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polydatin prevents the induction of secondary brain injury after traumatic brain injury by protecting neuronal mitochondria

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Neural Regeneration Research 2019年第9期14卷 1573-1582页

作者： Li Li Hong-ping Tan Cheng-Yong Liu Lin-Tao Yu Da-Nian Wei Zi-Chen Zhang Kui Lu Ke-Sen Zhao Marc Maegele Dao-Zhang Cai Zheng-Tao Gu Department of Treatment Center for Traumatic Injuries the Third Affiliated Hospital of Southern Medical UniversityAcademy of Orthopedics·Guangdong ProvinceGuangzhouGuangdong ProvinceChina Department of pathophysiology Southern Medical UniversityGuangdong Provincial Key Laboratory of Shock and Microcirculation ResearchGuangzhouGuangdong ProvinceChina Department of Epilepsy Surgery Guangdong Sanjiu Brain HospitalGuangzhouGuangdong ProvinceChina Department of Emergency the Third Affiliated Hospital of Southern Medical UniversityAcademy of Orthopedics·Guangdong ProvinceGuangzhouGuangdong ProvinceChina Department of Traumatology and Orthopedic Surgery Cologne-Merheim Medical Center(CMMC)University Witten/Herdecke(UW/H)Campus Cologne-MerheimCologneGermany Department of Orthopedics the Third Affiliated Hospital of Southern Medical UniversityAcademy of Orthopedics·Guangdong ProvinceGuangzhouGuangdong ProvinceChina

polydatin is thought to protect mitochondria in different cell types in various diseases.Mitochondrial dysfunction is a major contributing factor in secondary brain injury resulting from traumatic brain injury.To investigate the protective effect of polydatin after traumatic brain injury,a rat brain injury model of lateral fluid percussion was established to mimic traumatic brain injury insults.Rat models were intraperitoneally injected with polydatin(30 mg/kg)or the SIRT1 activator SRT1720(20 mg/kg,as a positive control to polydatin).At 6 hours post-traumatic brain injury insults,western blot assay was used to detect the expression of SIRT1,endoplasmic reticulum stress related proteins and p38 phosphorylation in cerebral cortex on the injured side.Flow cytometry was used to analyze neuronal mitochondrial superoxide,mitochondrial membrane potential and mitochondrial permeability transition pore opened.Ultrastructural damage in neuronal mitochondria was measured by transmission electron microscopy.Our results showed that after treatment with polydatin,release of reactive oxygen species in neuronal mitochondria was markedly reduced;swelling of mitochondria was alleviated;mitochondrial membrane potential was maintained;mitochondrial permeability transition pore opened.Also endoplasmic reticulum stress related proteins were inhibited,including the activation of p-pERK,spliced XBp-1 and cleaved ATF6.SIRT1 expression and activity were increased;p38 phosphorylation and cleaved caspase-9/3 activation were inhibited.Neurological scores of treated rats were increased and the mortality was reduced compared with the rats only subjected to traumatic brain injury.These results indicated that polydatin protectrd rats from the consequences of traumatic brain injury and exerted a protective effect on neuronal mitochondria.The mechanisms may be linked to increased SIRT1 expression and activity,which inhibits the p38 phosphorylation-mediated mitochondrial apoptotic pathway.This study was approved by the Animal Care and Use Committe

关键词： nerve regeneration traumatic brain injury polydatin mitochondria endoplasmic reticulum stress SIRT1 reactive oxygen species p38 mitochondrial membrane potential mitochondrial permeability transition pore lateral fluid percussion neural regeneration

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Neuroprotective effects of Activin A on endoplasmic reticulum stress-mediated apoptotic and autophagic pC12 cell death

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Neural Regeneration Research 2017年第5期12卷 779-786页

作者： Long-xing Xue Hong-yu Liu Yang Cui Yue Dong Jiao-qi Wang Qiu-ye Ji Jin-ting He Min Yao Ying-ying Wang Yan-kun Shao Jing Mang Zhong-xin Xu Department of Neurology China-Japan Union Hospital lilin University Changchun Jilin province China Research Center China-Japan Union Hospital Jilin University Changchun Jilin Province China

Activin A, a member of the transforming growth factor-beta superfamily, plays a neuroprotective role in multiple neurological diseases. Endoplasmic reticulum（ER） stress-mediated apoptotic and autophagic cell death is implicated in a wide range of diseases, including cerebral ischemia and neurodegenerative diseases. Thapsigargin was used to induce pC12 cell death, and Activin A was used for intervention. Our results showed that Activin A significantly inhibited morphological changes in thapsigargin-induced apoptotic cells, and the expression of apoptosis-associated proteins [cleaved-caspase-12, C/EBp homologous protein（CHOp） and cleaved-caspase-3] and biomarkers of autophagy（Beclin-1 and light chain 3）, and downregulated the expression of thapsigargin-induced ER stress-associated proteins [inositol requiring enzyme-1（IRE1）, tumor necrosis factor receptor-associated factor 2（TRAF2）, apoptosis signal-regulating kinase 1（ASK1）, c-Jun N-terminal kinase（JNK） and p38]. The inhibition of thapsigargin-induced cell death was concentration-dependent. These findings suggest that administration of Activin A protects pC12 cells against ER stress-mediated apoptotic and autophagic cell death by inhibiting the activation of the IRE1-TRAF2-ASK1-JNK/p38 cascade.

关键词： nerve regeneration Activin A endoplasmic reticulum stress apoptosis autophagy c-Jun N-terminal kinase p38 neural regeneration

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Crystal structure of the p38α MAp kinase in complex with a docking peptide from TAB1

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Science China(Life Sciences) 2013年第7期56卷 653-660页

作者： XIN FengJiao WU JiaWei Tsinghua-peking Center for Life Sciences and MOE Key Laboratory of protein Science School of Life Sciences Tsinghua University

The mitogen-activated protein kinase (MApK) p38α is a key regulator in many cellular processes, whose activity is tightly regulated by upstream kinases, phosphatases and other regulators. Transforming growth factor-β activated kinase 1 (TAK1) is an upstream kinase in p38α signaling, and its full activation requires a specific activator, the TAK1-binding protein (TAB1). TAB1 was also shown to be an inducer of p38α's autophosphorylation and/or a substrate driving the feedback control of p38α signaling. Here we determined the complex structure of the unphosphorylated p38α and a docking peptide of TAB1, which shows that the TAB1 peptide binds to the classical MApK docking groove and induces long-range conformational changes on p38α. Our structural and biochemical analyses suggest that TAB1 is a reasonable substrate of p38α, yet the interaction between the docking peptide and p38α may not be sufficient to trigger trans-autophosphorylation of p38α.

关键词： MAp激酶 p38 晶体结构对接丝裂原活化蛋白激酶自身磷酸化肽转化生长因子

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Activation of the pattern recognition receptor NOD1 augments colon cancer metastasis

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protein & Cell 2020年第3期11卷 187-201页

作者： Henry Y.Jiang Sara Najmeh Guy Martel Elyse MacFadden-Murphy Raquel Farias paul Savage Arielle Leone Lucie Roussel Jonathan Cools-Lartigue Stephen Gowing Julie Berube Betty Giannias France Bourdeau Carlos HFChan Jonathan D.Spicer Rebecca McClure Morag park Simon Rousseau Lorenzo E.Ferri Thoracic and Upper GI Cancer Research Laboratories Research Institute of McGill University Health Centre1001 Decarie BoulevardBlock ELab#E02-4134MontrealQC H4A 3J1Canada Department of Experimental Surgery and Department of Surgery McGill University1650 Cedar AvenueMontrealQC H3G 1A4Canada Meakins-Christie Laboratories Research Institute of McGill University Health Centre1001 Decarie BoulevardMontrealQC H4A 3J1Canada The Rosalind and Morris Goodman Cancer Research Centre McGill University1160 Pine AvenueMontrealQC H3A 1A3Canada Department of Surgery Roy J.and Lucille A.Carver College of MedicineUniversity of IowaUniversity of Iowa Hospitals and Clinics200 Hawkins DriveIowa CityIA 52242USA Department of pathology Health Sciences North41 Ramsey Lake RoadSudburyONCanada

While emerging data suggest nucleotide oligomerization domain receptor 1(NOD1),a cytoplasmic pattern recognition receptor,may play an important and complementary role in the immune response to bacterial infection,its role in cancer metastasis is entirely unknown.Hence,we sought to determine the effects of NOD1 on metastasis.NOD1 expression in paired human primary colon cancer,human and murine colon cancer cells were determined using immunohistochemistry and immunoblotting(WB).Clinical significance of NOD1 was assessed using TCGA survival data.A series of in vitro and in vivo functional assays,including adhesion,migration,and metastasis,was conducted to assess the effect of NOD1.C12-iE-DAp,a highly selective NOD1 ligand derived from gram-negative bacteria,was used to activate NOD1.ML130,a specific NOD1 inhibitor,was used to block C12-iE-DAp stimulation.Stable knockdown(KD)of NOD1 in human colon cancer cells(HT29)was constructed with shRNA lentiviral transduction and the functional assays were thus repeated.Lastly,the predominant signaling pathway of NOD1-activation was identified using WB and functional assays in the presence of specific kinase inhibitors.Our data demonstrate that NOD1 is highly expressed in human colorectal cancer(CRC)and human and murine CRC cell lines.Clinically,we demonstrate that this increased NOD1 expression negatively impacts survival in patients with CRC.Subsequently,we identify NOD1 activation by C12-iE-DAp augments CRC cell adhesion,migration and metastasis.These effects are predominantly mediated via the p38 mitogen activated protein kinase(MApK)pathway.This is the first study implicating NOD1 in cancer metastasis,and thus identifying this receptor as a putative therapeutic target.

关键词： NOD1 iE-DAp ML130 colon cancer metastasis cancer-extracellular matrix adhesion cancer migration p38 MApK activation intravital microscopy survival analysis

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Role of the IL-33/ST2/p38 signaling pathway in the immune response of corneal epithelial cells to Aspergillus fumigatus infection

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International Journal of Ophthalmology(English edition) 2019年第4期12卷 549-556页

作者： Jia You Jing Lin Yi-Fan Zhou Xu-Dong peng Hong He Cui Li Guo-Qiang Zhu Xue-Qi Zhao Gui-Qiu Zhao Department of Ophthalmology the Affiliated Hospital of Qingdao University Department of Clinical Laboratory the Affiliated Hospital of Qingdao University

AIM: To investigate the expression of interleukin(IL)-33 in the cornea and human corneal epithelial cells(HCECs) exposed to Aspergillus fumigatus(A. fumigatus), and to determine the function of IL-33/ST2/p38 signaling pathway in the immune response of corneal epithelial cells to A. fumigatus infection.METHODS: The mRNA and protein expression of IL-33 in HCECs and mice corneas were examined by quantitative real-time reverse transcription polymerase chain reaction(q RT-pCR) and Western blot analysis, respectively. IL-33 expression was also detected in cornea samples from healthy donors and patients with fungal keratitis with immunohistochemistry. The cultured HCECs were treated with inactive A. fumigatus hyphae at various concentrations with or without recombinant human IL-33 protein, soluble recombinant ST2 protein, specific ST2 neutralizing antibody, or the mitogen-activated protein kinase(MApK) p38 inhibitor SB203580 for evaluation of the expression and activation of IL-33/ST2/p38 signaling in the regulation of proinflammatory cytokines. The production levels of IL-6 and IL-1β were determined by qR T-pCR and enzymelinked immunosorbent assay(ELISA). The proliferation of HCECs was determined by a Cell Counting Kit-8(CCK8) assay and cell count.RESULTS: IL-33 expression levels increased in the corneal tissues of patients with fungal keratitis and in mice corneas of experimental A. fumigatus infection,as well as in HCECs with infection of A. fumigatus. A. fumigatus strongly stimulated HCECs-generated proinflammatory cytokine(IL-6 and IL-1β) production at both the mRNA and protein levels. This production of proinflammatory mediators stimulated by A. fumigatus was further stimulated by IL-33 and was prevented by soluble ST2 protein or ST2 neutralizing antibody. Moreover, IL-33 naturally promoted the p38 phosphorylation induced by A. fumigatus, which was suppressed by soluble ST2 protein. The MApK p38 inhibitor SB203580 also inhibited the A. fumigatus-induced proinflammatory cytokine production. IL-33 administration for

关键词： ST2 interleukin 33 Aspergillus fumigatus cornea p38 mitogen-activated protein kinase proliferation

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Alleviation of acute pancreatitis-associated lung injury by inhibiting the p38 mitogen-activated protein kinase pathway in pulmonary microvascular endothelial cells

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World Journal of Gastroenterology 2021年第18期27卷 2141-2159页

作者： Xiao-Xin Zhang Hao-Yang Wang Xue-Fei Yang Zi-Qi Lin Na Shi Chan-Juan Chen Lin-Bo Yao Xin-Min Yang Jia Guo Qing Xia ping Xue Department of Integrated Traditional Chinese and Western Medicine West China Hospital of Sichuan UniversityChengdu 610041Sichuan ProvinceChina

BACKGROUND previous reports have suggested that the p38 mitogen-activated protein kinase signaling pathway is involved in the development of severe acute pancreatitis(SAp)-related acute lung injury(ALI).Inhibition of p38 by SB203580 blocked the inflammatory responses in SAp-ALI.However,the precise mechanism associated with p38 is unclear,particularly in pulmonary microvascular endothelial cell(pMVEC)injury.AIM To determine its role in the tumor necrosis factor-alpha(TNF-α)-induced inflammation and apoptosis of pMVECs in vitro.We then conducted in vivo experiments to confirm the effect of SB203580-mediated p38 inhibition on SAp-ALI.METHODS In vitro,pMVEC were transfected with mitogen-activated protein kinase kinase 6(Glu),which constitutively activates p38,and then stimulated with TNF-α.Flow cytometry and western blotting were performed to detect the cell apoptosis and inflammatory cytokine levels,respectively.In vivo,SAp-ALI was induced by 5%sodium taurocholate and three different doses of SB203580(2.5,5.0 or 10.0 mg/kg)were intraperitoneally injected prior to SAp induction.SAp-ALI was assessed by performing pulmonary histopathology assays,measuring myeloperoxidase activity,conducting arterial blood gas analyses and measuring TNF-α,interleukin(IL)-1βand IL-6 levels.Lung microvascular permeability was measured by determining bronchoalveolar lavage fluid protein concentration,Evans blue pulmonary cells was confirmed by performing a terminal deoxynucleotidyl transferase-mediated dUTp nick end labeling analysis and examining the Bcl2,Bax,Bim and cle-caspase3 levels.The proteins levels of p-p38,NFκB,IκB,p-signal transducer and activator of transcription-3,nuclear factor erythroid 2-related factor 2,HO-1 and Myd88 were detected in the lungs to further evaluate the potential mechanism underlying the protective effect of SB203580.RESULTS In vitro,mitogen-activated protein kinase(Glu)transfection resulted in higher apoptotic rates and cytokine(IL-1βand IL-6)levels in TNF-α-treated pMVECs.In vivo,SB2035080 attenuated lung

关键词： Acute pancreatitis Acute lung injury pulmonary microvascular endothelial cells p38 SB203580 Apoptosis

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基于NOX4/ROS/p38信号通路探讨三焦祛湿方对膜性肾病小鼠的抗氧化应激作用

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中草药 2022年第4期53卷 1076-1083页

作者：赵亚云方敬刘海平陈静洁杨帆陈志强河北中医学院河北石家庄050091 河北省中医院河北石家庄050011 河北中医学院河北省中西医结合肝肾病证研究重点实验室河北石家庄050091

目的研究三焦祛湿方对阳离子化牛血清白蛋白(cationic bovine serum albumin,C-BSA)诱导的膜性肾病(membranous nephropathy,MN)小鼠的作用及其对烟酰胺腺嘌呤二核苷酸磷酸氧化酶4(nicotinamide adenine dinucleotide phosphate oxidase 4,NOX4)/活性氧(reactive oxygen species,ROS)/p38信号通路的影响,以阐明其抗氧化应激的作用机制。方法将60只小鼠随机分为对照组10只和造模组50只,造模组尾iv 6.5 mg/kg C-BSA建立MN小鼠模型,随机分为模型组及三焦祛湿方低、高剂量(3.71、7.42 g/kg)组和盐酸贝那普利(1.3 mg/kg)组,各给药组ig相应药物干预4周,检测各组小鼠24 h尿蛋白;腹主动脉取血,检测血清丙二醛(malondialdehyde,MDA)水平和超氧化物歧化酶(superoxide dismutase,SOD)活性;取肾组织进行苏木素-伊红(HE)、Masson、过碘酸-六胺银(pASM)染色及透射电镜(TEM),观察肾组织病理形态变化,采用免疫荧光法检测肾组织免疫球蛋白G(immunoglobulin G,IgG)沉积和ROS表达情况;采用Western blotting法检测肾组织NOX4、p38和磷酸化p38(p-p38)蛋白表达情况。结果与对照组相比,模型组小鼠24 h尿蛋白显著升高(pppp-p38蛋白表达水平显著升高(ppppp-p38蛋白表达水平显著降低(pp38信号通路有关。

关键词：三焦祛湿方膜性肾病氧化应激烟酰胺腺嘌呤二核苷酸磷酸氧化酶4 活性氧 p38

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TLR8 in the Trigeminal Ganglion Contributes to the Maintenance of Trigeminal Neuropathic pain in Mice

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Neuroscience Bulletin 2021年第4期37卷 550-562页

作者： Lin-Xia Zhao Ming Jiang Xue-Qiang Bai De-Li Cao Xiao-Bo Wu Jing Zhang Jian-Shuang Guo Tong-Tong Chen Juan Wang Hao Wu Yong-Jing Gao Zhi-Jun Zhang Department of Human Anatomy School of MedicineNantong UniversityNantong 226001China Institute of pain Medicine Institute of Nautical MedicineNantong UniversityNantong 226019China Department of Otolaryngology Head Neck Surgery The Affiliated Hospital of Nantong UniversityNantong 226001China Co-innovation Center of Neuroregeneration Nantong UniversityNantong 226001China

Trigeminal neuropathic pain(TNp)is a significant health problem but the involved mechanism has not been completely elucidated.Toll-like receptors(TLRs)have recently been demonstrated to be expressed in the dorsal root ganglion and involved in chronic pain.Here,we show that TLR8 was persistently increased in the trigeminal ganglion(TG)neurons in model of TNp induced by partial infraorbital nerve ligation(pIONL).In addition,deletion or knockdown of Tlr8 in the TG attenuated pIONL-induced mechanical allodynia,reduced the activation of ERK and p38-MApK,and decreased the expression of pro-inflammatory cytokines in the TG.Furthermore,intra-TG injection of the TLR8 agonist VTX-2337 induced pain hypersensitivity.VTX-2337 also increased the intracellular Ca^(2+)concentration,induced the activation of ERK and p38,and increased the expression of pro-inflammatory cytokines in the TG.These data indicate that TLR8 contributes to the maintenance of TNp through increasing MApK-mediated neuroinflammation.Targeting TLR8 signaling may be effective for the treatment of TNp.

关键词： TLR8 ERK p38 pro-inflammatory cytokine Trigeminal ganglion Trigeminal neuropathic pain Mouse

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paeoniflorin Attenuates Myocardial Fibrosis in Isoprenaline-induced Chronic Heart F ailure Rats via Inhibiting p38 MA pK pathway

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Current Medical Science 2020年第2期40卷 307-312页

作者： Mao LIU Jie FENG Qian DU Jiao AI Zhan LV Department of Cardiology Cardiovascular Research CenterAfiliated Hospital of North Sichuan Medical CollegeNanchong 637000China Department of Clinical Medicine North Sichuan Medical CollegeNanchong 637000China

paconiflorin(pae)is a monoterpenoid glycoside compound and has many biological activitics,such as immunosuppression,anti-inflammation and anti-cell proliferation.However,the effects and mechanisms of pae on chronic heart failure(CHF)remain unclear.This study was conducted to assess the effects and mechanisms of pae on myocardial fibrosis in isoprenaline(Iso)-induced CHF rats.pae(20 mgkg)was intragastrically administrated to CHF rats for 6 weeks.Cardiac structure and function were assessed.The protein and mRNA levels of transforming growth factorβ1(TGF-β1)and p38 were detected.C ompared to Iso group,pae could alleviate myocardial fbrosis and improve cardiac function in CHF rats.The levels of collagen volume fraction(13.75%+3.77%vs.30.97%+4.22%,pperivascular collagen volume area(14.32%+2.50%v8.28.31%+3.16%,ppae group as compared with those in Iso group.The expression of TGF-BI protein(0.30+0.07 vs.0.66+0.07,pppac group as compared with that in Iso group.The expression of p38 protein(0.36+0.12 vs.0.81+0.38,pppae group as compared with that in Iso group.pae could attenuate myocardial fibrosis and improve cardiac function in CHF rats by down-regulating the p38 MApK signaling pathway.

关键词： chronic heart failure paconiflorin myocardial fibrosis p38 transforming growth factorβ1

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Senescence in adipose-derived stem cells and its implications in nerve regeneration

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Neural Regeneration Research 2014年第1期9卷 10-15页

作者： Cristina Mantovani Giorgio Terenghi Valerio Magnaghi Dipartimento di Scienze Farmacologiche e Biomolecolari Universitàdegli Studi di Milano Blond McIndoe Laboratories Faculty of Medical and Human SciencesThe University of Manchester

Adult mesenchymal stem cells, specifically adipose-derived stem cells have self-renewal and multiple differentiation potentials and have shown to be the ideal candidate for therapeutic applications in regenerative medicine, particularly in peripheral nerve regeneration. Adipose-de- rived stem cells are easily harvested, although they may show the effects of aging, hence their potential in nerve repair may be limited by cellular senescence or donor age. Cellular senescence is a complex process whereby stem cells grow old as consequence of intrinsic events （e.g., DNA damage） or environmental cues （e.g., stressful stimuli or diseases）, which determine a permanent growth arrest. Several mechanisms are implicated in stem cell senescence, although no one is exclusive of the others. In this review we report some of the most important factors modulating the senescence process, which can influence adipose-derived stem cell morphology and function, and compromise their clinical application for peripheral nerve regenerative cell therapy.

关键词： aging adipose-derived stem cell DNA damage p38 p53 mitochondria Sirtuins pe- ripheral nervous system

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