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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 ***: 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 ***: 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 proinflammato

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

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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 ***,the effects and mechanisms of pae on chronic heart failure(CHF)remain *** study was conducted to assess the effects and mechanisms of pae on myocardial fibrosis in isoprenaline(Iso)-induced CHF ***(20 mgkg)was intragastrically administrated to CHF rats for 6 *** structure and function were *** 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 *** 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 *** expression of TGF-BI protein(0.30+0.07 vs.0.66+0.07,pppac group as compared with that in Iso *** expression of p38 protein(0.36+0.12 vs.0.81+0.38,pppae group as compared with that in Iso *** 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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Lonicera Japonica Caulis Ameliorates LpS and TNF-α-Induced HT-29 Cell Injury by Inhibiting the MApK/ERK/JNK/p38 pathway

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Biomedical and Environmental Sciences 2024年第7期37卷 805-810页

作者： Hanxiu Lu Wei Yan Xiao Yuan Yongbo Kang Zhongjian Liu Qiang Guo Faculty of Life science and Technology Kunming University of Science and TechnologyKunming 650031YunnanChina School of medicine Kunming University of Science and TechnologyKunming 650031YunnanChina Department of Gastroenterology The First People’s Hospital of Yunnan ProvinceKunming 650032YunnanChina Department of Gastroenterology The First People’s Hospital of Yuxi CityYuxi 653100YunnanChina Institute of Basic and Clinical Medicine The First People’s Hospital of Yunnan ProvinceKunming 650032YunnanChina

Inflammatory bowel disease(IBD)is characterized by chronic inflammation of the intestinal tract,and shows a high rate of *** have accumulated extensive experience in the treatment of IBD,with biologics and small molecule drugs having greatly expanded the therapeutic scope of IBD in recent ***,such treatments involve a high price and a single target of drug action.

关键词： drugs treatment p38

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Topical dihydroartemisinin inhibits suture-induced neovascularization in rat corneas through ERK1/2 and p38 pathways

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International Journal of Ophthalmology(English edition) 2011年第2期4卷 150-155页

作者： Yan-Yan Zhong, Xiao-He Lu Department of Ophthalmology Zhujiang Hospital Southern Medical University Guangzhou 510282 Guangdong Province China Department of Febrile Disease the First Affiliated Hospital Guangzhou University of Chinese Medicine Guangzhou 510405 Guangdong Province China Department of Ophthalmology Nanfang Hospital Southern Medical University Guangzhou 510515 Guangdong Province China

AIM: To determine if topical instillation of dihydroartemisinin (DHA) inhibits corneal neovascularization (NV) in rats and to investigate the role of the extracellular regulated kinases (ERK) 1/2 and p38 pathways in this process. O METHODS: Suture-induced corneal NV was produced in rats and the eyes were topically treated with different concentrations of DHA (20mg/L, 10mg/L or 5mg/L) or normal saline 4 times a day for 7 days. The corneal NV was quantified as the proportion of NV area to the whole cornea. Western blot was used to determine the expressions of vascular endothelial growth factor (VEGF) and the phosphorylation status of VEGF receptor-2, ERK1/2 and p38 in the corneas. Immunofluorescent staining was used to determine the expressions of phospho-ERK1/2 and phospho-p38 in the corneal tissues from the eyes treated with 20 mg/L DHA (DHA group) or normal saline (control group). RESULTS: The proportion of corneal NV area in the eyes treated with normal saline or DHA at dosages of 20mg/L, 10mg/L or 5mg/L was (23.74 +/- 3.00)%, (15.73 +/- 2.88)%, (19.53 +/- 2.42)%, and (23.38 +/- 2.79)%, respectively. In the eyes treated with 20mg/L or 10mg/L DHA, the corneal NV area was significantly reduced when compared to that in eyes with normal saline (p pressions of VEGF and phospho-VEGFR-2. Both 20mg/L and 10mg/L DHA inhibited the expressions of phospho-ERK1/2 and phospho-p38. Immunofluorescent staining further demonstrated that 20mg/L DHA lowered the Expression levels of phospho-ERK1/2 and phospho-p38 in the corneas with suture-induced NV. O CONCLUSION: Suture-induced NV in rat corneas was significantly inhibited by topical treatment with 20mg/L and 10mg/L DHA. The results suggest that the effects could be partially dependent on the DHA-mediated inhibitions of the ERK1/2 and p38 pathways.

关键词： cornea neovascularization dihydroartemisinin extracellular regulated kinases 1/2 p38

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Activation of p38/HSp27 pathway counters melatonin-induced inhibitory effect on proliferation of human gastric cancer cells

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The Journal of Biomedical Research 2019年第5期33卷 317-324页

作者： Chenchen Zhu Haonan Jiang Wenjie Deng Shuo Zhao Kaiquan Li Yuting Wang Qinjun Wei Jun Du School of Basic Medical Sciences Nanjing Medical UniversityNanjingJiangsu 211166China Department of physiology Nanjing Medical UniversityNanjingJiangsu 211166China The Fourth School of Clinical Medicine Nanjing Medical UniversityNanjingJiangsu 211166China The Laboratory Center for Basic Medical Sciences School of Basic Medical SciencesNanjing Medical UniversityNanjingJiangsu 211166China.

Overexpression of heat shock protein 27(HSp27)in gastric cancer is correlated with poor clinical ***,an endogenous hormone,shows promise in gastric cancer ***,there is limited study on the biological activity of HSp27 in response to melatonin *** this study,we show an anti-proliferative action of melatonin on human gastric cancer cell lines BGC-823 and ***,the inhibitory effect of melatonin is accompanied by the upregulation of HSp27 phosphorylation *** of gastric cancer cells with HSp27-specific siRNA effectively reduces HSp27 phosphorylation and potentiated melatonininduced inhibitory effect on cell *** reduction of cyclin D1 in melatonin-treated cells is also aggravated by HSp27 ***,melatonin stimulation increases p38 *** with p38 inhibitor SB203580 not only remarkably suppresses melatonin-induced HSp27 phosphorylation,but also augment the inhibitory effect of melatonin on cyclin D1 expression as well as cell *** together,our study indicates the protective pathway of p38/HSp27 against melatonin-induced inhibitory effect on gastric cancer cell proliferation,suggesting that combined with p38/HSp27 pathway inhibitor,the therapeutic efficacy of melatonin on gastric cancer may be improved.

关键词： melatonin p38 HSp27 gastric cancer proliferation

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p38γand p38δas biomarkers in the interplay of colon cancer and inflammatory bowel diseases

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Cancer Communications 2022年第9期42卷 897-901页

作者： pilar Fajardo Maria Taskova Miguel A.Martín-Serrano Jonas Hansen Sofie Slott Anna K.Jakobsen Marie-Louise Wibom Beñat Salegi Alberto Muñoz Antonio Barbachano Arpita Sharma John Mark Gubatan Aida Habtezion Juan J.Sanz-Ezquerro Kira Astakhova Ana Cuenda Department of Immunology and Oncology National Centre of Biotechnology/Consejo Superior de Investigaciones CientíficasDarwin 3Madrid 28049Spain phD programme in Molecular Bioscience Doctoral SchoolUniversidad Autónoma de MadridMadrid 28049Spain Department of Chemistry Technical University of Denmark2800 Kongens LyngbyDenmark Adolphe Merkle Institute University of FribourgChemin des Verdiers 41700 FribourgSwitzerland Stanford School of Medicine StanfordCA 94305USA Instituto de Investigaciones Biomédicas“Alberto Sols” Consejo Superior de Investigaciones CientíficasUniversidad Autónoma de MadridMadrid 28029Spain Centro de Investigación Biomédica en Red-Cáncer Instituto de Salud Carlos IIIMadrid 28029Spain Instituto de Investigación Sanitaria del Hospital Universitario La paz Madrid 28029Spain Department of Medicine Division of Gastroenterology and HepatologyStanford University School of MedicineStanfordCA 94305USA Department of Molecular and Cellular Biology Centro Nacional de Biotecnología/Consejo Superior de Investigaciones CientíficasDarwin 3Madrid 28049Spain

Dear Editor,Colorectal cancer(CRC)is the second leading cause of cancer death according to the World Health *** with inflammatory bowel disease(IBD),ulcerative colitis(UC)or Crohn’s disease(CD)are at increased risk of developing colitis-associated CRC(CAC)[1];however,our understanding of the inflammationcancer interplay at the molecular level is still limited.

关键词： inflammatory death p38 CRC

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TIpE-mediated up-regulation of MMp-9 promotes colorectal cancer invasion and metastasis through MKK-3/p38/NF-κB pro-oncogenic signaling pathway

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Signal Transduction and Targeted Therapy 2020年第1期5卷 1049-1051页

作者： Huiyu Chen Yuhan Ye Yan Yang Mengya Zhong Lei Gu Zhaopu Han Jinhua Qiu Zhongchen Liu Xingfeng Qiu Guohong Zhuang Cancer Research Center School of MedicineXiamen UniversityXiamenFujianChina Department of pathology Zhongshan Hospital Affiliated to Xiamen UniversityXiamenFujianChina Department of General Surgery Shanghai 10th People’s Hospital Affiliated to Tongji UniversityShanghaiChina Department of Gastrointestinal Surgery Zhongshan Hospital Affiliated to Xiamen UniversityXiamenFujianChina Organ Transplantation Institute of Xiamen University Fujian Provincial Key Laboratory of Organ and Tissue RegenerationSchool of MedicineXiamen UniversityXiamenFujianChina

Dear Editor,Colorectal cancer(CRC)is the third most common malignant tumor in human,ranking third in cancer-related mortality.1 Most colon cancer patients die of metastasis.2 Intriguingly,the deregulation of tumor necrosis factorα‑induced protein 8(TIpE)has been shown to play a vital regulatory role in tumor cell growth,proliferation,invasion,and metastasis.3 TIpE is a kind of cytoplasmic protein of 23 kDa.A large number of studies have shown that TIpE is closely related to the development of colon cancer.4 In addition,decreased expression of TIpE was linked to down-regulation of matrix metallopeptidase-1(MMp-1),MMp-9,and vascular endothelial growth factor receptor-2 in breast cancer.

关键词： metastasis TIp p38

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N-acetylcysteine blocked hypoxia-reoxygenation induced apoptosis through ROS-p38 MApK signaling pathway in neonatal rat cardiomyocytes

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Journal of Geriatric Cardiology 2009年第3期6卷 168-172页

作者： Feng-Xiang Zhang Ming-Long Chen Bing Yang Ke-Jiang Cao Cardiovascular Medical Center of Jiangsu the First Affiliated Hospital of Nanjing Medical University Nanjing China

Objective previous investigations have shown that N-acetylcysteine （NAC） could regulate diverse cell type＇s apoptosis. The purpose of this study was to evaluate the mechanism of NAC reversed apoptosis of cardiomyocytes induced by hypoxia-reoxygenation （H/R）. Methods Cardiomyocytes were treated with hypoxia 6 h and reoxygenation 72 h in the absence and presence of NAC （100/2mol/ L）. The ROS was assayed by using Image-iTTM LIVE green reactive oxygen species detection kit. The viability of cell was assayed with trypan blue. Early stages ofapoptosis were assessed by flow cytometry using Annexin V, and late stages of apoptosis were assessed using TUNEL system. Bcl2 and bax mRNA levels were determined by real-time quantitative pCR. Bcl2, bax, p38 and pp38 protein levels were determined by western blot. Results We found that H/R could markedly increase ROS generation and induce the apoptosis of cardiomyocytes （p〈0.01）. NAC （10012 mol/L） significantly reduced the generation of ROS and apoptosis （p all 〈0.01）. NAC also significantly reduced the protein ratio of pp38 and p38 and increased the RNA and protein ratio of bcl2 and bax （p all 〈0.01）. Conclusion The results showed that NAC significantly reduced apoptosis through inhibiting the phosphorylation of p38 signal pathway, which has potential value for clinical cardiac diseases （J Geriatr Cardio12009; 6：168-172）.

关键词： NAC apoptosis hypoxia-reoxygenation ROS p38

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Comparison of p38 MApK, soluble endoglin and endothelin-1 level in severe preeclampsia and HELLp syndrome patients

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Asian pacific Journal of Reproduction 2019年第2期8卷 83-87页

作者： Efendi Lukas Maisuri T Chalid Upik A Miskad Syakib Bakri Department of Obstetrics and Gynecology Faculty of MedicineHasanuddin University of MakassarIndonesia Department of phatology Faculty of MedicineHasanuddin University of MakassarIndonesia Departement of Internal Medicine Faculty of MedicineHasanuddin University of MakassarIndonesia

Objective: To compare the levels of p38 mitogen-activated protein kinase (MApK), soluble endoglin and endothelin-1 in the serum of patients with severe preeclampsia, hemolysis, elevated liver enzymes, and low platelets (HELLp) syndrome and normal pregnancies. Methods: This study was an observational analytic cross-sectional study performed at Wahidin Sudirohusodo Hospital, Makassar, Indonesia, in the period of 5th February 2016 to 20th January 2017. p38 MApK, soluble endoglin and endothelin-1 levels of patients with normal pregnancies, severe preeclampsia and HELLp syndrome were measured by enzyme-linked immunoabsorbentassay technique, using kits of human soluble endoglin, endothelin-1 and p38 MApK, Quantikine immunoassay: R&D System Inc. Results: Level of serum p38 MApK in HELLp syndrome group was higher than in severe preeclampsia and normal pregnancy groups. Soluble endoglin and endothelin-1 levels in pregnancies with severe preeclampsia and HELLp syndrome were higher than normal pregnancy but there was no significant difference between these two groups (p>0.05). Levels of p38 MApK, soluble endoglin and endothelin-1 also had a positive linear correlation with systolic and diastolic blood pressures (pp38 MApK in serum may be a marker for evidence of the severe hypoxia and its application may be considered for the diagnosis of HELLp syndrome.

关键词： preeclampsia HELLp syndrome p38 MApK Soluble endoglin Endothelin-1

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Realgar transforming solution is involved of JNK, p38 MApK pathway in down-regulating Ras/MApK pathway in Caenorhabditis elegans

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中国药理学与毒理学杂志 2019年第9期33卷 690-691页

作者： LIU Dong-ling ZHI De-juan WAN Feng-qi WANG Meng-qi ZHOU Ting BAI Yan-li LI Hong-yu Institute of Microbiology School of Life SciencesLanzhou UniversityLanzhou 730000China Gansu University of Chinese Medicine Lanzhou 730000China

OBJECTIVE To investigate the effect and the mechanisms of realgar transforming solution(RTS)on down-regulating over activated *** we used the optimizing technical processes to obtain the RTS,and eval⁃uate the mechanisms of RTS on down-regulating overactivated ras in Caenorhabditis *** We found that the mRNA level of let60 and lin45 significantly decreased following exposure to RTS,but mRNA levels of mpk1 were not statistically significant in let60/ras(gf)*** together with sorafenib(RAF inhibitors)significantly enhanced the activity of RTS on down-regulating overactivated ras more than RTS only,but 50μmol·L^-1 pD98059,a specific ERK inhibitor did ***45 gene RNAi decreased the ability of RTS on down-regulating overactivated ras significantly,but mpk1 gene RNAi did not,indicating that the activity of RTS on down-regulating overactivated ras mainly through targeting to lin45/*** addition,RTS significantly increased mRNA level of pmk1/p38 and jnk1/jnk in let-60/ras(gf)mutant,50μmol·L^-1 SB203580(p38 inhibitor)and Sp600125(JNK inhibitor)significantly attenuated the effects of RTS on down-regulating overactivated ras in some degree,and pmk1,jnk1 gene RNAi displayed the similar results,suggesting that p38 and JNK/MApK pathways in some degree were involved in the effects of RTS on down-regulating overactivated ras in ***⁃*** Realgar transforming solution down-regulate the Ras/MApK pathway through JNK and p38 MApK pathways.

关键词： realgar transforming solution C.elegans p38 JNK/MApK pathway

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