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| 1 | Interaction between autophagy and the NLRP3 inflammasome显示文摘Autophagy,a metabolic pathway that plays an important role in maintaining the dynamic balance of cells,has two types,i.e.non-selective autophagy and selective autophagy.The role of nonselective autophagy is primarily to allow cells to circulate nutrients in an energy-limited environment,while selective autophagy primarily cleans up the organelles inside the cells to maintain the cell structure.The NLRP3 inflammasome is an innate immune response produced by the organism that can promote the secretion of interleukin-1f3 and interleukin-18 through caspase-1 activation and resist the damage of some pathogens.However,when the NLRP3 inflammasome is overactivated,it can cause various inflammatory diseases,such as inflammatory liver disease and inflammatory bowel disease.Many previous studies have shown that autophagy can inhibit the NLRP3 inflammasome,while in recent years,new studies have found that autophagy can also promote the NLRP3 inflammasome in some cases,and the NLRP3 inflammasome can,in turn,affect autophagy.In this review,the interaction between autophagy and the NLRP3 inflammasome is explored,and then the application of this interaction in disease treatment is discussed. | Zhenrui Cao Yanhao Wang Zhimin Long Guiqiong He | 2019 | Acta Biochimica et Biophysica Sinica2019，51，11： | 14 |
| 2 | Cellular apoptosis and Caspase-12 expression in a rat model of progressive spinal cord compression显示文摘BACKGROUND:Studies have demonstrated that the mechanisms underlying cellular apoptosis signal transduction focus on two pathways:intracellular mitochondria and extracellular death receptor.The current evidence supports that signal transduction of cellular apoptosis also includes endoplasmic reticulum stress signal transduction. OBJECTIVE:To observe Caspase-12 expression and cellular apoptosis following ischemia in rats with progressive spinal cord compression,and to verify the influence of endoplasmic reticulum stress on the apoptosis induced by spinal cord injury. DESIGN,TIME AND SETTING:A randomized,controlled,animal trial was performed at the Institute of Neuroscience in Chongqing Medical University between January and October in 2006. MATERIALS:Immunohistochemical kit,diaminobenzidine,and TUNEL kit were purchased from Beijing Zhongshan Biotechnology,China;rabbit anti-rat Caspase-12 monoclonal antibody was provided by Santa Cruz,USA. METHODS:Sixty Wistar rats,aged 3-4 months,were randomly assigned to a model group(n=50), which underwent spinal cord compression in the L_1 segment following L_1 laminectomy and articular process excision to establish a model of progressive spinal cord compression,and a sham-surgery group(n=10),which underwent only laminectomy.Starting with the first day after surgery,the rats were locally anesthetized,the skin was opened,and the screw was rotated by 1/4 of a cycle,twice weekly. MAIN OUTCOME MEASURES:At 3,7,14,21,and 28 days after surgery,rats from each group were anesthetized,and the spinal cords were resected.Pathological changes following spinal cord compression were determined using hematoxylin-eosin staining,Nissl dye,and transmission electron microscopy.The TUNEL method was used to observe neuronal apoptosis in the compressed spinal cord segments.Immunohistochemistry and Western blot were utilized to detect Caspase-12 expression in the compressed segments. RESULTS:Cellular swelling,neural degeneration,and altered endoplasmic reticulum structures were observed at 3 days following compression.Symptoms became gradually aggravated with increasing compression time.Compared with the sham-surgery group,the number of apoptotic neurons was remarkably increased in compressed segments of the model group(P<0.05),and Caspase-12 expression was also shown to increase(P<0.05). CONCLUSION:Neuronal apoptosis was a predominant pathological factor resulting in secondary spinal cord injury during progressive spinal cord compression,and Caspase-12 was shown to be possibly involved in neuronal apoptosis induced by progressive spinal cord compression. | Yijian Liang Kejian Wang Shanquan Sun Wei Li Jianhua Ran Guiqiong He | 2009 | Neural Regeneration Research2009，4，8： | 4 |
| 3 | Effects of ovarian hormone loss on neuritic plaques and autophagic flux in the brains of adult female APP/PS1 double-transgenic mice显示文摘流行病的研究证明了女人们说明疾病(广告) 案例,在传播 gonadal 荷尔蒙的衰落为被认为是专业之一冒险的三分之二 Alzheimers 因素。另外,卵巢的荷尔蒙缺乏可以影响淀粉的(A) 免职,它与 autophagic 流动有一种靠近的关系。在这研究,我们在二个老鼠模型,上调查了短期或长期的卵巢的荷尔蒙剥夺的影响非转基因(野类型) 并且 APP/PS1 双 transgenic | Qiuhui Yao Min Feng Bo Yang Zhimin Long Shifang Luo Min Luo Guiqiong He Kejian Wang | 2018 | Acta Biochimica et Biophysica Sinica2018，50，5： | 2 |
| 4 | MKP-1 reduces Aβ generation and alleviates cognitive impairments in Alzheimer’s disease models显示文摘Mitogen-activated protein kinase(MAPK)phosphatase 1(MKP-1)is an essential negative regulator of MAPKs by dephosphorylating MAPKs at both tyrosine and threonine residues.Dysregulation of the MAPK signaling pathway has been associated with Alzheimer’s disease(AD).However,the role of MKP-1 in AD pathogenesis remains elusive.Here,we report that MKP-1 levels were decreased in the brain tissues of patients with AD and an AD mouse model.The reduction in MKP-1 gene expression appeared to be a result of transcriptional inhibition via transcription factor specificity protein 1(Sp1)cis-acting binding elements in the MKP-1 gene promoter.Amyloid-β(Aβ)-induced Sp1 activation decreased MKP-1 expression.However,upregulation of MKP-1 inhibited the expression of both Aβprecursor protein(APP)andβ-site APP-cleaving enzyme 1 by inactivating the extracellular signal-regulated kinase 1/2(ERK)/MAPK signaling pathway.Furthermore,upregulation of MKP-1 reduced Aβproduction and plaque formation and improved hippocampal long-term potentiation(LTP)and cognitive deficits in APP/PS1 transgenic mice.Our results demonstrate that MKP-1 impairment facilitates the pathogenesis of AD,whereas upregulation of MKP-1 plays a neuroprotective role to reduce Alzheimer-related phenotypes.Thus,this study suggests that MKP-1 is a novel molecule for AD treatment. | Yehong Du Yexiang Du Yun Zhang Zhilin Huang Min Fu Junjie Li Yayan Pang Peng Lei Yu Tian Wang Weihong Song Guiqiong He Zhifang Dong | 2019 | Signal Transduction and Targeted Therapy2019，4，1： | 2 |
| 5 | Distribution and expression of Pen-2 in the central nervous system of APP/PS1 double transgenic mice显示文摘-secretase 建筑群催化淀粉的蛋白质先锋应用软件的最后的劈开步产生淀粉的 A 肽,在 Alzheimer 的疾病广告病人的大脑的老年的匾的一个病原的部件。最近的研究显示出那 presenilin enhancer-2 1 是的 Pen-2, presenilin PS,包括的 PS1 和 PS2, nicastrin,和前面的咽有缺陷者 -secretase 的必要部件。在 vitro 的 Pen-2 的结构和功能是明确的。然而,很少在广告模型老鼠的中央神经系统 CNS 对 Pen-2 的神经解剖学的分发和表示被知道。我们这里报导,用象染色的 immunohistochemical 和 immunoblotting 那样的各种各样的方法,那 Pen-2 广泛地在广告模型老鼠在主要区域的特定的 neuronal 房间被表示包括嗅觉的灯泡,基础前脑, striatum ,外皮,马头鱼尾的怪兽,杏仁之类,丘脑,视下丘,小脑, brainstem ,并且针的绳索。它在老鼠大脑在特定的 neuronal 房间与 PS1 被共同表示。Pen-2 比细胞外的淀粉的存款广泛地更分布式,建议在局部性的淀粉的免职的另外的因素的重要性。Pen-2 在成年广告鼠标在房间膜和 cytoplasma 主要是局部性的,但是仅仅在控制在房间膜散布。在出生后的开发的早阶段, Pen-2 的表达式水平在 CNS 相对高,但是在成年鼠标逐渐地衰退。现在的学习作为一个关键部件为 Pen-2 提供一个解剖基础在发展和成年老鼠的大脑复杂的 -secretase,和 Pen-2 可能是仔细与在老化的负担有关神经系统。 | Yanan Chu Xuehua Peng Zhiming Long Kejian Wang Shifang Luo Akhilesh Sharma Guiqiong He | 2015 | Acta Biochimica et Biophysica Sinica2015，47，4： | 1 |
| 6 | Aquaporin-4 in the formation of cerebral edema following severe burns What role do arginine vasopressin levels play?显示文摘BACKGROUND: Aquaporin-4 (AQP-4), which is able to rapidly transport water within the brain, is highly expressed in brain tissue. It also plays an important role in the formation of cerebral edema following brain injury. However, the role of AQP-4 in the formation of cerebral edema following severe burns remains unknown. OBJECTIVE: To study changes in AQP-4 protein and mRNA expression during formation of cerebral edema following severe burns, and to explore the correlation between AQP-4 protein and mRNA expression with plasma levels of arginine vasopressin (AVP). DESIGN, TIME AND SETTING: A randomized, controlled, animal experiment was performed at the Research Center of Neuroscience, Chongqing Medical University from 2007 to 2008. MATERIALS: Biotin-labeled goat anti-rabbit antibody was provided by Beijing Zhongshan Biotechnology, China; in situ hybridization kit was provided by Wuhan Boster Biotechnology, China; rabbit anti-AQP-4 polyclonal antibody and horseradish peroxidase-labeled goat anti-rabbit IgG were provided by Chemicon, USA; AVP radioimmunoassay kit was provided by the Research Department of Neurobiology, the Second Military Medical University of Shanghai, China. METHODS: A total of 180 adult, healthy, Wistar rats were randomly assigned to control and burn groups with 30 rats in each group. The burn group was observed at five different time points: 2, 6, 12, 24, and 48 hours after burn. Hair on the mouse back was removed to expose skin on the back. After 1 day, skin with the hair removed was dipped into 100 °C water for 15 seconds to induce grade III burn injury that measures 30% of total burn surface area. MAIN OUTCOME MEASURES: Brain water content was measured using the dry-wet weight method. AQP-4 protein and mRNA expressions were detected using immunohistochemistry, in situ hybridization, Western blot, and reverse transcription-polymerase chain reaction; dynamic changes in plasma AVP were detected using radioimmunoassay. RESULTS: Brain water content gradually increased following severe burn injury. AQP-4 protein and mRNA expressions were upregulated in the supraoptic nucleus, suprachiasmatic nucleus, paraventricular nucleus, hippocampus, choroid plexus, and cerebral cortex. Plasma AVP levels increased following burn injury. AQP-4 protein and mRNA expressions positively correlated with brain water content and AVP levels during formation of cerebral edema (r = 0.870, 0.848, P < 0.01). CONCLUSION: AQP-4 participated in the formation of cerebral edema following burn injury. Plasma AVP upregulated AQP-4 expression in brain tissue, thereby promoting formation of cerebral edema. | Shifang Luo | 2010 | Neural Regeneration Research2010，5，7： | 1 |
| 7 | Estrogen deficiency exacerbates learning and memory deficits associated with glucose metabolism disorder in APP/PS1 double transgenic female mice显示文摘Alterations in glucose metabolism occur in the brain in the early stage of Alzheimer's disease(AD),and menopausal women have more severe metabolic dysfunction and are more prone to dementia than men.Although estrogen deficiency-induced changes in glucose metabolism have been previously studied in animal models,their molecular mechanisms in AD remain elusive.To investigate this issue,double transgenic(APP/PS1)female mice were subjected to bilateral ovariectomy at 3 months of age and were sacrificed 1 week,1 month and 3 months after surgery to simulate early,middle and late postmenopause,respectively.Our analysis demonstrated that estrogen deficiency exacerbates learning and memory deficits in this mouse model of postmenopause.Estrogen deficiency impairs the function of mitochondria in glucose metabolism.It is possible that the occurrence of AD is associated with the aberrant mitochondrial ERβ-mediated IGF-1/IGF-1R/GSK-3βsignaling pathway.In this study,we established a potential mechanism for the increased risk of AD in postmenopausal women and proposed a therapeutic target for AD due to postmenopause. | Min Luo Qinghua Zeng Kai Jiang Yueyang Zhao Zhimin Long Yexiang Du Kejian Wang Guiqiong He | 2022 | Genes & Diseases2022，9，5： | 1 |
| 8 | Gender difference in valproic acid-induced neuroprotective effects on APP/PS1 double transgenic mice modeling Alzheimer's disease显示文摘Alzheimers 疾病(广告) 是在广告的特定的认知能力领域,病理,和风险与性差别引起进步记忆和认知缺陷的 neurodegenerative 混乱。自从 valproic 酸(VPA ) ,是广泛地使用的心情 stabilizer 和镇癫痫剂药,它在广告上展出多重 neuroprotective 活动,这研究打算在 APP/PS1 双转基因的老鼠建模上在 VPA 的效果调查性差别广告。行为的实验证明 VPA 减少了自治行为,学习改进并且存储器,和在广告鼠标的展出的性差别与控制鼠标相比。在老年的匾的减少,淀粉的(A) 40,并且 VPA 在男广告老鼠引起的 A42 在女广告老鼠是比那更著名的。同时, VPA 保护了大脑房间免受在女广告老鼠尤其是在男广告老鼠,但是仅仅稍微死的伤害,并且 VPA 处理变厚 postsynaptic 密度并且显著地在男、女的广告老鼠增加了 presynaptic 泡的数字和密度。然而, rescuing 的效果结构的早 synaptic 和由 VPA 的功能的赤字在雄的老鼠是更明显的。总的来说,这些结果支持了性差别显著地影响的假设广告并且如果基本生物差别和性特性谨慎地被考虑,显示 VPA 可以是为广告的有希望的疗法。 | Zhimin Long Qinghua Zeng Kejian Wang Akhilesh Sharma Guiqiong He | 2016 | Acta Biochimica et Biophysica Sinica2016，48，10： | 1 |
| 9 | Dihydroartemisinin ameliorates learning and memory in Alzheimer's disease through promoting autophagosome-lysosome fusion and autolysosomal degradation for Aβclearance显示文摘Dihydroartemisinin(DHA)is the primary active metabolite of Artemisia annua,which is used to treat malaria worldwide.DHA can activate autophagy to remove the harmful or useless su bstances from eukaryotic cells,and maintain the cell viability through autolysosomal degradation system.Autophagy activation and autophagy flux are playing an important neuroprotective role in the CNS,as they accelerate the removal of toxic protein aggregates intracellularly and extracellularly to prevent Alzheimer's disease(AD). | Zhao Yueyang Long Zhimin Ding Ya Jiang Tingting Liu Jiajun Li Yimin Liu Yuanjie Peng Xuehua Wang Kejian Feng Min He Guiqiong | 2021 | 解剖学杂志2021，44，S01： | 0 |
| 10 | Dynamic changes of autophagic flux induced by A in the brain of postmortem Alzheimer's disease patients,animal models and cell models显示文摘Autophagy has been reported to play a dual'double-edged sword'role in the occurrence and development of Alzheimer's disease(AD).To assess the relationship between AD and autophagy,the dynamic changes of autophagic flux in the brain of postmortem AD patients,animal models and cell models were studied.The results showed that in AD patients,LC3 was accumulated in large amount,but the expression of Lamp1 and CTSB decreased,and the co-expression of LC3 and CTSB decreased.In the brain of APP/PS1 double transgenic mice,autophagosomes(APs)and autolysosomes(ALs)accumulation occur with the deposition of senile plaques(SPs),and the levels of lysosomal markers CTSB and Lamp1 protein decreased significantly.In the brain of APP/PS1/LC3 triple transgenic mice,the number of APs increased with the age of mice,but the number of ALs did not increase accordingly. | Long Zhimin Zhao Yueyang He Guiqiong | 2021 | 解剖学杂志2021，44，S01： | 0 |
| 11 | Coexistence of dopamine-beta-hydroxylase and activated protein-2 alpha in rat cerebellar Purkinje cells显示文摘BACKGROUND:Tyrosine hydroxylase and phenylethanolamine-n-methyl transferase expression coexist in Purkinje cells of the rat cerebellum.Numerous reports have also been published addressing whether dopamine-beta-hydroxylase(DBH) expression exists in cerebellar Purkinje cells. OBJECTIVE:To investigate the coexistence of DBH and activator protein-2αexpression in rat cerebellar Purkinje cells. DESIGN,TIME AND SETTING:A cell morphological study was performed at the Institute of Neuroscience,Chongqing Medical University,China in May 2007. MATERIALS:Ten healthy Wistar rats,of either gender,aged 14 weeks,served as experimental animals.Rabbit anti-mouse DBH,goat anti-mouse activator protein-2αand rabbit anti-mouseβ-actin (Santa Cruz Biotechnology,Inc.,USA),horseradish peroxidase-labeled goat anti-rabbit IgG, FITC-labeled mouse anti-rabbit IgG,and Cy3-labeled mouse anti-goat IgG(Boster,Wuhan,China), were used in this study. METHODS:Immunohistochemical staining was used to measure the expression of DBH or activator protein-2α,with double-label immunofluorescence being employed to determine coexpression of both,in the cerebellum of 5 randomly selected rats.Western blot assay was utilized to determine the expression of DBH and activator protein-2αin the cerebellum of the remaining 5 rats. MAIN OUTCOME MEASURES:Expression,localization and coexistence of DBH and activator protein-2αin the cerebellum were measured separately. RESULTS:Immunohistochemical staining demonstrated that cerebellar Purkinje cells stained positive for DBH and activator protein-2α.Western blot assay also demonstrated DBH and activator protein-2αexpression in the cerebellum.Double-labeling immunofluorescence showed the coexistence of DBH and activator protein-2αin cerebellar Purkinje cells. CONCLUSION:Norepinephrine and activator protein-2αcoexist in rat cerebellar Purkinje cells. | Kejian Wang Wei Li Shanquan Sun Zhongqin Ren Guiqiong He | 2009 | Neural Regeneration Research2009，4，6： | 0 |
| 12 | miR-429-3p mediates memory decline by targeting MKP-1 to reduce surface GluA1- containing AMPA receptors in a mouse model of Alzheimer’s disease显示文摘Alzheimer ’s disease(AD) is a leading cause of dementia in the elderly.Mitogen-activated protein kinase phosphatase 1(MKP-1) plays a neuroprotective role in AD.However,the molecular mechanisms underlying the effects of MKP-1 on AD have not been extensively studied.MicroRNAs(miRNAs) regulate gene expression at the post-transcriptional level,thereby repressing mRNA translation.Here,we reported that the microRNA-429-3p(miR-429-3p) was significantly increased in the brain of APP23/PS45 AD model mice and N2AAPPAD model cells.We further found that miR-429-3p could downregulate MKP-1 expression by directly binding to its 3’-untranslated region(3’ UTR).Inhibition of miR-429-3p by its antagomir(A-miR-429) restored the expression of MKP-1 to a control level and consequently reduced the amyloidogenic processing of APP and Aβ accumulation.More importantly,intranasal administration of A-miR-429 successfully ameliorated the deficits of hippocampal CA1 long-term potentiation and spatial learning and memory in AD model mice by suppressing extracellular signal-regulated kinase(ERK1/2)-mediated GluAl hyperphosphorylation at Ser831 site,thereby increasing the surface expression of GluAl-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors(AMPARs).Together,these results demonstrate that inhibiting miR-429-3p to upregulate MKP-1 effectively improves cognitive and synaptic functions in AD model mice,suggesting that miR-429/MKP-1 pathway may be a novel therapeutic target for AD treatment. | Man Luo Yayan Pang Junjie Li Lilin Yi Bin Wu Qiuyun Tian Yan He Maoju Wang Lei Xia Guiqiong He Weihong Song Yehong Du Zhifang Dong | 2024 | Acta Pharmaceutica Sinica B2024，14，2： | 0 |
| 13 | Structure,function,and pathology of Neurexin-3显示文摘Neurexin-3 is primarily localized in the presynaptic membrane and forms complexes with various ligands located in the postsynaptic membrane.Neurexin-3 has important roles in synapse development and synapse functions.Neurexin-3 mediates excitatory presynaptic differentiation by interacting with leucine-rich-repeat transmembrane neuronal proteins.Meanwhile,neurexin-3 modulates the expression of presynapticα-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors andγ-aminobutyric acid A receptors by interacting with neuroligins at excitatory and inhibitory synapses.Numerous studies have documented the potential contribution of neurexin-3 to neurodegenerative and neuropsychiatric disorders,such as Alzheimer's disease,addiction behaviors,and other diseases,which raises hopes that understanding the mechanisms of neurexin-3 may hold the key to developing new strategies for related illnesses.This review comprehensively covers the literature to provide current knowledge of the structure,function,and clinical role of neurexin-3. | Rui Zhang HanXiao Jiang YuanJie Liu GuiQiong He | 2023 | Genes & Diseases2023，10，5： | 0 |
| 14 | Nonlinear stability of rarefaction waves for a viscous radiative and reactive gas with large initial perturbation显示文摘We investigate the time-asymptotically nonlinear stability of rarefaction waves to the Cauchy problem of a one-dimensional compressible Navier-Stokes type system for a viscous,compressible,radiative and reactive gas,where the constitutive relations for the pressure p,the speci c internal energy e,the speci c volume v,the absolute temperature θ,and the specific entropy s are given by p=Rθv+aθ^(4)/3,e=C_(v)θ+avθ^(4),and s=C_(v)lnθ+4avθ^(3)/3+Rln v with R>0,C_(v)>0 and a>0 being the perfect gas constant,the speci c heat and the radiation constant,respectively.For such a specific gas motion,a somewhat surprising fact is that,generally speaking,the pressure p(v,s)is not a convex function of the specific volume v and the specific entropy s.Even so,we show in this paper that the rarefaction waves are time-asymptotically stable for large initial perturbation provided that the radiation constant a and the strength of the rarefaction waves are sufficiently small.The key point in our analysis is to deduce the positive lower and upper bounds on the specific volume and the absolute temperature,which are uniform with respect to the space and the time variables,but are independent of the radiation constant a. | Guiqiong Gong Lin He Yongkai Liao | 2021 | Science China Mathematics2021，64，12： | 0 |
| 15 | Liquiritigenin promotes osteogenic differentiation and prevents bone loss via inducing auto-lysosomal degradation and inhibiting apoptosis显示文摘Osteoporosis(OP)is a debilitating skeletal abnormality involving bone remodeling and bone cell homeostasis characterized by decreased bone strength and high fracture risk.A novel therapeutic intervention for OP by manipulating cellular autophagy-apoptosis processes to promote skeletal homeostasis is presented.Protective effects of the naturally occurring plant extract Liquiritigenin(LG)were demonstrated in an ovariectomy(OvX)-OP mouse model and preosteoblast MC3T3-E1 cells.Micro-CT and histological staining assessments of skeletal phenotype were applied alongside detection of autophagy activity in osteocytes and MC3T3-E1 cells by transmission electron microscopy(TEM).The effects of LG on chloroquine(CQ)-and the apoptosis-inducing TS-treated osteogenic differentiations and status of lysosomes within MC3T3-E1 cells were analyzed by Neutral red,Alizarin red S and alkaline phosphatase(ALP)staining and Western blot assays.Treatment with LG prevented bone loss,increased osteogenic differentiation in vivo and in vitro,and inhibited osteoclast formation to some extent.TEM analyses revealed that LG can improve auto-lysosomal degradation within osteocytes from OVX mice and MC3T3-E1 cells.The abnormal status of lysosomes associated with CQ and TS treatments was notably alleviated by LG which also reduced levels of apoptosis-induced inhibition of osteogenic differentiation and averted abnormal osteogenic differentiation as a consequence of a blockage in autolysosome degradation.Overall,LG stimulates bone growth in Oovx mice through increased osteogenic differentiation and regulation of autophagyapoptosis mechanisms,presenting an auspicious natural therapy for Op. | Yu Qiu Yueyang Zhao Zhimin Long Aijia Song Peng Huang Kejian Wang Ling Xu David Paul Molloy Guiqiong He | 2023 | Genes & Diseases2023，10，1： | 0 |
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