) by lateral ventricular injection of the lentivirus. Four weeks after injection of the virus, the immunofluorescence of brain slices were used to detect the level of β-amyloid protein(Aβ). Golgi staining was used to detect the changes of dendritic spine density and morphology. Electron microscopy was applied to detect the thickness of postsynaptic density(PSD). The Morris water maze test was applied to examine the learning and memory abilities of the mice.RESULTS: Up-regulation of PP2A in the astrocytes attenuated Aβ level increasing in APP/PS1 group. Up-regulation of PP2A in the astrocytes significantly attenuated both decreases in the dendritic spine density and the percentage of mushroom-like dendritic spines in the hippocampal CA3 region of APP/PS1 mice. Up-regulation of PP2A in the astrocytes significantly attenuated the reduced thickness of PSD in APP/PS1 group. Up-regulation of PP2A in the astrocytes attenuated the escape latency extending in APP/PS1 group.CONCLUSION: Up-regulation of PP2A in the astrocytes reduces AD-like pathological changes, and attenuates synaptic impairment, synaptic plasticity deficits and cognitive impairment in the APP/PS1 double transgenic mice. 相似文献
6.
GU Qing-fang YU Jie-zhong GUO Min-fang WEI Wen-yue XIAO Bao-guo ZHANG Guang-xian MA Cun-gen 《园艺学报》2019,35(12):2227-2234
AIM: To explore the neuroprotective effect of novel Rho kinase inhibitor FSD-C10 on Alzheimer disease (AD) model of APP/PS1 double transgenic (Tg) mice. METHODS: Male APP/PS1 Tg mice (n=20) at 8 months of age were randomly divided into 2 groups:model group and FSD-C10 treatment group. The mice were treated with normal saline or FSD-C10 (25 mg·kg-1·d-1) by intraperitoneal injection, once daily for 2 months. Age-and sex-matched wild-type (WT) mice without treatment were used as the control. The Morris water maze (MWM) test and SMART 3.0 behavioral record system were applied to examine and analyze the spatial cognitive function of the mice. The protein levels and distribution of Aβ, p-tau and synapse-associated proteins such as synaptophysin, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) and postsynaptic density protein 95 (PSD-95) were determined by immunofluorescence staining. The protein levels of phosphorylated amyloid precursor protein at Thr668[p-APP(Thr668)], beta-site APP-cleaving enzyme 1 (BACE1) and synapse-associated proteins in the brain were analyzed by Western blot. RESULTS: Compared with model group, FSD-C10 treatment significantly improved the cognitive function of the APP/PS1 Tg mice, accompanied by reduced Aβ deposition and p-tau level, increased protein level of p-APP (Thr668) in the central nervous system, decreased expression of BACE1, and increased expression of synapse-associated proteins in the brain of the mice (P<0.05). CONCLUSION: FSD-C10 has neuroprotective potential in the APP/PS1 Tg mice. The mechanism may be related to enhancing the non-amyloidogenic APP cleavage pathway, reducing the production of Aβ oligomers, the deposition of senile plaques and the amount of tau protein, up-regulating synapse-associated proteins, and increasing synaptic plasticity. 相似文献
7.
XIE Chang-ning WU Jian WANG Xin-meng PENG Si-cong WU Jing XIAO Ling-hui LIU Tao 《园艺学报》2018,34(4):739
AIM: To investigate whether oxytocin has neuroprotective effects on hippocampal CA1 pyramidal neurons from neonatal rats exposed to hypoxic-ischemic brain injury and the underlying mechanisms. METHODS: An in vitro model of hypoxic-ischemic injury was used by exposing the brain slices to oxygen-glucose deprivation (OGD) solution. Acute dissociated brain slices (6~8 slices per rat) from 8 Sprague-Dawely rats of 7~10 d old were used. The slices were randomly divided into 4 groups:control group, OGD 20 min group, OGD 40 min group and OGD+oxytocin group. The effect of oxytocin on neuronal death was evaluated by TO-PRO-3 staining. Fresh brain slices from other 20 neonatal rats were divided into OGD group, OGD+oxytocin group, OGD+dVOT (oxytocin receptor antagonist)+oxytocin group, and OGD+bicucuclline (GABAA receptor antagonist)+oxytocin group. The onset of anoxic depolarization in the hippocampal neurons treated with different drugs was recorded by whole-cell patch-clamp techniques. RESULTS: The results of TO-PRO-3 staining showed that neuronal deaths in hippocampal CA1 area were increased over the prolonged OGD time. Oxytocin significantly reduced the hypoxic-ischemic deaths. Oxytocin dramatically prolonged the onset time of anoxic depolarization after the application of OGD solution. Both dVOT and bicuculline blocked this effect. CONCLUSION: Oxytocin plays a neuroprotective role in neonatal rat hippocampal CA1 pyramidal neurons by enhancing the inhibitory synaptic transmission via oxytocin receptors. Therefore, oxytocin is useful as a candidate for neuroprotective treatment after neonatal hypoxic-ischemic brain injury. 相似文献
8.
椭圆嗜蓝层孔菌(Phellinus ellipsoidea)子实体甲醇提取物依次用石油醚和乙酸乙酯萃取,其乙酸乙酯分部经柱层析分离得到11个化合物。经鉴定这11个化合物分别为:苯并(1,2-b,5,4-b′)二呋喃-3,5-二酮-8-甲酸甲酯(1)、原儿茶酸(2)、4-(3,4-二羟苯基)-3-丁烯-2-酮(3)、原儿茶醛(4)、Hispidin(5)、Hispolon(6)、Inoscavin A(7)、Phelligridin K(8)、Inoscavin C(9)、Inoscavin E(10)和Inonoblins B(11),其中化合物2、4、7、10为首次从该物种中分离得到。 相似文献
9.
两种无公害药剂对小菜蛾的防治效果比较 总被引：1，自引：0，他引：1
利用两种苦参碱复配型生物源性杀虫剂防治甘蓝小菜蛾。试验结果表明,1％除虫菊素·苦参碱微囊悬浮剂1000倍液具有良好的速效性和防治效果;1％苦参碱·印楝素乳油2000～2500倍液虽然速效性较差,但持效期长,效果良好;两种药剂对甘蓝无药害,对小菜蛾防效高,毒性小,残留少,适宜在无公害蔬菜生产中推广使用。 相似文献
10.
CAI Chen-chen YE Li-xia ZHU Jiang-hu BAI Jun-jie ZENG Shan-shan CHEN Shang-qin LIN Zhen-lang 《园艺学报》2019,35(2):311-319
AIM:To investigate whether ellagic acid (EA) attenuates hypoxic-ischemic encephalopathy (HIE) by down-regulating autophagy. METHODS:In vivo, Sprague-Dawley rats (n=17) were randomly divided into 3 groups:5 rats for sham group, 6 rats for HIE group and 6 rats for HIE+EA pretreatment group. The rats in HIE+EA pretreatment group were treated with EA (10 mg/kg, 10 mL/kg, suspended in corn oil, ig). After 24 h of operation, the rats from each group were sacrificed and their brains were collected. TTC staining and HE staining were used to define the infarct areas and brain structure. The autophagy-related proteins beclin-1, P62, LC3-Ⅱ/-I and Atg5 in the cortex in each group were compared by Western blot. In vitro, PC12 cells were divided into 3 groups:control group, CoCl2 group and CoCl2+EA pretreatment group. CoCl2 at 800 μmol/L was added to the PC12 cells to induce an anoxic environment. The PC12 cells were pretreated with EA at 8 μmol/L and the cell viability was measured by CCK-8 assay. The production of reactive oxidative species (ROS) in the cells was detected by flow cytometry with DCFH-DA staining. MDC staining and TMRE staining were applied to reflect the extent of autophagy and the state of apoptosis, respectively. The autophagy-related proteins in PC12 cells were also investigated. RESULTS:In HIE group, 7-day-old rats were given the operations and the their large infarct areas in the hemisphere were observed by TTC staining. HE staining displayed the injured hemispheres which contained few neurons, and exhibited edema status and serious structural damage. EA pretreatment decreased the infarct area and alleviated the damage to hemisphere with more visible neurons, compared with HIE group. Compared with sham group, the levels of autophagy-related proteins Atg5, beclin-1 and LC3-Ⅱ/-I in the cortex were increased (P<0.01), and P62 protein expression was decreased (P<0.01) in HIE group. Compared with HIE group, the protein expression of Atg5, beclin-1 and LC3-Ⅱ/-I was decreased (P<0.01) and P62 protein expression was increased in HIE+EA pretreatment group (P<0.01). In vitro, compared with CoCl2 group, the PC12 cells in CoCl2+EA pretreatment group showed a lower ROS level. Moreover, the cells in CoCl2+EA pretreatment group exhibited higher mitochondrial membrane potential than that in CoCl2 group. MDC staining in CoCl2 group showed high value of fluorescence and increased number of autophagosomes. EA pretreatment reduced the number of autophagosomes and the extent of autophagy to protect PC12 cells. Furthermore, the protein levels of Atg5, beclin-1 and LC3-Ⅱ/-I in CoCl2 group were higher (P<0.01), and the protein expression of P62 was lower (P<0.01) than those in control group. In CoCl2+EA pretreatment group, the protein levels of Atg5, beclin-1 and LC3-Ⅱ/-I were decreased (P<0.01) and the protein expression of P62 was increased as compared with CoCl2 group (P<0.01). CONCLUSION:EA pretreatment attenuates autophagy to protect the neurons against HIE injury. 相似文献
11.
利用两种苦参碱复配型生物源性杀虫剂防治甘蓝小菜蛾.试验结果表明,1%除虫菊素·苦参碱微囊悬浮剂1000倍液具有良好的速效性和防治效果;1%苦参碱·印楝素乳油2000～2500倍液虽然速效性较差,但持效期长,效果良好;两种药剂对甘蓝无药害,对小菜蛾防效高,毒性小,残留少,适宜在无公害蔬菜生产中推广使用. 相似文献
12.
虎奶菇抑菌物质与食品防腐剂抑菌活性的比较 总被引：6，自引：0，他引：6
分别以几种细菌、酵母菌和霉菌为指示菌,比较了虎奶菇发酵液乙酸乙酯提取物与苯甲酸、山梨酸、苯甲酸钠、山梨酸钾、乳酸链球菌素和钠他霉素等几种食品防腐剂的抑菌能力。结果表明,虎奶菇发酵液的乙酸乙酯提取物对几种细菌指示菌均有较好抑制作用,尤其对金黄色葡萄球菌(Staphylococcus aureus),枯草芽孢杆菌(Bacillus subtilis),大肠杆菌(Escherichia coli),蜡样芽孢杆菌(Bacillus cereus)和肠炎沙门氏菌(Sal monellaenteritidis)的抑制效果都显著高于其它防腐剂;对白色念珠菌(Candida albicans)和啤酒酵母(Saccharomyces cerevisiae)的抑制作用仅次于钠他霉素;对黄曲霉(Aspergillus flavus)和黑曲霉(Aspergillusniger)的抑制效果较差;对金黄色葡萄球菌、枯草芽孢杆菌、蜡样芽孢杆菌、大肠杆菌、肠炎沙门氏菌和绿浓杆菌的最小抑菌浓度分别为1.250mg/mL、1.250mg/mL、2.500mg/mL、5.000mg/mL、5.000mg/mL和10.000mg/mL。 相似文献
13.
AIM:To investigate the possible mechanism of deferoxamine on angiogenesis in rat hypoxic-ischemic encephalopathy (HIE). METHODS:SD rats (7 days of age) were used to make HIE model. Model group and treatment group were injected with deferoxamine or normal saline alone 24 hours before hypoxic-ischemic insult. Rats were sacrificed at 1,3,7 or 14 days after hypoxic-ischemic insult. Brain capillary density index (BCDI),the number of proliferating capillary,brain water content and extent of brain atrophy were determined. The expression of vascular endothelial growth factor (VEGF) and hypoxia-inducible factor-1α(HIF-1α) mRNA was measured. RESULTS:Early water content and late atrophic ratio of the left brain were significantly improved in the treatment group compared to model group (P<0.01). The number of proliferating capillary in the treatment group was significantly higher than that in the model group ［(2.01±0.31)/HPF vs (0.90±0.25)/HPF,P<0.01］. Deferoxamine markedly up-regulated the expression of VEGF and HIF-1α mRNA in the brain ［VEGF at 12 h: (1.41±0.07) vs (1.10±.15),P<0.05; HIF-1α at 12 h: (1.49±0.12) vs (1.11±0.16),P<0.05］.CONCLUSION:Deferoxamine may promote angiogenesis and attenuate hypoxic-ischemic induced brain injury via up-regulation of HIF-1α and VEGF expression. 相似文献
14.
为探明EMS诱变西瓜种子的最佳条件,以石红为试材,设置种子切口与不切口2种处理方式,采用6个诱变浓度(0.40%,1.00%,1.20%,1.40%,1.60%和2.00%)和5个诱变时间(4、10、12、14、16 h)共30个不同处理组合对西瓜种子萌发的影响进行研究。结果表明,切口处理能显著提高西瓜种子对EMS诱变剂的敏感性,共筛选出6个处理组合,诱变效果最接近半致死剂量,分别是1.20%+12 h、1.20%+14 h、1.20%+16 h、1.40%+12 h、1.40%+14 h和1.40%+16 h,对应的西瓜种子相对发芽率分别为50.38%、52.21%、51.97%、48.95%、49.97%和48.82%。以用量少且用时短为原则,确定EMS诱变西瓜种子的最佳组合是1.20%EMS诱变12 h。 相似文献
15.
AIM:To investigate the effect of resveratrol (RSV) on apoptosis and stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor 4 (CXCR4) pathway in hypoxia-ischemia-induced neurons from the brain of newborn rats and its mechanism. METHODS:The cortex neurons from the brain of newborn rats were given oxygen-glucose deprivation (OGD) treatment to mimic neonatal hypoxic-ischemic encephalopathy (HIE). The cortex neurons were randomly divided into 4 groups:control group, HIE model group, HIE+RSV-low (10 μmol/L) group, and HIE+RSV-high (50 μmol/L) group. After OGD treatment for 2 h, the neurons were cultured with indicated dose of RSV for 24 h. The apoptosis was analyzed by flow cytometry. Western blot was used to determine the levels of apoptosis-related proteins, SDF-1 and CXCR4. Real-time PCR was used to detect the mRNA expression of SDF-1 and CXCR4. Additionally, to explore the effects of RSV on cell apoptosis and apoptosis-related proteins after the suppression of SDF-1/CXCR4 signaling, a CXCR4 antagonist AMD3100, and RSV were used to co-treat OGD-injured neurons for 24 h. RESULTS:RSV alleviated OGD-induced neuronal apoptosis, down-regulated cleaved caspase-3 and cytochrome C levels, and up-regulated the ratio of Bcl-2/Bax. Compared with the control group, OGD treatment increased the expression of SDF-1 and CXCR4 (P<0.05). Compared with the HIE model group, RSV further up-regulated the expression of SDF-1 and CXCR4 (P<0.05). AMD3100 reversed the effects of RSV on OGD-induced cell apoptosis. CONCLUSION:RSV suppresses hypoxia-ischemia-induced apoptosis of neurons from the brain of newborn rats via up-regulating SDF-1/CXCR4 signaling pathway. 相似文献
16.
为创制用于番茄遗传育种和基因功能研究的新种质,用0.7% 的甲基磺酸乙酯（EMS）浸泡处理TTD302A 种子 8 h,清水冲洗后催芽育苗,定植于塑料大棚中,单株观察、单株留种。对M2 群体进行株系和单株的系统观察,表型表现一致的株系混合留种,有表型变异的单株进行单株留种,获得M3 种子。另外选取了15 份出现典型变异性状的M2 材料进行SSR 检测。通过对M2 群体表型性状的观察,共发现373 个变异性状,297 个变异单株,总的单株变异频率为7.1%。叶、花、果实和植株的表型变异频率依次为1.5%、2.8%、1.3% 和2.4%。SSR 分析结果表明9 份材料在 DNA 水平上有变异。 相似文献
17.
冷害导致砂糖橘果实品质劣变 总被引：7，自引：1，他引：7
将砂糖橘（Citrus Reticulata Blanco CV. Shiyueju）果实置于1℃、3℃、6℃和9℃下贮藏,比较其贮藏效果及冷害对果实品质的影响。结果表明：砂糖橘最适贮藏温度为6℃,在1~3℃温度贮藏易发生冷害。冷害导致果实外观品质下降,果肉乙醛和乙醇含量累积,果肉异味,品质下降。1℃贮藏果实的呼吸强度和乙烯释放速率较6℃高,丙二醛（MDA）含量增加,丙酮酸脱羧酶（PDC）和乙醇脱氢酶（ADH）活性大幅度提高。说明在冷害温度下,砂糖橘果肉异味是由于乙醛和乙醇累积,而果实呼吸强度的提高与PDC和ADH活性的增加密切相关。 相似文献
18.
Newly released × Cupressocyparis hybrids have been tested for their tolerance to exposed coastal conditions. Preliminary data show that the hybrids × C. notabilis and × C. ovensii were severely damaged by salt-laden winds, whilst × C. leylandii clones ‘Rostrevor’ and ‘Leighton Green’ were not seriously affected. 相似文献
19.
Volvariella volvacea is a mushroom well-adapted to high temperature. It optimally grows at 30–35 °C. To breed cold-tolerant strains to expand cultivation region and season, the basidiospores and gills of V. volvacea were treated with chemical mutagens, ethyl methane sulfonate (EMS) and diethyl sulfate (DES), respectively. Two cold-tolerant strains, strains Em-16 and Em-18, were successfully obtained from EMS mutagenesis of gills through 0 °C screening, colony morphology screening and fruiting screening. The biological efficiencies of Em-16 and Em-18 strains were 24.55% and 23.61% in the first flush at 27 °C and their biological efficiencies were 46.1% and 40.5% higher than the control strain V41, respectively. Their fruiting bodies had a longer storage life at 16 °C, compared with the control strain V41. Amplified fragment length polymorphism analysis shows that the strains Em-16 and Em-18 are new strains. 相似文献
20.
AIM To investigate the activation of related repair pathways after bupivacaine-induced neuronal DNA damage by cDNA gene screening. METHODS The bupivacaine-induced SH-SY5Y neuronal damage and DNA damage model was established. The technique of cDNA microplate array was used to screen the 21 important regulatory factors in the DNA damage repair pathway. Post-analysis of these differentially expressed repair genes for the repair pathway enrichment and distribution was performed. The data were analyzed by GraphPad Prism 6 statistical software to compare differences between groups. RESULTS The viability of SH-SY5Y cells treated with bupivacaine at different concentrations （detected by CCK-8 assay） showed that the IC50 value of bupivacaine was 1.5 mmol/L. The comet assay related index （the comet tail） was increased （P <0.05）, the phosphorylation level of γH2AX protein was increased （P <0.05）, indicating that DNA damage in the SH-SY5Y cells was significantly aggravated after bupivacaine treatment. The results of cDNA microplate assay showed that compared withcontrol group, the differentially expressed genes after bupivacaine treatment were DNA-PKcs , PTEN , NTH1 , RAD9 , CSB , GADD45 , XPD, XPC-HR23B and P53 . The analysis showed that these repair genes were mainly concentrated in the following 3 repair mechanisms： base excision repair, nucleotide excision repair, and non-homologous reconstitution. CONCLUSION The repair genes differentially expressed after neuronal DNA damage caused by local anesthetics are mainly concentrated in the pathways of non-homologous end-joining, base excision repair and nucleotide excision repair. 相似文献