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Physalin B reduces Aβ secretion through down-regulation of BACE1 expression by activating FoxO1 and inhibiting stat3 phosphorylation

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Chinese Journal of Natural Medicines 2021年第10期19卷 732-740页

作者： ZHANG Wei BAI Shan-Shan ZHANG Qi SHI Ru-Ling WANG He-Cheng LIU You-Cai NI Tian-Jun WU Ying YAO Zhao-Yang SUN Yi WANG Ming-Yong school of Basic Medical Sciences Xinxiang Medical UniversityXinxiang 453003China Grade 2019 School of Basic Medical SciencesXinxiang Medical UniversityXinxiang 453003China school of Public Health Xinxiang Medical UniversityXinxiang 453003China school of Life and Pharmaceutical Sciences Dalian University of TechnologyPanjin 124221China school of Basic Medical Sciences Sanquan College of Xinxiang Medical UniversityXinxiang 453003China school of Nursing Care Xinxiang Medical UniversityXinxiang 453003China Institute of Chinese Materia Medica China Academy of Chinese Medical SciencesBeijing 100700China school of Laboratory Medicine Xinxiang Medical UniversityXinxiang 453003China Xinxiang Key Laboratory of Immunoregulation and Molecular Diagnostics Xinxiang 453003China Central Laboratory the First Affiliated Hospital of Henan University of Science and TechnologyLuoyang 471003China

Physalin B(PB),one of the major active steroidal constituents of Solanaceae Physalis plants,has a wide variety of biological *** found that PB significantly down-regulatedβ-amyloid(Aβ)secretion in N2a/APPsw ***,the underlying mechanisms are not well *** the current study,we investigated the changes in key enzymes involved inβ-amyloid precursor protein(APP)metabolism and other APP metabolites by treating N2a/APPsw cells with PB at different *** results indicated that PB reduced Aβ secretion,which was caused by down-regulation of β-secretase(BACE1)expression,as indicated at both the protein and mRNA *** research revealed that PB regulated BACE1 expression by inducing the activation of forkhead box O1(FoxO1)and inhibiting the phosphorylation of signal transducer and activator of transcription 3(stat3).In addition,the effect of PB on BACE1 expression and Aβsecretion was reversed by treatment with FoxO1 siRNA and stat3 antagonist *** conclusion,these data demonstrated that PB can effectively down-regulate the expression of BACE1 to reduce Aβsecretion by activating the expression of FoxO1 and inhibiting the phosphorylation of stat3.

关键词： Physalin B β-amyloid BACE1 FoxO1 Alzheimer’s disease

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Osteopontin Promotes Macrophage M1 Polarization by Activation of the JAK1/stat1/HMGB1 Signaling Pathway in Nonalcoholic Fatty Liver Disease

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Journal of Clinical and Translational Hepatology 2023年第2期11卷 273-283页

作者： Zhihao Xu Feiyang Xi Xinxin Deng Yuqi Ni Changqin Pu Dan Wang Weiming Lou Xufang Zeng Ning Su Chen Chen Ziqiang Zeng Libin Deng Meixiu Jiang The Institute of Translational Medicine Nanchang UniversityNanchangJiangxiChina school of Pharmacy Nanchang UniversityNanchangJiangxiChina Central Laboratory Affiliated Jinhua HospitalZhejiang University School of MedicineJinhuaZhejiangChina Jiangxi Provincial Key Laboratory of Preventive Medicine School of Public HealthNanchang UniversityNanchangJiangxiChina school of Basic Medical Science Nanchang UniversityNanchangJiangxiChina

Background and Aims:Osteopontin(OPN)is reported to be associated with the pathogenesis of nonalcoholic fatty liver disease(NAFLD).However,the function of OPN in NAFLD is still ***,our aim in this study was to evaluate the role of OPN in NAFLD and clarify the involved ***:We analyzed the expression change of OPN in NAFLD by bioinformatic analysis,qRT-PCR,western blotting and immunofluorescence *** clarify the role of OPN in NAFLD,the effect of OPN from HepG2 cells on macrophage polarization and the involved mechanisms were examined by FACS and western ***:OPN was significantly upregulated in NAFLD patients compared with normal volunteers by microarray data,and the high expression of OPN was related with disease stage and *** level was also significantly increased in liver tissue samples of NAFLD from human and mouse,and in HepG2 cells treated with oleic acid(OA).Furthermore,the supernatants of OPN-treated HepG2 cells promoted the macrophage M1 ***,OPN activated the janus kinase 1(JAK1)/signal transducers and activators of transcription 1(stat1)signaling pathway in HepG2 cells,and consequently HepG2 cells secreted more high-mobility group box 1(HMGB1),thereby promoting macrophage M1 ***:OPN promoted macrophage M1 polarization by increasing JAK1/stat1-induced HMGB1 secretion in hepatocytes.

关键词： OPN NAFLD Macrophage M1 polarization HMGB1 JAK1/stat1 signaling

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Nanoparticle-linked antagonist for leptin signaling inhibition in breast cancer

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World Journal of Clinical Oncology 2017年第1期8卷 54-66页

作者： Tia Harmon Adriana Harbuzariu Viola Lanier Crystal C Lipsey Ward Kirlin Lily Yang Ruben R Gonzalez-Perez Department of Microbiology Biochemistry and Immunology Morehouse School of Medicine Department of Pathology and Laboratory Medicine Emory University School of Medicine

AIM To develop a leptin peptide receptor antagonist linked to nanoparticles and determine its effect on viability of breast cancer *** The leptin antagonist, LPrA2, was coupled via EDAC [1-Ethyl-3-(3-dimethylaminopropyl)carbodiimide] to iron oxide nanoparticles(IONP-LPrA2) to increase its ***-LPrA2 conjugation was confirmed by Western blot and nanoparticle tracking *** triple negative breast cancer(TNBC) MDA-MB-231, HCC1806 and estrogen receptor positive(ER+) MCF-7 cells were analyzed for the expression of the leptin receptor, *** effects of leptin and antagonist on levels of leptin-induced stat3 phosphorylation and cyclin D1, cell cycle progression, cell proliferation, and tumorsphere formation in breast cancer cells were *** of the chemotherapeutics [cisplatin(Cis), cyclophosphamide(CTX), doxorubicin(Dox) and paclitaxel(PTX)] to effectively reduce cell viability were *** effects of combination treatments of IONP-LPrA2 and chemotherapeutics on cell viability were *** Western blot analysis of coupling reaction products identified IONP-LPrA2 at approximately 100 ***2 significantly decreased leptin-induced p stat3 levels in HCC1806 cells and drastically decreased cyclin D1 levels in all cell ***-LPrA2 significantly reduced leptin-induced S phase progression and cell proliferation in all breast cancer cell lines and the formation of tumorspheres in MDA-MB-231 ***, IONP-LPrA2 showed an additive effect on the reduction of breast cancer cell survival with *** plus IONP-LPrA2 produced a significant reduction in the survival of MDA-MB-231 and HCC1806 *** plus IONP-LPrA2 caused a significant decrease in the survival of MDA-MB-231 *** plus IONP-LPrA2 caused a marked reduction in the survival of HCC1806 ***, PTX plus IONP-LPrA2 did not have a major effect on the viability of the breast cancer cells when compared to PTX *** Prese

关键词： Triple negative breast cancer Obesity Leptin Leptin peptide receptor antagonist 2 Iron oxide nanoparticles Chemotherapy adjuvant

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Rational fusion design inspired by cell-penetrating peptide:SS31/S-14 G Humanin hybrid peptide with amplified multimodal efficacy and bio-permeability for the treatment of Alzheimer’s disease

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Asian Journal of Pharmaceutical Sciences 2024年第4期19卷 128-143页

作者： Kang Qian Peng Yang Yixian Li RanMeng Yunlong Cheng Lingling Zhou Jing Wu Shuting Xu Xiaoyan Bao Qian Guo Pengzhen Wang Minjun Xu Dongyu Sheng Qizhi Zhang Key Laboratory of Smart Drug Delivery Ministry of EducationSchool of PharmacyFudan UniversityShanghai 201203China school of Pharmaceutical Sciences Wenzhou Medical UniversityWenzhou 325035China

Alzheimer’s disease is a neurodegenerative disease induced by multiple interconnected *** drug candidates with multi-modal efficacy generated from fusion strategy are suitable for addressing multi-facet ***,clinical translation of peptide drugs is greatly hampered by their low permeability into ***,a hybrid peptide HNSS is generated by merging two therapeutic peptides(SS31 and S-14 G Humanin(HNG)),using a different approach from the classical shuttle-therapeutic peptide conjugate *** demonstrated increased bio-permeability,with a 2-fold improvement in brain distribution over HNG,thanks to its structure mimicking the design of signal peptide-derived cell-penetrating *** efficiently alleviated mitochondrial dysfunction through the combined effects of mitochondrial targeting,ROS scavenging and p-stat3 ***,HNSS with increased Aβaffinity greatly inhibited Aβoligomerization/fibrillation,and interrupted Aβinteraction with neuron/microglia by reducing neuronal mitochondrial Aβdeposition and promoting microglial phagocytosis of Aβ.In3×Tg-AD transgenic mice,HNSS treatment efficiently inhibited brain neuron loss and improved the cognitive *** work validates the rational fusion design-based strategy for bio-permeability improvement and efficacy amplification,providing a paradigm for developing therapeutic peptide candidates against neurodegenerative disease.

关键词： Hybrid peptide S-14 G Humanin SS31 Permeability Aβ Alzheimer’s disease

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Prediction model of air infiltration in single-zone buildings with high airtightness

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Energy and Built Environment 2023年第6期4卷 653-668页

作者： Yongming Ji Lin Duanmu Songtao Hu school of Environmental and Municipal Engineering Qingdao University of TechnologyQingdaoShandong Province 266033China school of Civil Engineering Dalian University of TechnologyDalianLiaoning Province 116024China

Air infiltration through building envelopes has a considerable impact on the comprehensive performance of build-ings,especially in terms of their energy demand and indoor air ***,it is important to accurately predict building air infiltration rates under various *** airtightness is one of the typical character-istics of passive ultra-low energy *** the rapid application of passive technology in building energy efficiency,the airtightness of new urban buildings has been significantly *** centralized air leakage path distribution assumption of current prediction model for building air infiltration rate is inconsistent with the actual situation of high airtightness buildings,which reduces its prediction accuracy and application ***,it is of great practical significance and academic value to carry out the research on the prediction model of air infiltration rate of buildings with high *** paper presents an air infiltration prediction model for single-zone buildings with adventitious *** building envelope was broken down into permeable parts and impermeable parts,and the air leakage path-ways were assumed to be uniformly and continuously distributed in the permeable envelope.A linear pressure distribution over the building facade was assumed,and the airflow rate was integrated in the vertical and hori-zontal planes to theoretically predict the air infiltration *** feasibility of the proposed model was tested by comparing the air infiltration rates simulated by this model with those determined using the tracer gas attenua-tion method of an airtight *** initial test results suggest that this model is mathematically robust and is capable of modeling the air infiltration of a building in a wide variety of *** agreement was found between the tested and simulated *** study can provide basic theoretical support for the coupling performance analysis of high air

关键词： Prediction model Air infiltration Airtightness Natural ventilation Modeling

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Numerical Simulation of Blood Flow in Aorta with Dilation:A Comparison between Laminar and LES Modeling Methods

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Computer Modeling in Engineering & Sciences 2020年第8期124卷 509-526页

作者： Lijian Xu Tianyang Yang Lekang Yin Ye Kong Yuri Vassilevski Fuyou Liang school of Naval Architecture Ocean and Civil EngineeringShanghai Jiao Tong UniversityShanghai200240China Shanghai Chest Hospital Shanghai Jiao Tong UniversityShanghai200030China Zhongshan Hospital Fudan UniversityShanghai200032China Marchuk Institute of Numerical mathematics Russian Academy of SciencesMoscow119333Russia Institute for Personalized Medicine Sechenov UniversityMoscow119991Russia Key Laboratory of Hydrodynamics(Ministry of Education) Shanghai Jiao Tong UniversityShanghai200240China

Computational modeling methods have been increasingly employed to quantify aortic hemodynamic parameters that are challenging to in vivo measurements but important for the diagnosis/treatment of aortic *** the presence of turbulence-like behaviors of blood flow in normal or diseased aorta has long been confirmed,the majority of existing computational model studies adopted the laminar flow assumption(LFA)in the treatment of sub-grid flow *** far,it remains unclear whether LFA would significantly compromise the reliability of hemodynamic *** the present study,we addressed the issue in the context of a specific aortopathy,namely aortic dilation,which is usually accompanied by disturbed flow *** patient-specific aortas with treated/untreated dilation of the ascending segment were investigated,and their geometrical models were reconstructed from computed tomography angiographic images,with the boundary conditions being prescribed based on flow velocity information measured in vivo with the phase contrast magnetic resonance imaging *** the modeling of blood flow,apart from the traditional LFA-based method in which sub-grid flow dynamics is ignored,the large eddy simulation(LES)method capable of incorporating the dissipative energy loss induced by turbulent eddies at the sub-grid level,was adopted and taken as a reference for examining the performance of the LFA-based *** results showed that the simulated large-scale flow patterns with the two methods had high similarity,both agreeing well with in vivo measurements,although locally large between-method discrepancies in computed hemodynamic quantities existed in regions with high intensity of flow ***,a switch from the LES to the LFAbased modeling method led to mild(stat

关键词： Blood flow aortic dilation computational modeling turbulence laminar flow assumption large eddy simulation

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Role of Epstein-Barr Virus Encoded Latent Membrane Protein 1 in the Carcinogenesis of Nasopharyngeal Carcinoma

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Cellular & Molecular Immunology 2007年第3期4卷 185-196页

作者： Hui Zheng Lili Li Duosha Hu Xiyun Deng Ya Cao Cancer Research Institute Xiangya School of Medicine Central South University Changsha Hunan China

Epstein-Barr virus （EBV）-encoded latent membrane protein 1 （LMPI） has been known to have oncogenic properties during latent infection in nasopharyngeal carcinoma （NPC）. Our studies focused on the role of LMP1 in NPC, and showed that LMP1 triggers the NF-κB, AP-1 and stat signaling pathways. Strikingly, LMP1 was found to mediate the formation of a new heterodimer between c-Jun and JunB. Also, we have identified JAK/stat and PI-PLC-PKC activation triggered by LMP1 through upregulating the expression of JAK3 and enhancing the phosphorylation of stato The constitutive activation of these signaling cascades explains LMP1＇s ability to induce such a diverse array of morphological and phenotypic effects in cells and provides insight into how LMP1 may induce cell transformation, in which multihit targeted genes in the downstream play an essential role. All signaling cascades triggered by LMP1 ultimately lead to the disruption of the cell cycle： the acceleration of G1/S phase and the arrest of G2/M phase. We also found that LMP1 induced the expression of hTERT and promoted cell immortalization. Importantly, by intervening physical intracellular signal transduction pathways and disturbing the progression of the cell cycle, LMP1, an important oncoprotein encoded by EBV, is thought to be a key modulator in the pathogenesis of NPC. Interfering LMP1 signaling could be a promising strategy to target the malignant phenotype of NPC. Cellular ＆ Molecular Immunology.

关键词： latent membrane protein 1 nasopharyngeal carcinoma signal transduction

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Signal transducer and activator of transcription 3 promotes the Warburg effect possibly by inducing pyruvate kinase M2 phosphorylation in liver precancerous lesions

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World Journal of Gastroenterology 2019年第16期25卷 1936-1949页

作者： Yang-Hui Bi Wen-Qi Han Ruo-Fei Li Yun-Jiao Wang Zun-Shu Du Xue-Jiang Wang Ying Jiang Department of Physiology and Pathophysiology School of Basic Medical Sciences Capital Medical University

BACKGROUND Study shows that signal transducer and activator of transcription 3(stat3) can increase the Warburg effect by stimulating hexokinase 2 in breast cancer and upregulate lactate dehydrogenase A and pyruvate dehydrogenase kinase 1 in myeloma. stat3 and pyruvate kinase M2(PKM2) can also be activated and enhance the Warburg effect in hepatocellular carcinoma. Precancerous lesions are critical to human and rodent hepatocarcinogenesis. However, the underlying molecular mechanism for the development of liver precancerous lesions remains unknown. We hypothesized that stat3 promotes the Warburg effect possibly by upregulating p-PKM2 in liver precancerous lesions in *** To investigate the mechanism of the Warburg effect in liver precancerous lesions in *** A model of liver precancerous lesions was established by a modified Solt-Farber method. The liver pathological changes were observed by HE staining and immunohistochemistry. The transformation of WB-F344 cells induced with Nmethyl-N'-nitro-N-nitrosoguanidine and hydrogen peroxide was evaluated by the soft agar assay and aneuploidy. The levels of glucose and lactate in the tissue and culture medium were detected with a spectrophotometer. The protein levels of glutathione S-transferase-π, proliferating cell nuclear antigen(PCNA), stat3,and PKM2 were examined by Western blot and *** We found that the Warburg effect was increased in liver precancerous lesions in rats. PKM2 and p-stat3 were upregulated in activated oval cells in liverprecancerous lesions in rats. The Warburg effect, p-PKM2, and p-stat3 expression were also increased in transformed WB-F344 cells. stat3 activation promoted the clonal formation rate, aneuploidy, alpha-fetoprotein expression,PCNA expression, G1/S phase transition, the Warburg effect, PKM2 phosphorylation, and nuclear translocation in transformed WB-F344 ***, the Warburg effect was inhibited by stattic, a specific inhibitor of stat3, and furthe

关键词： Warburg effect Hepatic progenitor cell Signal transducer and activator of transcription 3 Pyruvate kinase M2 Liver precancerous lesion

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The Life-Cycle Model with Optimal Individual Years of schooling and Simulation

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数学计算（中英文版） 2014年第2期3卷 44-48页

作者： Donghan Cai Huan Yang Zhongbin Chen College of Math. & stat. Wuhan Univ. Wuhan 430072 PR. China school of Econ. & Management Wuhan Univ. Wuhan 430072 P.R. China

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SENP1 regulates IFN-γ-stat1 signaling throug stat3-SOCS3 negative feedback loop

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Journal of Molecular Cell Biology 2017年第2期9卷 144-153页

作者： Tingting Yu Yong Zuo Rong Cai Xian Huang Shuai Wu Chenxi Zhang Y. Eugene Chin Dongdong Li Zhenning Zhang Nansong Xia Qi Wang Hao Shen Xuebiao Yao Zhong-Yin Zhang Song Xue Lei Shen Jinke Cheng Department of Biochemistry and Molecular Cell Biology Shanghai Key Laboratory for Tumor Microenvironment and Inflammation Shanghai Jiao Tong University School of Medicine Shanghai 200025 China Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education Shanghai Jiao Tong University School of Medicine Shanghai 200025 China Department of Developmental Genetics School of Basic Medical Sciences Nanjing Medical University Nanjing 211166 China Shanghai Institute of Immunology Shanghai Jiao Tong University School of Medicine Shanghai 200025 China Institute of Health Sciences Chinese Academy of Sciences Shanghai Jiao Tong University School of Medicine Shanghai 200025 China Department of Microbiology University of Pennsylvania Perelman School of Medicine Philadelphia PA 19104 USA Anhui Key Laboratory of Cellular Dynamics Hefei National Laboratory for Physical Sciences at Nanoscale University of Science and Technology of ChinaHefei 230026 China Department of Biochemistry and Molecular Biology Indiana University School of Medicine Indianapolis IN 46202 USA Shanghai Renji Hospital Affiliated to Shanghai Jiao Tong University school of Medicine Shanghai 200127 China

Interferon-γ （IFN-γ） triggers macrophage for inflammation response by activating the intracellular JAK-stat1 signaling. Suppressor of cytokine signaling 1 （SOCS1） and protein tyrosine phosphatases can negatively modulate IFN-γ signaling. Here, we identify a novel negative feedback loop mediated by stat3-SOCS3, which is tightly controlled by SENP1 via de-SUMOylation of protein tyrosine phosphatase 1B （PTPIB）, in IFN-y signaling. SENP1-deficient macrophages show defects in IFN-γ signaling and M1 macrophage activation. PTP1B in SENP1-deficient macrophages is highly SUMOylated, which reduces PTP1B-induced de-phosphorylation of stat3. Activated stat3 then suppresses stat1 activation via SOCS3 induction in SENP1-deficient macro- phages. Accordingly, SENP1-deficient macrophages show reduced ability to resist Listerio rnonocytogenes infection. These results reveal a crucial role of SENP1-controlled stat1 and stat3 balance in rnacrophage polarization.

关键词： IFN-γ macrophage SENP1 SUMOylation

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