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Journal of Integrative Agriculture 2012年第2期11卷 303-311页

作者： LI Fang-fang XIA Jun LI Jun-min LIU Shu-sheng WANG Xiao-wei Key Laboratory of Agricultural Entomology Ministry of Agriculture/Institute of Insect SciencesZhejiang UniversityHangzhou 310029P.R.China

Cold stress responses help insects to survive under low temperatures that would be lethal *** phenomenon might contribute to the invasion of some Bemisia tabaci cryptic species from subtropical areas to temperate ***,the molecular mechanisms regulating cold stress responses in whitefly are yet ***-activated protein kinases（MApKs）which including p38,ERK,and JNK,are well known for their roles in regulating metabolic responses to cold stress in many *** this study,we explored the possible roles of the MApKs in response to low temperature stresses in the Mediterranean cryptic species（the Q-biotype）of the *** species ***,we cloned the p38 and ERK genes from the whitefly cDNA ***,we analyzed the activation of MApKs during cold stress in the Mediterranean cryptic species by *** cold stress,the level of phospho-p38 increased but no significant change was observed in the phosphorylation of ERK and JNK,thus suggesting that the p38 might be responsible for the defense response to low temperature ***,we demonstrated that：i）3 min chilling at 0°C was sufficient for the activation of p38 MApK pathway in this whitefly;and ii）the amount of phosphorylated p38 increased significantly in the first 20 min of chilling,reversed by 60 min,and then returned to the original level by 120 *** together,our results suggest that the p38 pathway is important during response to low temperature stress in the Mediterranean cryptic species of the *** species complex.

关键词： Bemisia tabaci cold stress MApK p38 phosphorylation signal transduction

The involvement of p38 MApK in transforming growth factor β1-induced apoptosis in murine hepatocytes

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Cell Research 2001年第2期11卷 89-94页

作者： LIAO JIN HUI, JUN SONG CHEN, MIN QIANG CHAI, SHENG ZHAO, JIAN GUO SONG State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, 320 Yue Yang Road, Shan 1State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences 320 Yue Yang Road Shanghai 200031 China 1State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences 320 Yue Yang Road Shanghai 200031 China 1State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences 320 Yue Yang Road Shanghai 200031 China 1State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences 320 Yue Yang Road Shanghai 200031 China 1State Key Laboratory of Molecular Biology Institute of Biochemistry and Cell Biology Shanghai Institutes for Biological Sciences Chinese Academy of Sciences 320 Yue Yang Road Shanghai 200031 China

We reported in this manuscript that TGF-β1 induces apoptosis in AML12 murine hepatocytes, which is associated with the activation of p38 MApK signaling pathway. SB202190, a specific inhibitor of p38 MApK, strongly inhibited the TGF-β1-induced apoptosis and pAI-1 promoter activity. Treatment of cells with TGF-β1 activates p38. Furthermore, over-expression of dominant negative mutant p38 also reduced the TGF-β1-induced apoptosis. The data indicate that the activation of p38 is involved in TGF-β1-mediated gene expression and apoptosis.

关键词： Transforming growth factor β apoptosis p38 hepatocyte signal transduction.

Echinatin inhibits tumor growth and synergizes with chemotherapeutic agents against human bladder cancer cells by activating p38 and suppressing Wnt/β-catenin pathways

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Genes & Diseases 2024年第2期11卷 1050-1065页

作者： Xiaoxuan Wang Lijuan Luo Jingtao Xu Qiuping Lu Haichao Xia Yanran Huang Lulu Zhang Liping Xie Habu Jiwa Shiqiong Liang Xiaoji Luo Jinyong Luo Key Laboratory of Diagnostic Medicine Designated By the Chinese Ministry of Education School of Laboratory MedicineChongqing Medical UniversityChongqing 400016China Department of Orthopedics The First Affiliated Hospital of Chongqing Medical UniversityChongqing 400042China

Bladder cancer (BC) is one of the most common malignant tumors in the urinary *** to the poor prognosis and high mortality rate of the disease,it is urgent to develop new drugs with high efficacy and low toxicity to treat *** (Ecn) is a bioactive natural flavonoid oflicorice that has attracted special attention for its promising anti-tumor ***,we explored the inhibitory effects of Echinatin on BC cells and probed the possible molecular *** found that Ecnin vitro inhibited the proliferation,migration,and invasion,arrested the cell cycle at the G2/M phase,and promoted apoptosis in BC ***,Ecn had no notable cytotoxicity towards human normal *** subsequently confirmed that Ecn restrained xenograft tumor growth and metastasis of BC cells in vivo .Mechanistically,Ecn activated the p38 signaling pathway but inactivated the Wnt/β-catenin signaling pathway,while over-expression of β-catenin and the p38 inhibitor both attenuated the inhibitory effects of Ecn on BC ***,Ecn combined with cisplatin (DDp) or gemcitabine (Gem) had synergistic inhibitory effects on BC *** summary,our results validate that Ecn inhibits the tumor growth of human BC cells via p38 and Wnt/β-catenin signaling *** meaningfully,our results suggest a potential strategy to enhance DDp- or Gem-induced inhibitory effects on BC cells by combining with Ecn.

关键词： Bladder cancer Combination chemotherapy Echinatin p38 Wnt/β-catenin

Erucic acid from Isatis indigotica Fort. suppresses influenza A virus replication and inflammation in vitro and in vivo through modulation of NF-kB and p38 MApK pathway

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Journal of pharmaceutical Analysis 2020年第2期10卷 130-146页

作者： Xiaoli Liang Yuan Huang Xiping pan Yanbing Hao Xiaowei Chen Haiming Jiang Jing Li Beixian Zhou Zifeng Yang State Key Laboratory of Respiratory Diseases Guangzhou Institute of Respiratory HealthNational Clinical Centre of Respiratory DiseaseThe First Affiliated HospitalGuangzhou Medical UniversityGuangzhou510120China Hutchison Whampoa Guangzhou Baiyunshan Chinese Medicine Co. LtdGuangzhou510515China Institute of Combination Chinese and Western Medicine Guangzhou Medical UniversityGuangzhou511436China Department of pharmacy The People's Hospital of GaozhouGaozhou525200GuangdongChina State Key Laboratory of Quality Research in Chinese Medicine Macao Institute for Applied Research in Medicine and HealthMacao University of Science and TechnologyAvenida Wai LongTaipaMacao999078PR China

Isatis indigotica Fort.(Ban-Lan-Gen)is an herbal medicine prescribed for influenza ***,its active components and mode of action remain mostly *** the present study,erucic acid was isolated from Isatis indigotica Fort.,and subsequently its underlying mechanism against influenza A virus(IAV)infection was investigated in vitro and in *** results demonstrated that erucic acid exhibited broad-spectrum antiviral activity against IAV resulting from reduction of viral polymerase transcription *** acid was found to exert inhibitory effects on IAV or viral(v)RNA-induced pro-inflam-matory mediators as well as interferons(IFNs).The molecular mechanism by which erucic acid with antiviral and anti-inflammatory properties was attributed to inactivation of NF-kB and p38 MApK ***,the NF-kB and p38 MApK inhibitory effect of erucic acid led to diminishing the transcriptional activity of interferon-stimulated gene factor 3(ISGF-3),and thereby reducing IAV-triggered pro-inflammatory response amplification in IFN-β-sensitized ***,IAV-or vRNA-triggered apoptosis of alveolar epithelial A549 cells was prevented by erucic *** vivo,erucic acid administration consistently displayed decreased lung viral load and viral antigens ***,erucic acid markedly reduced CD8+cytotoxic T lymphocyte(CTL)recruitment,pro-apoptotic signaling,hyperactivity of multiple signaling pathways,and exacerbated immune inflammation in the lung,which resulted in decreased lung injury and mortality in mice with a mouse-adapted A/FM/1/47-MA(H1N1)strain *** findings provided a mechanistic basis for the action of erucic acid against IAV-mediated inflammation and injury,suggesting that erucic acid may have a therapeutic potential in the treatment of influenza.

关键词： Influenza A virus Isatis indigotica Fort. Erucic acid Antiviral Anti-inflammatory NF-kB p38 MApK Lung injury

The binding of actin to p38 MApK and inhibiting its kinase activity in vitro

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Science China(Life Sciences) 2003年第1期46卷 87-94页

作者：杨琨姜勇韩家淮顾军 Research Center of Molecular Medicine Sun Yet-sen University of Medical Sciences Department of pathophysiology and Key Laboratory for Shock and Microcirculation of pLA The First Military Medical University Department of Immunology The Scripps Research Institute Laboratory of Genetics College of Life SciencePeking University

p38 MAp kinase mediates a signal pathway that is involved in many physiological and pathological processes such as inflammation, cellular stress, apoptosis, cell cycle and growth, ischemia/re-perfusion, and myocardium hypertrophy. To determine the molecular and regulative mechanism of p38 signal pathway, we used in vitro binding methods to screen the proteins that interact with p38. Here we report two proteins from mouse macrophage RAW264.7 strain treated with lipopolysaccharide (LpS) or ultraviolet radiation (UV), binding directly to p38. One of them is b-actin identified by peptide mass spectrum and proFound program. Actin can inhibit the auto-phosphorylation of p38 and the phosphorylation of ATF by p38. It suggests that the binding of actin to p38 in vitro may represent a negative feedback to the kinase activity of p38, which leads to the regulation of p38 pathway and cellular function.

关键词： mitogen-activated protein kinase (MAp kinase, MApK), p38 MApK, actin, protein-protein interaction, signal transduction.

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 ***,the precise mechanism associated with p38 is unclear,particularly in pulmonary microvascular endothelial cell(pMVEC)*** To determine its role in the tumor necrosis factor-alpha(TNF-α)-induced inflammation and apoptosis of pMVECs in *** then conducted in vivo experiments to confirm the effect of SB203580-mediated p38 inhibition on *** 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,*** 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 ***-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 *** 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 *** 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 *** In vitro,mitogen-activated protein kinase(Glu)transfection resulted in higher apoptotic rates and cytokine(IL-1βand IL-6)levels in TNF-α-t

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

Caenorhabditis elegans mom-4 is required for the activation of the p38 MApK signaling pathway in the response to pseudomonas aeruginosa infection

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protein & Cell 2013年第1期4卷 53-61页

作者： Ajing Xu Guojun Shi Feng Liu Baoxue Ge Department of pharmacology Xinhua HospitalSchool of MedicineShanghai 200092China Shanghai pulmonary hospital Tongji University School of MedicineShanghai 200092China Lab of Signal Transduction Institute of Health SciencesShanghai Institutes for Biological SciencesChinese Academy of Sciences and Shanghai Jiao-Tong University School of MedicineShanghai 200025China Graduate School of the Chinese Academy of Sciences Beijing 100049China

The p38 mitogen-activated protein kinase(MApK)plays an evolutionarily conserved role in the cellular re-sponse to microbial infection and environmental *** of p38 is mediated through phosphorylation by upstream MApKK,which in turn is activated by *** the Caenorhabditis elegans,the p38 MApK(also called pMK-1)signaling pathway has been shown to be required in its resistance to bacterial ***,how different upstream MAp2Ks and MAp3Ks specifically contribute to the activation of pMK-1 in response to bacterial infection still is not clearly *** using double-stranded RNA-mediated interference(RNAi)and genetic mutants of ***,we demonstrate that *** MOM-4,a mammalian TAK1 homolog,is required for the resistance of *** to a *** *** have also found that the MKK-4 of *** is required for *** resistance,but not through the regulation of *** summary,our results indicate that different upstream MApKKKs or MApKKs regulate the activation of pMK-1 in response to ***.

关键词： C.elegans MApK innate immunity p38 p.aeruginosa pA-14 MOM-4

Semi-synthetic chondroitin sulfate CS-semi5 upregulates miR-122-5p,conferring a therapeutic effect on osteoarthritis via the p38/MMp13 pathway

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Acta pharmaceutica Sinica B 2024年第8期14卷 3528-3542页

作者： Xiang Li Ya Zhou Xuefeng Chen Hongjun Wang Shuang Yang Jun Yang Yunfeng Song Zhehui Zhao Haijing Zhang Lianqiu Wu State Key Laboratory of Digestive Health Institute of Materia MedicaChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100050China Tide pharmaceutical Co. Ltd.Beijing 100176China Camford Royal School Beijing 100093China

Osteoarthritis(OA)is an aging-associated disease characterized by joint stiffness pain and destroyed articular *** treatments for OA are limited to alleviating various OA *** is a lack of drugs available in clinical practice that can truly repair cartilage ***,we developed the chondroitin sulfate analog CS-semi5,semi-synthesized from chondroitin sulfate *** vivo,CS-semi5 alleviated inflammation,provided analgesic effects,and protected cartilage in the modified Hulth OA rat model and papain-induced OA rat model.A bioinformatics analysis was performed on samples from OA patients and an exosome analysis on papain-induced OA rats,revealing miR-122-5p as the key regulator associated with CS-semi5 in OA *** prediction revealed that miR-122-5p acted on the 30-untranslated region of p38 mitogen-activated protein kinase,which was related to MMp13 *** in vitro experiments revealed that CS-semi5 effectively reduced cartilage degeneration and maintained matrix homeostasis by inhibiting matrix breakdown through the miR-122-5p/p38/MMp13 axis,which was further validated in the articular cartilage of OA *** is the first study to investigate the semi-synthesized chondroitin sulfate CS-semi5,revealing its cartilageprotecting,anti-inflammatory,and analgesic properties that show promising therapeutic effects in OA via the miR-122-5p/p38/MMp13 pathway.

关键词： Chondroitin sulfate Cartilage Osteoarthritis Extracellular matrix Inflammation miRNA p38 MMp13

Effect of electrical stimulation on neural regeneration via the p38-RhoA and ERK1/2-Bcl-2 pathways in spinal cord-injured rats

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Neural Regeneration Research 2018年第2期13卷 340-346页

作者： Min Cheol Joo Chul Hwan Jang Jong Tae park Seung Won Choi Seungil Ro Min Seob Kim Moon Young Lee Department of Rehabilitation Medicine and Institute of Wonkwang Medical Science School of Medicine Wonkwang University Department of Neurosurgery School of Medicine Wonkwang University Department of Anesthesiology and pain Medicine School of Medicine Wonkwang University Department of physiology and Cell Biology School of Medicine University of Nevada Department of physiology and Institute of Wonkwang Medical Science School of Medicine Wonkwang University

Although electrical stimulation is therapeutically applied for neural regeneration in patients, it remains unclear how electrical stimulation exerts its effects at the molecular level on spinal cord injury （SCI）. To identify the signaling pathway involved in electrical stimulation improving the function of injured spinal cord, 21 female Sprague-Dawley rats were randomly assigned to three groups： control （no surgical intervention, n = 6）, SCI （SCI only, n = 5）, and electrical simulation （ES; SCI induction followed by ES treatment, n = 10）. A complete spinal cord transection was performed at the 10^th thoracic level. Electrical stimulation of the injured spinal cord region was applied for 4 hours per day for 7 days. On days 2 and 7 post SCI, the Touch-Test Sensory Evaluators and the Basso-Beattie-Bresnahan locomotor scale were used to evaluate rat sensory and motor function. Somatosensory-evoked potentials of the tibial nerve of a hind paw of the rat were measured to evaluate the electrophysiological function of injured spinal cord. Western blot analysis was performed to measure p38-RhoA and ERK1/2-Bcl-2 pathways related protein levels in the injured spinal cord. Rat sensory and motor functions were similar between SCI and ES groups. Com- pared with the SCI group, in the ES group, the latencies of the somatosensory-evoked potential of the tibial nerve of rats were significantly shortened, the amplitudes were significantly increased, RhoA protein level was significantly decreased, protein gene product 9.5 expression, ERK1/2, p38, and Bcl-2 protein levels in the spinal cord were significantly increased. These data suggest that ES can promote the recovery of electrophysiological function of the injured spinal cord through regulating p38-RhoA and ERK1/2-Bcl-2 pathway-related protein levels in the injured spinal cord.

关键词： Bcl-2 ERKI/2 p38 pGp9.5 RhoA spinal cord injury somatosensory evoked potential muscle contraction electrical impulses neural regeneration

Serine metabolism orchestrates macrophage polarization by regulating the IGF1–p38 axis

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Cellular & Molecular Immunology 2022年第11期19卷 1263-1278页

作者： Xiao Shan penghui Hu Lina Ni Long Shen Yanan Zhang Zemin Ji Yan Cui Meihua Guo Haoan Wang Liyuan Ran Kun Yang Ting Wang Lei Wang Bin Chen Zhi Yao Vingjie Wu Qiujing Yu Tianjin Institute of Immunology Key Laboratory of Immune Microenvironment and Disease of the Ministry of EducationThe Province and Ministry Co-sponsored Collaborative Innovation Center for Medical EpigeneticsTianjin Key Laboratory of Inflammation BiologyDepartment of ImmunologySchool of Basic Medical SciencesTianjin Medical University Division of Infectious Disease Second Hospital of Tianjin Medical UniversityTianjin300070China Institute for Genome Engineered Animal Models of Human Diseases National Center of Genetically Engineered Animal Models for International ResearchDalian Medical UniversityDalian116044LiaoningChina Shandong provincial Hospital School of Laboratory Animal and Shandong Laboratory Animal CenterScience and Technology Innovation CenterShandong First Medical University and Shandong Academy of Medical SciencesJinan250021ShandongChina The province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics Department of Pharmacology and Tianjin Key Laboratory of Inflammation BiologySchool of Basic Medical SciencesTianjin Medical UniversityTianjin300070China Tianjin Institute of Immunology Key Laboratory of Immune Microenvironment and Disease of the Ministry of EducationDepartment of ImmunologySchool of Basic Medical SciencesTianjin Medical UniversityTianjinChina Department of Molecular pathobiology New York University College of DentistryNew YorkNY10010USA

Serine metabolism is reportedly involved in immune cell functions, but whether and how serine metabolism regulates macrophage polarization remain largely unknown. Here, we show that suppressing serine metabolism, either by inhibiting the activity of the key enzyme phosphoglycerate dehydrogenase in the serine biosynthesis pathway or by exogenous serine and glycine restriction, robustly enhances the polarization of interferon-γ-activated macrophages (M(IFN-γ)) but suppresses that of interleukin-4-activated macrophages (M(IL-4)) both in vitro and in vivo. Mechanistically, serine metabolism deficiency increases the expression of IGF1 by reducing the promoter abundance of S-adenosyl methionine-dependent histone H3 lysine 27 trimethylation. IGF1 then activates the p38-dependent JAK–STAT1 axis to promote M(IFN-γ) polarization and suppress STAT6-mediated M(IL-4) activation. This study reveals a new mechanism by which serine metabolism orchestrates macrophage polarization and suggests the manipulation of serine metabolism as a therapeutic strategy for macrophage-mediated immune diseases.

关键词： Serine metabolism pHGDH Macrophage polarization SAM IGF1 p38