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学者姓名：张蓬勃
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Abstract ：
Astrocytes experience significant metabolic shifts in the "sensitive period" of neurological function recovery following cerebral ischemia. However, the changes in astrocyte lipid metabolism and their implications for neurological recovery remain unknown. In the present study, we employed a mouse middle cerebral artery occlusion model to investigate the changes in de novo lipogenesis and interleukin-33 (IL-33) production in astrocytes and elucidate their role in blood-brain barrier (BBB) repair in the subacute phase of cerebral ischemia. Neurological behavior evaluation was used to assess functional changes in mice. Pharmacological inhibition and astrocyte-specific downregulation of fatty acid synthase (FASN) were used to evaluate the role of de novo lipogenesis in brain injury. Intracerebroventricular administration of recombinant IL-33 was performed to study the contribution of IL-33 to BBB disruption. Extravasation of Evans blue dye, dextran and IgG were used to assess BBB integrity. Western blotting of tight junction proteins ZO-1, Occludin, and Claudin-5 were performed at defined time points to evaluate changes in BBB. It was found that de novo lipogenesis was activated, and IL-33 production increased in astrocytes at the subacute stage of cerebral ischemia injury. Inhibition of lipogenesis in astrocytes decreased IL-33 production in the peri-infarct area, deteriorated BBB damage and interfered with neurological recovery. In addition, supplementation of IL-33 alleviated BBB destruction and improved neurological recovery worsened by lipogenesis inhibition. These findings indicate that astrocyte lipogenesis increases the production of IL-33 in the peri-infarct area, which promotes BBB repair in the subacute phase of cerebral ischemia injury and improves long-term functional recovery.
Keyword ：
brain repair fatty acid synthase ischemic stroke neurological recovery
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| GB/T 7714 | Wei Haidong , Zhen Luming , Wang Shiquan et al. De novo Lipogenesis in Astrocytes Promotes the Repair of Blood-Brain Barrier after Transient Cerebral Ischemia Through Interleukin-33. [J]. | Neuroscience , 2022 , 488 : 132-134 . |
| MLA | Wei Haidong et al. "De novo Lipogenesis in Astrocytes Promotes the Repair of Blood-Brain Barrier after Transient Cerebral Ischemia Through Interleukin-33." . | Neuroscience 488 (2022) : 132-134 . |
| APA | Wei Haidong , Zhen Luming , Wang Shiquan , Zhang Yuanyuan , Wang Kui , Jia Pengyu et al. De novo Lipogenesis in Astrocytes Promotes the Repair of Blood-Brain Barrier after Transient Cerebral Ischemia Through Interleukin-33. . | Neuroscience , 2022 , 488 , 132-134 . |
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Abstract ：
目的 探讨慢性失眠患者认知功能与主客观睡眠质量、血清鸢尾素和脑源性神经营养因子(BDNF)水平的相关性.方法 选取慢性失眠患者67例为慢性失眠组,再按失眠严重程度分为轻、中、重度失眠亚组;另选择同期体检的健康者28例为对照组.两组年龄、性别、受教育年限、体质指数(BMI)、体育活动等级量表得分比较,差异无显著性.用多导睡眠监测、匹兹堡睡眠质量指数(PSQI)评估受试者的主客观睡眠质量,MoCA量表评估认知功能,测定血清鸢尾素和BDNF水平.结果 慢性失眠组PSQI得分、睡眠潜伏期、N1期睡眠时间占比(N1％)高于对照组,睡眠效率、N3期睡眠时间占比(N3％)及快速动眼睡眠(REM)％、MoCA量表总分、视空间执行功能、注意力、记忆力评分、血清鸢尾素和BDNF水平低于对照组,差异均有统计学意义(P<0.05).轻、中和重度慢性失眠亚组的组间MoCA总分及视空间与执行功能、记忆力得分、血清鸢尾素和BDNF水平比较,差异均有统计学意义(均P<0.05);3亚组MoCA量表总分及视空间与执行功能、记忆力、血清鸢尾素和BDNF水平均依次降低(均P<0.05).相关分析示慢性失眠组MoCA评分与N3％、REM％水平、血清鸢尾素和BDNF呈正相关(P<0.05),与PSQI量表评分、N1％呈负相关(P<0.05).结论 慢性失眠患者认知功能较正常人降低,与睡眠质量下降、睡眠结构紊乱、血清鸢尾素和BDNF水平降低有关.
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| GB/T 7714 | 范清雨 , 杨新利 , 张桂莲 et al. 慢性失眠患者认知功能与睡眠质量、血清鸢尾素和脑源性神经营养因子水平的相关性研究 [J]. | 中国临床神经科学 , 2021 , 29 (4) : 399-405 . |
| MLA | 范清雨 et al. "慢性失眠患者认知功能与睡眠质量、血清鸢尾素和脑源性神经营养因子水平的相关性研究" . | 中国临床神经科学 29 . 4 (2021) : 399-405 . |
| APA | 范清雨 , 杨新利 , 张桂莲 , 张茹 , 展淑琴 , 王虎清 et al. 慢性失眠患者认知功能与睡眠质量、血清鸢尾素和脑源性神经营养因子水平的相关性研究 . | 中国临床神经科学 , 2021 , 29 (4) , 399-405 . |
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Abstract ：
BackgroundGlioblastoma (GBM) is a highly malignant brain tumor with poor survival and prognosis. Randomized trials have demonstrated that chemotherapy improves survival in patients with GBM. This study aims to examine the clinical characteristics that are potentially associated with the efficacy of chemotherapy and the risk factors of GBM.MethodsA total of 25,698 patients diagnosed with GBM were identified between 2004 and 2015 from the Surveillance, Epidemiology, and End Results (SEER). The clinical and demographic variables between groups were examined by Student's t-test and Pearson's chi-square test. GBM-specific survival (GBMSS) and overall survival (OS) were evaluated using the Kaplan-Meier method with the log-rank test. Univariable and multivariable analyses were also performed using the Cox proportional hazards model to identify statistically significant prognostic factors.ResultsPatients who received chemotherapy had better overall survival (median OS 13 vs. Threemonths, HR=1.9224, 95%CI 1.8571-1.9900, p<0.0001) and better GBMSS (median GBMSS of 12 vs. Threemonths, HR=1.9379, 95%CI 1.8632-2.0156, p<0.0001), compared to patients who did not. Further subgroup analysis revealed that among patients who underwent chemotherapy, those who were younger, with a supratentorial tumor, received surgery, or radiotherapy had both improved OS and GBMSS. Age, race, tumor location, tumor size, and treatments were identified as independent prognostic factors by multivariable analyses for patients with glioblastoma.ConclusionPatients with GBM who were younger (<65years), underwent surgery, or radiotherapy can benefit more from chemotherapeutic regimens. Age, race, tumor size, tumor location, surgery, radiotherapy, and chemotherapy were factors associated with the prognosis of patients with GBM.
Keyword ：
Chemotherapy Glioblastoma SEER Survival
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| GB/T 7714 | Wen, Jieqiong , Chen, Wanbin , Zhu, Yayun et al. Clinical features associated with the efficacy of chemotherapy in patients with glioblastoma (GBM): a surveillance, epidemiology, and end results (SEER) analysis [J]. | BMC CANCER , 2021 , 21 (1) . |
| MLA | Wen, Jieqiong et al. "Clinical features associated with the efficacy of chemotherapy in patients with glioblastoma (GBM): a surveillance, epidemiology, and end results (SEER) analysis" . | BMC CANCER 21 . 1 (2021) . |
| APA | Wen, Jieqiong , Chen, Wanbin , Zhu, Yayun , Zhang, Pengbo . Clinical features associated with the efficacy of chemotherapy in patients with glioblastoma (GBM): a surveillance, epidemiology, and end results (SEER) analysis . | BMC CANCER , 2021 , 21 (1) . |
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Abstract ：
Exploring a strategy to effectively repair cerebral ischemic injury is a critical requirement for neuroregeneration. Herein, we transplanted a neural stem cell (NSC)-laden self-healing and injectable hydrogel into the brains of ischemic rats and evaluated its therapeutic effects. We observed an improvement in neurological functions in rats transplanted with the NSC-laden hydrogel. This strategy is sufficiently efficient to support neuroregeneration evidenced by NSC proliferation, differentiation, and athletic movement recovery of rats. This therapeutic effect relates to the inhibition of the astrocyte reaction and the increased expression of vascular endothelial growth factor. This work provides a novel approach to repair cerebral ischemic injury. © 2021 American Chemical Society. All rights reserved.
Keyword ：
Cell engineering Hydrogels Molecular biology Rats Self-healing materials Stem cells
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| GB/T 7714 | Zheng, Juan , Wei, Zhao , Yang, Kuan et al. Neural Stem Cell-Laden Self-Healing Polysaccharide Hydrogel Transplantation Promotes Neurogenesis and Functional Recovery after Cerebral Ischemia in Rats [J]. | ACS Applied Bio Materials , 2021 , 4 (4) : 3046-3054 . |
| MLA | Zheng, Juan et al. "Neural Stem Cell-Laden Self-Healing Polysaccharide Hydrogel Transplantation Promotes Neurogenesis and Functional Recovery after Cerebral Ischemia in Rats" . | ACS Applied Bio Materials 4 . 4 (2021) : 3046-3054 . |
| APA | Zheng, Juan , Wei, Zhao , Yang, Kuan , Lu, Yang , Lu, Pan , Zhao, Jingyi et al. Neural Stem Cell-Laden Self-Healing Polysaccharide Hydrogel Transplantation Promotes Neurogenesis and Functional Recovery after Cerebral Ischemia in Rats . | ACS Applied Bio Materials , 2021 , 4 (4) , 3046-3054 . |
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Abstract ：
目的 探究舒芬太尼与帕瑞昔布钠对瑞芬太尼术中镇痛后痛觉过敏的预防效果.方法 选取2017年6月至2018年6月在<em>西安</em><em>交通</em><em>大学</em>第二附属医院择期全麻下行妇科开腹手术的病人60例,根据随机数字表法分成两组,A组:舒芬太尼+帕瑞昔布钠组30例,B组:舒芬太尼组30例.两组病人均采用气管插管全麻,A组于手术终止前30 min静注舒芬太尼5μg,帕瑞昔布钠40 mg;B组于手术终止前30 min静注舒芬太尼10μg;记录所有病人的手术用时和苏醒用时.于拔管后即刻、术后30、60、90 min对病人进行Ramsay镇静程度评分、BCS舒适度评分并VAS疼痛视觉模拟评分评估病人疼痛程度,记录术后不良反应及追加镇痛药品情况.结果 A组病人Ramsay评分在拔管即刻(2.5±0.3)分及术后30 min(2.0±0.2)分低于B组(3.8±0.2)分、(3.2±0.3)分(P<0.05);A、B两组之间各时间点VAS评分差异无统计学意义(P>0.05);A组病人BCS评分在拔管后即刻(2.1±0.4)分、术后30 min(2.4±0.5)分、60 min(2.3±0.4)分、90 min(2.1±0.5)分高于B组(2.0±0.6)分、(2.3±0.4)分、(2.2±0.3)分、(2.2±0.4)分,差异有统计学意义(P<0.05);A组病人术后头晕4例,及追加药物人次3人次少于B组13例和10人次(P<0.05);B组苏醒用时(10.2±2.9)min比A组(7.6±3.3)min显著延长(P<0.05),两组病人均无嗜睡、寒战、低血压、心动过缓等术后不良反应.结论 联合应用舒芬太尼和帕瑞昔布钠预防术后痛觉过敏,病人舒适度高,镇痛效果更好.
Keyword ：
安定镇痛 帕瑞昔布纳 瑞芬太尼 舒芬太尼 疼痛,手术后 痛觉过敏
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| GB/T 7714 | 白洁 , 李卫松 , 孟丽华 et al. 舒芬太尼复合帕瑞昔布钠预防瑞芬太尼麻醉后痛觉过敏的效果观察 [J]. | 安徽医药 , 2020 , 24 (3) : 569-572 . |
| MLA | 白洁 et al. "舒芬太尼复合帕瑞昔布钠预防瑞芬太尼麻醉后痛觉过敏的效果观察" . | 安徽医药 24 . 3 (2020) : 569-572 . |
| APA | 白洁 , 李卫松 , 孟丽华 , 张蓬勃 . 舒芬太尼复合帕瑞昔布钠预防瑞芬太尼麻醉后痛觉过敏的效果观察 . | 安徽医药 , 2020 , 24 (3) , 569-572 . |
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Abstract ：
目的:观察氯胺酮复合咪达唑仑在无水乙醇治疗儿童先天性周围血管畸形的应用效果.方法:选择择期全麻下行无水乙醇治疗周围血管畸形儿童50例,随机分为两组:氨胺酮复合咪达唑仑组(M组)和丙泊酚持续输注组(P组),M组以咪达唑仑和氯胺酮基础下全麻,P组采用芬太尼镇痛基础下丙泊酚持续静注全麻,观察并记录入室(T0)、麻醉诱导后5 min(T1)、手术开始后30、60、90 min(分别为T2、T3、T4)、拔管后5 min(T5)的MAP与HR,监测脑电双频指数(bispectral index,BIS)并记录BIS＜40次数、平均注射无水乙醇量、术中输液量、苏醒时间及苏醒后5 min视觉模拟评分(Visual analog scales,VAS)、Ramsay镇静评分结果.结果:(1)与M组相比,P组MAP(T2～T54个时间点)、HR(T1～T55个时间点)和BIS值(T3和T42个时间点)均显著降低,差异有统计学意义(P＜0.05);三个指标其余时间点两组患儿相比,差异均无统计学意义(P＞0.05);(2)与M组患儿相比,P组BIS值＜40的患儿例数以及应用阿托品和麻黄碱例数均显著增加,差异具有统计学差异(P＜0.05);两组患儿平均无水乙醇注射量比较显著差异无统计学意义(P＞0.05);(3)与M组相比,P组患儿全麻苏醒拔管后5 min VAS评分显著降低,Ramsay评分显著升高(P＜0.05);两组患儿不良事件发生率均无统计学差异(P＞0.05).结论:氯胺酮复合咪达唑仑下全麻应用于无水乙醇注射治疗儿童周围血管畸形,能维持术中血流动力学平稳,且缩短苏醒时间.
Keyword ：
丙泊酚 氯胺酮 咪达唑仑 无水乙醇 周围血管畸形
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| GB/T 7714 | 赵茜娟 , 袁浩峥 , 张鹏 et al. 氯胺酮复合咪达唑仑全麻在无水乙醇治疗先天性周围血管畸形中的效果评价 [J]. | 现代生物医学进展 , 2020 , 20 (18) : 3474-3477,3489 . |
| MLA | 赵茜娟 et al. "氯胺酮复合咪达唑仑全麻在无水乙醇治疗先天性周围血管畸形中的效果评价" . | 现代生物医学进展 20 . 18 (2020) : 3474-3477,3489 . |
| APA | 赵茜娟 , 袁浩峥 , 张鹏 , 王龙 , 贺海萌 , 张蓬勃 . 氯胺酮复合咪达唑仑全麻在无水乙醇治疗先天性周围血管畸形中的效果评价 . | 现代生物医学进展 , 2020 , 20 (18) , 3474-3477,3489 . |
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Abstract ：
目的:观察持续气道正压通气(CPAP)治疗对中重度阻塞性睡眠呼吸暂停低通气综合征患者认知功能的影响,并探讨其与生长激素(GH)、胰岛素样生长因子1(IGF-1)的关系.方法:中重度OSAHS患者39例为OSAHS组,根据治疗方法分为CPAP治疗亚组20例和保守治疗亚组19例.另选取同期健康体检者20例为对照组,治疗3月.治疗前后所有受试者经多导睡眠监测(PSG)、认知功能评估、GH/IGF-1水平测定.结果:与对照组相比,OSAHS组的AHI、TS90％、(N1+N2)％明显升高,LSaO2、N3％、REM％、睡眠潜伏期明显降低,MoCA总分、视空间及执行功能、注意力、延迟回忆评分、IGF-1及GH水平明显降低(均P<0.01).Pearson相关分析显示,OSAHS组的MOCA评分与ESS评分、AHI、(NI+N2)％、TS90％呈负相关,与LSaO2、N3及REM％、IGF-1水平呈正相关.治疗3月后,CPAP亚组与治疗前及保守治疗亚组相比,AHI、TS90％、(N1+N2)％明显降低,LSaO2、N3％、REM％、MoCA总分、视空间及执行功能、注意力、延迟回忆分数、IGF-1及GH水平均明显升高(均P<0.05).结论:CPAP治疗可改善中重度OSAHS患者的睡眠呼吸参数及认知功能,提高GH、IGF-1水平.
Keyword ：
持续气道正压通气治疗 认知功能 生长激素 胰岛素样生长因子-1 阻塞性睡眠呼吸暂停低通气综合征
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| GB/T 7714 | 范清雨 , 杨新利 , 曹会芳 et al. 持续气道正压通气治疗对中重度阻塞性睡眠呼吸暂停低通气综合征患者认知功能的影响 [J]. | 神经损伤与功能重建 , 2020 , 15 (9) : 510-514,539 . |
| MLA | 范清雨 et al. "持续气道正压通气治疗对中重度阻塞性睡眠呼吸暂停低通气综合征患者认知功能的影响" . | 神经损伤与功能重建 15 . 9 (2020) : 510-514,539 . |
| APA | 范清雨 , 杨新利 , 曹会芳 , 张桂莲 , 张茹 , 张蓬勃 . 持续气道正压通气治疗对中重度阻塞性睡眠呼吸暂停低通气综合征患者认知功能的影响 . | 神经损伤与功能重建 , 2020 , 15 (9) , 510-514,539 . |
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Ketamine inhibits neural stem/progenitor cell (NSPC) proliferation and disrupts normal neurogenesis in the developing brain. 17β-Estradiol alleviates neurogenesis damage and enhances behavioral performance after ketamine administration. However, the receptor pathway of 17β-estradiol that protects NSPCs from ketamine-induced injury remains unknown. In the present study, we investigated the role of estrogen receptor α (ER-α) and estrogen receptor β (ER-β) in 17β-estradiol's protection against ketamine-exposed NSPCs and explored its potential mechanism. The primary cultured NSPCs were identified by immunofluorescence and then treated with ketamine and varying doses of ER-α agonist 4,4',4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (PPT) or ER-β agonist 2,3-bis(4-hydroxyphenyl)-propionitrile (DPN) for 24 h. NSPC proliferation was analyzed by 5-bromo-2-deoxyuridine incorporation test. The expression of phosphorylated glycogen synthase kinase-3β (p-GSK-3β) was quantified by western blotting. It was found that treatment with different concentrations of PPT did not alter the inhibition of ketamine on NSPC proliferation. However, treatment with DPN attenuated the inhibition of ketamine on NSPC proliferation at 24 h after their exposure (P < 0.05). Furthermore, treatment with DPN increased p-GSK-3β expression in NSPCs exposed to ketamine. These findings indicated that ER-β mediates probably the protective effects of 17β-estradiol on ketamine-damaged NSPC proliferation and GSK-3β is involved in this process.
Keyword ：
17β-estradiol ER-α ER-β GSK-3β ketamine neural stem/progenitor cells
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| GB/T 7714 | Li Weisong , Lu Pan , Lu Yang et al. 17β-Estradiol Protects Neural Stem/Progenitor Cells Against Ketamine-Induced Injury Through Estrogen Receptor β Pathway. [J]. | Frontiers in neuroscience , 2020 , 14 : 576813 . |
| MLA | Li Weisong et al. "17β-Estradiol Protects Neural Stem/Progenitor Cells Against Ketamine-Induced Injury Through Estrogen Receptor β Pathway." . | Frontiers in neuroscience 14 (2020) : 576813 . |
| APA | Li Weisong , Lu Pan , Lu Yang , Wei Haidong , Niu Xiaoli , Xu Jing et al. 17β-Estradiol Protects Neural Stem/Progenitor Cells Against Ketamine-Induced Injury Through Estrogen Receptor β Pathway. . | Frontiers in neuroscience , 2020 , 14 , 576813 . |
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Abstract ：
Background: Clinical studies have shown that dexmedetomidine ameliorates cognitive decline in both the postoperative and critical care settings. This study determined the mechanism(s) for the benefit provided by dexmedetomidine in a medical illness in mice induced by lipopolysaccharide. Methods: Cognitive decline, peripheral and hippocampal inflammation, blood-brain barrier permeability, and inflammation resolution were assessed in male mice. Dexmedetomidine was administered in the presence of lipopolysaccharide and in combination with blockers. Cultured macrophages ( RAW 264.7; BV-2) were exposed to lipopolysaccharide +/- dexmedetomidine +/- yohimbine; tumor necrosis factor a release into the medium and monocyte NF kappa B activity was determined. Results: In vivo, lipopolysaccharide-induced cognitive decline and inflammation (mean +/- SD) were reversed by dexmedetomidine (freezing time, 55.68 +/- 12.31 vs. 35.40 +/- 17.66%, P = 0.0286, n = 14; plasma interleukin [IL]-1 beta: 30.53 +/- 9.53 vs. 75.68 +/- 11.04 pg/ml, P < 0.0001; hippocampal IL-1 beta: 3.66 +/- 1.88 vs. 28.73 +/- 5.20 pg/mg, P < 0.0001; n = 8), which was prevented by a 2 adrenoceptor antagonists. Similar results were found in 12-month-old mice. Lipopolysaccharide also increased blood-brain barrier leakage, inflammation-resolution orchestrator, and proresolving and pro-inflammatory mediators; each lipopolysaccharide effect was attenuated by dexmedetomidine, and yohimbine prevented dexmedetomidine's attenuating effect. In vitro, lipopolysaccharide-induced tumor necrosis factor a release ( RAW 264.7: 6,308.00 +/- 213.60 vs. 7,767.00 +/- 358.10 pg/ml, P < 0.0001; BV-2: 1,075.00 +/- 40.41 vs. 1,280.00 +/- 100.30 pg/ml, P = 0.0003) and NF kappa B-p65 activity (nuclear translocation [RAW 264.7: 1.23 +/- 0.31 vs. 2.36 +/- 0.23, P = 0.0031; BV-2: 1.08 +/- 0.26 vs. 1.78 +/- 0.14, P = 0.0116]; phosphorylation [RAW 264.7: 1.22 +/- 0.40 vs. 1.94 +/- 0.23, P = 0.0493; BV-2: 1.04 +/- 0.36 vs. 2.04 +/- 0.17, P = 0.0025]) were reversed by dexmedetomidine, which was prevented by yohimbine. Conclusions: Preclinical studies suggest that the cognitive benefit provided by dexmedetomidine in mice administered lipopolysaccharide is mediated through a 2 adrenoceptor-mediated anti-inflammatory pathways.
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| GB/T 7714 | Li, Rong , Lai, Ieng K. , Pan, Jonathan Z. et al. Dexmedetomidine Exerts an Antiinflammatory Effect via alpha(2) Adrenoceptors to Prevent Lipopolysaccharide-induced Cognitive Decline in Mice [J]. | ANESTHESIOLOGY , 2020 , 133 (2) : 393-407 . |
| MLA | Li, Rong et al. "Dexmedetomidine Exerts an Antiinflammatory Effect via alpha(2) Adrenoceptors to Prevent Lipopolysaccharide-induced Cognitive Decline in Mice" . | ANESTHESIOLOGY 133 . 2 (2020) : 393-407 . |
| APA | Li, Rong , Lai, Ieng K. , Pan, Jonathan Z. , Zhang, Pengbo , Maze, Mervyn . Dexmedetomidine Exerts an Antiinflammatory Effect via alpha(2) Adrenoceptors to Prevent Lipopolysaccharide-induced Cognitive Decline in Mice . | ANESTHESIOLOGY , 2020 , 133 (2) , 393-407 . |
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Abstract ：
Midazolam, a widely used anesthetic, inhibits proliferation of neural stem cells (NSCs) and induces neuroapoptosis in neonates. Dexmedetomidine, an effective auxiliary medicine in clinical anesthesia, protects the developing brain against volatile anesthetic-induced neuroapoptosis. Whether dexmedetomidine protects against neurogenesis damage induced by midazolam remains unknown. This study aims to clarify the protective effect of dexmedetomidine on midazolam-induced neurogenesis damage and explore its potential mechanism. Postnatal 7-day-old Sprague-Dawley (SD) rats and cultured NSCs were treated with either normal saline, midazolam, or dexmedetomidine combined with midazolam. The rats were sacrificed at 1, 3, and 7 days after treatment. Cell proliferation was assessed by 5-bromodeoxyurdine (BrdU) incorporation. Cell viability was determined using MTT assay. Cell differentiation and apoptosis were detected by immunofluorescent staining and terminal dUTP nick-end labeling (TUNEL), respectively. The protein levels of p-JNK, p-P38, and cleaved caspase-3 were quantified using Western blotting. Midazolam decreased cell proliferation and increased cell apoptosis in the subventricular zone (SVZ), the subgranular zone (SGZ) of the hippocampus, and cultured NSCs. Moreover, midazolam decreased cell viability and increased the expression of p-JNK and p-P38 in cultured NSCs. Co-treatment with dexmedetomidine attenuated midazolam-induced changes in cell proliferation, viability, apoptosis, and protein expression of p-JNK and p-P38 in cultured NSCs. Midazolam and dexmedetomidine did not affect the differentiation of the cultured NSCs. These results indicate that dexmedetomidine alleviated midazolam-induced neurogenesis damage via JNK and P38 MAPK pathways.
Keyword ：
apoptosis dexmedetomidine differentiation midazolam neurogenesis proliferation
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| GB/T 7714 | Lei, Shan , Lu, Pan , Lu, Yang et al. Dexmedetomidine Alleviates Neurogenesis Damage Following Neonatal Midazolam Exposure in Rats through JNK and P38 MAPK Pathways [J]. | ACS CHEMICAL NEUROSCIENCE , 2020 , 11 (4) : 579-591 . |
| MLA | Lei, Shan et al. "Dexmedetomidine Alleviates Neurogenesis Damage Following Neonatal Midazolam Exposure in Rats through JNK and P38 MAPK Pathways" . | ACS CHEMICAL NEUROSCIENCE 11 . 4 (2020) : 579-591 . |
| APA | Lei, Shan , Lu, Pan , Lu, Yang , Zheng, Juan , Li, Weisong , Wang, Ning et al. Dexmedetomidine Alleviates Neurogenesis Damage Following Neonatal Midazolam Exposure in Rats through JNK and P38 MAPK Pathways . | ACS CHEMICAL NEUROSCIENCE , 2020 , 11 (4) , 579-591 . |
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