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  1. Article ; Online: Ferroptosis Mediates Pulmonary Fibrosis: Implications for the Effect of

    Wen, Jing / Wang, Cui / Song, Li-Yun / Wang, Yin-Ying / Liang, Peng-Tao / Pang, Wen-Lin / Yin, Wen / Zhang, Qiang / Zhao, Wei-Tian / Sun, Xue-Ping / Yan, Jin-Yuan / Yang, Zhong-Shan

    Canadian respiratory journal

    2024  Volume 2024, Page(s) 5554886

    Abstract: Objective: To investigate the mechanism through which : Materials and methods: First, the electromedical measurement systems were used to measure respiratory function in mice; the lungs were then collected for histological staining. Potential ... ...

    Abstract Objective: To investigate the mechanism through which
    Materials and methods: First, the electromedical measurement systems were used to measure respiratory function in mice; the lungs were then collected for histological staining. Potential pharmacologic targets were predicted via network pharmacology. Finally, tests including immunohistochemistry, reverse transcription-quantitative polymerase chain reaction, and western blotting were used to evaluate the relative expression levels of collagen, transforming growth factor
    Results: APD prevented the occurrence of restrictive ventilation dysfunction induced by ferroptosis. Extracellular matrix and collagen fiber deposition were significantly reduced when the APD group compared with the model group; furthermore, ferroptosis was attenuated, expression of PTGS2 and ACSL4 increased, and expression of GPX4 and SLC7A11 decreased. In the APD group, the candidates related to the mediation of ferroptosis (Hif-1
    MeSH term(s) Animals ; Mice ; Pulmonary Fibrosis/drug therapy ; Panax notoginseng ; Cyclooxygenase 2 ; Ferroptosis ; Collagen ; ErbB Receptors
    Chemical Substances Cyclooxygenase 2 (EC 1.14.99.1) ; Collagen (9007-34-5) ; ErbB Receptors (EC 2.7.10.1)
    Language English
    Publishing date 2024-03-29
    Publishing country Egypt
    Document type Journal Article
    ZDB-ID 1213103-9
    ISSN 1916-7245 ; 1198-2241
    ISSN (online) 1916-7245
    ISSN 1198-2241
    DOI 10.1155/2024/5554886
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  2. Article ; Online: Astragalus polysaccharide protects experimental colitis through an aryl hydrocarbon receptor-dependent autophagy mechanism.

    Ying, Yi / Song, Li-Yun / Pang, Wen-Lin / Zhang, Si-Qi / Yu, Jing-Ze / Liang, Peng-Tao / Li, Tian-Gang / Sun, Yi / Wang, Yin-Ying / Yan, Jin-Yuan / Yang, Zhong-Shan

    British journal of pharmacology

    2023  Volume 181, Issue 5, Page(s) 681–697

    Abstract: Background and purpose: Disruption of intestinal barriers plays a vital role in the pathogenesis of colitis. The aryl hydrocarbon receptor (AhR) is a recognition sensor that mediates intestinal immune homeostasis and minimizes intestinal inflammation. ... ...

    Abstract Background and purpose: Disruption of intestinal barriers plays a vital role in the pathogenesis of colitis. The aryl hydrocarbon receptor (AhR) is a recognition sensor that mediates intestinal immune homeostasis and minimizes intestinal inflammation. Astragalus polysaccharide (APS) exerts pharmacological actions in colitis; however, the mechanism has not been elucidated. We investigated whether APS protects through AhR-dependent autophagy.
    Experimental approach: The symptoms of dextran sulfate sodium (DSS)-induced colitis in mice involving intestinal barrier function and inflammatory injury were evaluated after APS administration. Intestinal-specific Becn1 conditional knockout (Becn1 cKO) mice were constructed and compared with wild-type mice. Autophagy and the effects of APS were investigated after the deactivation of AhRs. The relationship between APS-induced AhRs and autophagic Becn1 was investigated using a dual-luciferase reporter system and chromatin immunoprecipitation (ChIP)-quantitative polymerase chain reaction assay. Caco-2 cells were used to investigate inflammatory responses and AhR-dependent autophagy.
    Key results: APS improved intestinal barrier function in inflammatory injury in colitis mice. APS triggered autophagic flow; however, knockout of Becn1 in the gut increased susceptibility to colitis, leading to diminished epithelial barrier function and severe intestinal inflammation, impairing the protective effects of APS. Mechanistically, APS-triggered autophagy depends on AhR expression. Activated AhR binds to the promoter Becn1 to operate transcription of genes involved in anti-inflammation and intestinal barrier repair, while deactivation of AhR correlated with intestinal inflammation and the therapeutic function of APS.
    Conclusions and implications: APS protects colitis mice by targeting autophagy, especially as the AhR stimulates the repair of damaged intestinal barrier functions.
    MeSH term(s) Animals ; Humans ; Mice ; Autophagy ; Caco-2 Cells ; Colitis/chemically induced ; Colitis/drug therapy ; Colitis/prevention & control ; Dextran Sulfate ; Disease Models, Animal ; Inflammation ; Mice, Inbred C57BL ; Polysaccharides/pharmacology ; Polysaccharides/therapeutic use ; Receptors, Aryl Hydrocarbon/genetics
    Chemical Substances Dextran Sulfate (9042-14-2) ; Polysaccharides ; Receptors, Aryl Hydrocarbon
    Language English
    Publishing date 2023-10-12
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1111/bph.16229
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  3. Article ; Online: Astragaloside trigger autophagy: Implication a potential therapeutic strategy for pulmonary fibrosis.

    Yu, Jing-Ze / Wen, Jing / Ying, Yi / Yin, Wen / Zhang, Si-Qi / Pang, Wen-Ling / Wang, Cui / Bian, Yao / Yuan, Jia-Li / Yan, Jin-Yuan / Yang, Zhong-Shan

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    2022  Volume 154, Page(s) 113603

    Abstract: Pulmonary fibrosis is an abnormal wound-healing response to repeated alveolar injury, characterized by continuous inflammation and abnormal collagen deposition. Its treatment is problematic. Astragaloside (AST) is an active component of Astragalus ... ...

    Abstract Pulmonary fibrosis is an abnormal wound-healing response to repeated alveolar injury, characterized by continuous inflammation and abnormal collagen deposition. Its treatment is problematic. Astragaloside (AST) is an active component of Astragalus membranaceus with anti-inflammatory and anti-tumor properties. Although the underlying mechanisms are unknown, AST is also used to treat fibrotic diseases. This study aimed to investigate the mechanisms of action of AST in pulmonary fibrosis treatment. We found that AST significantly improved restrictive ventilatory impairment, compliance, total lung capacity, and functional residual capacity. In mice with pulmonary fibrosis, extracellular matrix deposition in the pulmonary parenchyma and intemperate inflammation were reversed. This therapeutic effect can be attributed to autophagy, activating the genes for autophagy flux and autophagic vacuoles. Impaired autophagy increased susceptibility to pulmonary fibrosis by exacerbating collagen deposition in vitro and in vivo. Using a combination of molecular docking and network pharmacology, the Ras/Raf/MEK/ERK signaling pathway was identified as a possible candidate for the pharmacologic target of AST. Functional dephosphorylation of MEK and ERK inhibited the Ras/Raf/MEK/ERK signaling pathway, which converges at the rapamycin switch to initiate autophagy. Inhibitors of Ras and MEK regulated autophagy. These findings suggest that AST might treat pulmonary fibrosis by modulating the Ras/Raf/MEK/ERK signaling pathway mediated by depression.
    MeSH term(s) Mice ; Animals ; Pulmonary Fibrosis/drug therapy ; Molecular Docking Simulation ; MAP Kinase Signaling System ; Mitogen-Activated Protein Kinase Kinases/metabolism ; Autophagy ; Inflammation ; Collagen/metabolism
    Chemical Substances Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; Collagen (9007-34-5)
    Language English
    Publishing date 2022-09-07
    Publishing country France
    Document type Journal Article
    ZDB-ID 392415-4
    ISSN 1950-6007 ; 0753-3322 ; 0300-0893
    ISSN (online) 1950-6007
    ISSN 0753-3322 ; 0300-0893
    DOI 10.1016/j.biopha.2022.113603
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  4. Article ; Online: Induction of autophagy via the TLR4/NF-κB signaling pathway by astragaloside Ⅳ contributes to the amelioration of inflammation in RAW264.7 cells.

    Ying, Yi / Sun, Chun-Bin / Zhang, Si-Qi / Chen, Bo-Jun / Yu, Jing-Ze / Liu, Fei-Yu / Wen, Jing / Hou, Jiong / Han, Si-Si / Yan, Jin-Yuan / Yang, Zhong-Shan / Xiong, Lei

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    2021  Volume 137, Page(s) 111271

    Abstract: Cigarette smoking-related lung injury is one of the most common and fatal etiologies of many respiratory diseases, for which no effective interventions are available. Astragaloside Ⅳ (ASⅣ) is an active component extracted from Astragalus membranaceus. It ...

    Abstract Cigarette smoking-related lung injury is one of the most common and fatal etiologies of many respiratory diseases, for which no effective interventions are available. Astragaloside Ⅳ (ASⅣ) is an active component extracted from Astragalus membranaceus. It is prescribed as a treatment for upper respiratory tract infections. Here, we report the potential anti-inflammatory effects and mechanisms of ASⅣ on cigarette smoking extract- (CSE)-exposed RAW264.7 cells. Murine macrophages were exposed to CSE, followed by administration of ASⅣ at 25-100 μg/mL for 24 h. ASⅣ significantly rescued CSE-induced cell death by inhibition of release pro-inflammatory cytokines. We measured autophagy as an intracellular scavenger by analyzing autophagic flux using tandem mRFP-GFP-LC3 fluorescence microscopy. Following administration with ASⅣ in CSE-exposed RAW264.7 cells, there was a notable increase in autophagosomes and a range of autophagic vacuoles were generated, as seen with transmission electron microscopy. Loss of autophagy following transfection siRNA aggravated inflammatory injury and release of inflammatory cytokines. Mechanistically, ASⅣ-triggered autophagy is mediated by the TLR4/NF-κB signaling pathway to reduce inflammation. Taken together, our findings suggest that ASⅣ acts stimulates autophagy, and that ASⅣ induces autophagy by inhibiting the TLR4/NF-κB signaling pathway, contributing to alleviation of inflammation.
    MeSH term(s) Animals ; Anti-Inflammatory Agents/pharmacology ; Autophagy/drug effects ; Cytokines/metabolism ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/pathology ; Inflammation/prevention & control ; Macrophages/drug effects ; Macrophages/immunology ; Macrophages/metabolism ; Macrophages/ultrastructure ; Mice ; NF-kappa B/metabolism ; Phosphorylation ; RAW 264.7 Cells ; Saponins/pharmacology ; Signal Transduction ; Toll-Like Receptor 4/metabolism ; Triterpenes/pharmacology
    Chemical Substances Anti-Inflammatory Agents ; Cytokines ; NF-kappa B ; Saponins ; Tlr4 protein, mouse ; Toll-Like Receptor 4 ; Triterpenes ; astragaloside A (3A592W8XKE)
    Language English
    Publishing date 2021-02-06
    Publishing country France
    Document type Journal Article
    ZDB-ID 392415-4
    ISSN 1950-6007 ; 0753-3322 ; 0300-0893
    ISSN (online) 1950-6007
    ISSN 0753-3322 ; 0300-0893
    DOI 10.1016/j.biopha.2021.111271
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  5. Article ; Online: Gastrodia remodels intestinal microflora to suppress inflammation in mice with early atherosclerosis.

    Liu, Fei-Yu / Wen, Jing / Hou, Jiong / Zhang, Si-Qi / Sun, Chun-Bin / Zhou, Luo-Chuan / Yin, Wen / Pang, Wen-Lin / Wang, Cui / Ying, Yi / Han, Si-Si / Yan, Jin-Yuan / Li, Chen-Xi / Yuan, Jia-Li / Xing, Hai-Jing / Yang, Zhong-Shan

    International immunopharmacology

    2021  Volume 96, Page(s) 107758

    Abstract: Atherosclsis is a critical actuator causing cardiac-cerebral vascular disease with a complicated pathogeneon, refered to the disorders of intestinal flora and persistent inflammation. Gastrodin (4-(hydroxymethyl) phenyl-β-D- Glucopyranoside) is the most ... ...

    Abstract Atherosclsis is a critical actuator causing cardiac-cerebral vascular disease with a complicated pathogeneon, refered to the disorders of intestinal flora and persistent inflammation. Gastrodin (4-(hydroxymethyl) phenyl-β-D- Glucopyranoside) is the most abundant glucoside extracted from the Gastrodiaelata, which is a traditional Chinese herbal medicine for cardiac-cerebral vascular disease, yet its mechanisms remain little known. In the present study, the gastrodia extract and gastrodin attenuate the lipid deposition and foam cells on the inner membrane of the inner membrane of the thoracic aorta in the early atherosclerosis mice. Blood lipid detection tips that TC and LDL-C were reduced in peripheral blood after treatment with the gastrodia extract and gastrodin. Furthermore, unordered gut microbes are remodeled in terms of bacterial diversity and abundance at family and genus level. Also, the intestinal mucosa damage and permeability were reversed, accompaniedwith the reducing of inflammatory cytokines. Our findings revealed that the functions of gastrodia extract and gastrodin in cardiac-cerebral vascular disease involved to rescued gut microbes and anti-inflammation may be the mechanismof remission lipid accumulation.
    MeSH term(s) Acetic Acid/metabolism ; Animals ; Aorta/drug effects ; Aorta/metabolism ; Aorta/pathology ; Atherosclerosis/drug therapy ; Atherosclerosis/microbiology ; Atherosclerosis/pathology ; Benzyl Alcohols/pharmacology ; Benzyl Alcohols/therapeutic use ; Butyric Acid/metabolism ; Disease Models, Animal ; Drugs, Chinese Herbal/pharmacology ; Fatty Acids, Volatile/metabolism ; Gastrodia/chemistry ; Gastrointestinal Microbiome/drug effects ; Gastrointestinal Microbiome/genetics ; Glucosides/pharmacology ; Glucosides/therapeutic use ; Inflammation/drug therapy ; Inflammation/microbiology ; Intercellular Adhesion Molecule-1/blood ; Interleukin-1beta/blood ; Intestinal Mucosa/drug effects ; Intestinal Mucosa/pathology ; Lipids/blood ; Mice, Inbred C57BL ; Propionates/metabolism ; Tight Junction Proteins/metabolism ; Tumor Necrosis Factor-alpha/blood ; Mice
    Chemical Substances Benzyl Alcohols ; Drugs, Chinese Herbal ; Fatty Acids, Volatile ; Glucosides ; IL1B protein, mouse ; Interleukin-1beta ; Lipids ; Propionates ; Tight Junction Proteins ; Tumor Necrosis Factor-alpha ; Butyric Acid (107-92-6) ; Intercellular Adhesion Molecule-1 (126547-89-5) ; gastrodin (5YS9U2W3RQ) ; propionic acid (JHU490RVYR) ; Acetic Acid (Q40Q9N063P)
    Language English
    Publishing date 2021-05-24
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 2043785-7
    ISSN 1878-1705 ; 1567-5769
    ISSN (online) 1878-1705
    ISSN 1567-5769
    DOI 10.1016/j.intimp.2021.107758
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  6. Article ; Online: Antifibrotic action of Yifei Sanjie formula enhanced autophagy via PI3K-AKT-mTOR signaling pathway in mouse model of pulmonary fibrosis.

    Yu, Jing-Ze / Ying, Yi / Liu, Yang / Sun, Chun-Bin / Dai, Chen / Zhao, Shan / Tian, Shou-Zheng / Peng, Jing / Han, Ni-Ping / Yuan, Jia-Li / Yan, Jin-Yuan / Yang, Zhong-Shan

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    2019  Volume 118, Page(s) 109293

    Abstract: Pulmonary fibrosis (PF) is a crippling disease characterized by progressive dyspnea and associated with a high mortality rate, but its origin is unknown and there is no effective treatment. Yifei Sanjie formula (YFSJF) is a Chinese medicine that is ... ...

    Abstract Pulmonary fibrosis (PF) is a crippling disease characterized by progressive dyspnea and associated with a high mortality rate, but its origin is unknown and there is no effective treatment. Yifei Sanjie formula (YFSJF) is a Chinese medicine that is widely used for treatment of respiratory systems disease. However, the molecular basis for the function of YFSJF has not been determined. Here we investigate the contribution of YFSJF in BLM-induced PF mice. Administration with YFSJF significantly alleviated the degree of BLM-induced collagen I and III deposition and the inflammatory injuring in the lungs and suppressed hydroxyproline release in PF animals. The active components of YFSJF are comprised with flavonoid, amino acids, saponins, oligosaccharide, organic acid, vitamin, esters, purine nucleosides. Additionally, there was a significant increase in autophagosomes, after treatment with YFSJF in PF animals. Interestingly, autophagy dysfunction by the blocker chloroquine (CQ) resulted in collagen deposition and inducing the expression of fibrosis-related genes. In addition, YFSJF-induced autophagy is mediated by the PI3K-AKT-mTOR pathway, and knockdown of PI3K by siRNA up-regulated the expression of autophagy-related genes and down-regulated the expression of collagen in human lung fibroblasts (HLF). Our findings provide a detailed understanding that YFSJF-antifibrotic effects are mainly mediated by triggering autophagy, and suppressing phosphorylation of the PI3K-AKT-mTOR pathway is required for YFSJF-curative effect.
    MeSH term(s) Animals ; Autophagosomes/metabolism ; Autophagosomes/ultrastructure ; Autophagy/drug effects ; Collagen/metabolism ; Disease Models, Animal ; Drugs, Chinese Herbal ; Humans ; Inflammation/complications ; Inflammation/pathology ; Lung/pathology ; Male ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphorylation/drug effects ; Proto-Oncogene Proteins c-akt/metabolism ; Pulmonary Fibrosis/complications ; Pulmonary Fibrosis/drug therapy ; Pulmonary Fibrosis/metabolism ; Pulmonary Fibrosis/pathology ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism ; Transforming Growth Factor beta1/metabolism
    Chemical Substances Drugs, Chinese Herbal ; Transforming Growth Factor beta1 ; Collagen (9007-34-5) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2019-08-08
    Publishing country France
    Document type Journal Article
    ZDB-ID 392415-4
    ISSN 1950-6007 ; 0753-3322 ; 0300-0893
    ISSN (online) 1950-6007
    ISSN 0753-3322 ; 0300-0893
    DOI 10.1016/j.biopha.2019.109293
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  7. Article: Anti-inflammatory effect of Yu-Ping-Feng-San

    Yang, Zhong-Shan / Yan, Jin-Yuan / Han, Ni-Ping / Zhou, Wei / Cheng, Yu / Zhang, Xiao-Mei / Li, Ning / Yuan, Jia-Li

    Iranian journal of basic medical sciences

    2016  Volume 19, Issue 9, Page(s) 993–1002

    Abstract: Objectives: Yu-Ping-Feng-San (YPFS) is a classical traditional Chinese medicine that is widely used for treatment of the diseases in respiratory systems, including chronic obstructive pulmonary disease (COPD) recognized as chronic inflammatory disease. ... ...

    Abstract Objectives: Yu-Ping-Feng-San (YPFS) is a classical traditional Chinese medicine that is widely used for treatment of the diseases in respiratory systems, including chronic obstructive pulmonary disease (COPD) recognized as chronic inflammatory disease. However, the molecular mechanism remains unclear. Here we detected the factors involved in transforming growth factor beta 1 (TGF-β1)/Smad2 signaling pathway and inflammatory cytokines, to clarify whether YPFS could attenuate inflammatory response dependent on TGF-β1/Smad2 signaling in COPD rats or cigarette smoke extract (CSE)-treated human bronchial epithelial (Beas-2B) cells.
    Materials and methods: The COPD rat model was established by exposure to cigarette smoke and intratracheal instillation of lipopolysaccharide, YPFS was administered to the animals. The efficacy of YPFS was evaluated by comparing the severity of pulmonary pathological damage, pro-inflammation cytokines, collagen related genes and the activation of TGF-β1/Smad2 signaling pathway. Furthermore, CSE-treated cells were employed to confirm whether the effect of YPFS was dependent on the TGF-β1/Smad2 signaling via knockdown Smad2 (Si-RNA), or pretreatment with the inhibitor of TGF-β1.
    Results: Administration of YPFS effectively alleviated injury of lung, suppressed releasing of pro-inflammatory cytokines and collagen deposition in COPD animals (
    Conclusion: YPFS accomplished anti-inflammatory effects mainly by suppressing phosphorylation of Smad2, TGF-β1/Smad2 signaling pathway was required for YPFS-mediated anti-inflammation in COPD rats or CSE-treated Beas-2B cells.
    Language English
    Publishing date 2016-10-17
    Publishing country Iran
    Document type Journal Article
    ZDB-ID 2500485-2
    ISSN 2008-3874 ; 2008-3866
    ISSN (online) 2008-3874
    ISSN 2008-3866
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  8. Article ; Online: Pseudomonas toxin pyocyanin triggers autophagy: Implications for pathoadaptive mutations.

    Yang, Zhong-Shan / Ma, Lan-Qing / Zhu, Kun / Yan, Jin-Yuan / Bian, Li / Zhang, Ke-Qin / Zou, Cheng-Gang

    Autophagy

    2016  Volume 12, Issue 6, Page(s) 1015–1028

    Abstract: Pseudomonas aeruginosa can establish life-long chronic infection in patients with cystic fibrosis by generating genetic loss-of-function mutations, which enhance fitness of the bacterium in the airways. However, the precise role of the pathoadaptive ... ...

    Abstract Pseudomonas aeruginosa can establish life-long chronic infection in patients with cystic fibrosis by generating genetic loss-of-function mutations, which enhance fitness of the bacterium in the airways. However, the precise role of the pathoadaptive mutations in persistence in chronic airways infection remains largely unknown. Here we demonstrate that pyocyanin, a well-described P. aeruginosa virulence factor that plays an important role in the initial infection, promotes autophagy in bronchial epithelial cells. Disruption of phzM, which is required for pyocyanin biosynthesis, leads to a significant reduction in autophagy in Beas-2B cells and lung tissues. Pyocyanin-induced autophagy is mediated by the EIF2AK4/GCN2-EIF2S1/eIF2α-ATF4 pathway. Interestingly, rats infected with the phzMΔ mutant strain have high mortality rate and numbers of colony-forming units, compared to those infected with wild-type (WT) P. aeruginosa PA14 strain, during chronic P. aeruginosa infection. In addition, the phzMΔ mutant strain induces more extensive alveolar wall thickening than the WT strain in the pulmonary airways of rats. As autophagy plays an essential role in suppressing bacterial burden, our findings provide a detailed understanding of why reduction of pyocyanin production in P. aeruginosa in chronic airways infections has been associated with better host adaptation and worse outcomes in cystic fibrosis.
    MeSH term(s) Adaptation, Physiological ; Animals ; Autophagosomes/drug effects ; Autophagosomes/metabolism ; Autophagy/drug effects ; Bacterial Toxins/chemistry ; Bacterial Toxins/pharmacology ; Bronchi/pathology ; Chronic Disease ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Epithelial Cells/ultrastructure ; Humans ; Inflammation/complications ; Inflammation/pathology ; Mutation/genetics ; Pneumonia/complications ; Pneumonia/microbiology ; Pneumonia/pathology ; Pseudomonas/metabolism ; Pseudomonas Infections/complications ; Pseudomonas Infections/microbiology ; Pseudomonas Infections/pathology ; Pyocyanine/chemistry ; Pyocyanine/pharmacology ; Rats, Sprague-Dawley ; Signal Transduction/drug effects
    Chemical Substances Bacterial Toxins ; Pyocyanine (9OQM399341)
    Language English
    Publishing date 2016-05-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2016.1170256
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Y55 and D78 are crucial amino acid residues of a new IgE epitope on trichosanthin.

    Zhang, Xin-Yue / Wu, Ye / Yan, Jin-Yuan / Gao, Yin / Wang, Ye / Mi, Shuang-Li / An, Cheng-Cai

    Biochemical and biophysical research communications

    2006  Volume 343, Issue 4, Page(s) 1251–1256

    Abstract: Trichosanthin (TCS) possesses many biological and pharmaceutical activities, but its strong immunogenicity limits its clinical application. To reduce the immunogenicity of TCS, we modified the reported method for the prediction of antigenic site and ... ...

    Abstract Trichosanthin (TCS) possesses many biological and pharmaceutical activities, but its strong immunogenicity limits its clinical application. To reduce the immunogenicity of TCS, we modified the reported method for the prediction of antigenic site and identified two crucial amino acid residues (Y55 and D78) for a new epitope. We mutated these two residues into glycine and serine, respectively, and obtained three mutants, Y55G, D78S, and Y55G/D78S. These mutants induced less amount of Ig and IgG antibodies in C57BL/6J mice than wild-type TCS (wTCS) (p<0.01) and almost lost the ability to induce IgE antibody production. The mutants stimulated fewer TCS-specific B cells in C57BL/6J mice than wTCS (p<0.01). Compared with wTCS, Y55G, D78S, and Y55G/D78S lost 26.9%, 17.9%, and 98.7% specific binding ability to anti-TCS monoclonal antibody TCS4E9, respectively. These mutants still retained RNA N-glycosidase activity. In conclusion, Y55 and D78 are two crucial amino acid residues of a new IgE epitope on TCS, and their mutation reduces the immunogenicity of TCS, but still retained the enzymatic activity.
    MeSH term(s) Amino Acid Substitution ; Amino Acids/genetics ; Amino Acids/immunology ; Animals ; B-Lymphocytes/immunology ; Epitopes ; Immunoglobulin E/blood ; Immunoglobulin E/immunology ; Immunoglobulin G/blood ; Immunoglobulins/blood ; Lymphocyte Activation ; Male ; Mice ; Mice, Inbred C57BL ; Models, Molecular ; Mutagenesis, Site-Directed ; N-Glycosyl Hydrolases/metabolism ; Ribosome Inactivating Proteins ; Trichosanthin/genetics ; Trichosanthin/immunology
    Chemical Substances Amino Acids ; Epitopes ; Immunoglobulin G ; Immunoglobulins ; Immunoglobulin E (37341-29-0) ; Trichosanthin (60318-52-7) ; N-Glycosyl Hydrolases (EC 3.2.2.-) ; Ribosome Inactivating Proteins (EC 3.2.2.22)
    Language English
    Publishing date 2006-05-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 205723-2
    ISSN 0006-291X ; 0006-291X
    ISSN (online) 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2006.03.097
    Database MEDical Literature Analysis and Retrieval System OnLINE

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