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Xi</title> <meta name="description" content="Search results for: Yongyong Xi"> <meta name="keywords" content="Yongyong Xi"> <meta name="viewport" content="width=device-width, initial-scale=1, minimum-scale=1, maximum-scale=1, user-scalable=no"> <meta charset="utf-8"> <link href="https://cdn.waset.org/favicon.ico" type="image/x-icon" rel="shortcut icon"> <link href="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/css/bootstrap.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/plugins/fontawesome/css/all.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/css/site.css?v=150220211555" rel="stylesheet"> </head> <body> <header> <div class="container"> <nav class="navbar navbar-expand-lg navbar-light"> <a class="navbar-brand" href="https://waset.org"> <img src="https://cdn.waset.org/static/images/wasetc.png" alt="Open Science Research Excellence" title="Open Science Research Excellence" /> </a> <button class="d-block d-lg-none navbar-toggler ml-auto" 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id="custom-search-input"> <div class="input-group"> <i class="fas fa-search"></i> <input type="text" class="search-query" name="q" placeholder="Author, Title, Abstract, Keywords" value="Yongyong Xi"> <input type="submit" class="btn_search" value="Search"> </div> </div> </form> </div> </div> <div class="row mt-3"> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Commenced</strong> in January 2007</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Frequency:</strong> Monthly</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Edition:</strong> International</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Paper Count:</strong> 9</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: Yongyong Xi</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">9</span> Hsa-miR-139-5p Acts as a Tumor Suppressor by Targeting C-Met in Non-Small Cell Lung Cancer</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun">Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Feng%20Zhang"> Feng Zhang</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Hsa-miRNA-139-5p (miR-139-5p) has recently been discovered having anticancer efficacy in different organs. However, the role of miR-139-5p on lung cancer is still ambiguous. In this study, we investigated the role of miR-139-5p on development of lung cancer. Results indicated miR-139-5p was significantly down-regulated in primary tumor tissues and very low levels were found in a non-small cell lung cancer (NSCLC) cell lines. Ectopic expression of miR-139-5p in NSCLC cell lines significantly suppressed cell growth through inhibition of cyclin D1 and up-regulation of p57(Kip2). In addition, miR-139-5p induced apoptosis, as indicated by up-regulation of key apoptosis gene cleaved caspase-3, and down-regulation of anti-apoptosis gene Bcl2. Moreover, miR-139-5p inhibited cellular metastasis through inhibition of matrix metalloproteinases (MMP)-7 and MMP-9. Further, oncogene c-Met was revealed to be a putative target of miR-139-5p, which was inversely correlated with miR-139-5p expression. Taken together, our results demonstrated that miR-139-5p plays a pivotal role in lung cancer through inhibiting cell proliferation, metastasis, and promoting apoptosis by targeting oncogenic c-Met. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=hsa-miRNA-139-5p%20%28miR-139-5p%29" title="hsa-miRNA-139-5p (miR-139-5p)">hsa-miRNA-139-5p (miR-139-5p)</a>, <a href="https://publications.waset.org/abstracts/search?q=c-Met" title=" c-Met"> c-Met</a>, <a href="https://publications.waset.org/abstracts/search?q=non-small%20cell%20lung%20cancer%20%28NSCLC%29" title=" non-small cell lung cancer (NSCLC)"> non-small cell lung cancer (NSCLC)</a>, <a href="https://publications.waset.org/abstracts/search?q=proliferation" title=" proliferation"> proliferation</a>, <a href="https://publications.waset.org/abstracts/search?q=apoptosis" title=" apoptosis"> apoptosis</a> </p> <a href="https://publications.waset.org/abstracts/41708/hsa-mir-139-5p-acts-as-a-tumor-suppressor-by-targeting-c-met-in-non-small-cell-lung-cancer" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/41708.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">343</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">8</span> Hsa-miR-326 Functions as a Tumor Suppressor in Non-Small Cell Lung Cancer through Targeting CCND1</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Cheng-Cao%20Sun">Cheng-Cao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Shu-Jun%20Li"> Shu-Jun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Feng%20Zhang"> Feng Zhang</a>, <a href="https://publications.waset.org/abstracts/search?q=De-Jia%20Li"> De-Jia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Hsa-miRNA-326 (miR-326) has recently been discovered having anticancer efficacy in different organs. However, the role of miR-326 on non-small cell lung cancer (NSCLC) is still ambiguous. In this study, we investigated the role of miR-326 on the development of NSCLC. The results indicated that miR-326 was significantly down-regulated in primary tumor tissues and very low levels were found in NSCLC cell lines. Ectopic expression of miR-326 in NSCLC cell lines significantly suppressed cell growth as evidenced by cell viability assay, colony formation assay and BrdU staining, through inhibition of cyclin D1, cyclin D2, CDK4, and up-regulation of p57(Kip2) and p21(Waf1/Cip1). In addition, miR-326 induced apoptosis, as indicated by concomitantly with up-regulation of key apoptosis protein cleaved caspase-3, and down-regulation of anti-apoptosis protein Bcl2. Moreover, miR-326 inhibited cellular migration and invasiveness through inhibition of matrix metalloproteinases (MMP)-7 and MMP-9. Further, oncogene CCND1 was revealed to be a putative target of miR-326, which was inversely correlated with miR-326 expression in NSCLC. Taken together, our results demonstrated that miR-326 played a pivotal role on NSCLC through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic CCND1. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=hsa-miRNA-326%20%28miR-326%29" title="hsa-miRNA-326 (miR-326)">hsa-miRNA-326 (miR-326)</a>, <a href="https://publications.waset.org/abstracts/search?q=cyclin%20D1" title="cyclin D1">cyclin D1</a>, <a href="https://publications.waset.org/abstracts/search?q=non-small%20cell%20lung%20cancer%20%28NSCLC%29" title=" non-small cell lung cancer (NSCLC)"> non-small cell lung cancer (NSCLC)</a>, <a href="https://publications.waset.org/abstracts/search?q=proliferation" title=" proliferation"> proliferation</a>, <a href="https://publications.waset.org/abstracts/search?q=apoptosis" title=" apoptosis"> apoptosis</a> </p> <a href="https://publications.waset.org/abstracts/41380/hsa-mir-326-functions-as-a-tumor-suppressor-in-non-small-cell-lung-cancer-through-targeting-ccnd1" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/41380.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">306</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">7</span> LncRNA NEAT1 Promotes NSCLC Progression through Acting as a ceRNA of miR-377-3p</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun">Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Feng%20Zhang"> Feng Zhang</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Recently, the long non-coding RNA (lncRNA) NEAT1 has been identified as an oncogenic gene in multiple cancer types and elevated expression of NEAT1 was tightly linked to tumorigenesis and cancer progression. However, the molecular basis for this observation has not been characterized in progression of non-small cell lung cancer (NSCLC). In our studies, we identified NEAT1 was highly expressed in NSCLC patients and was a novel regulator of NSCLC progression. Patients whose tumors had high NEAT1 expression had a shorter overall survival than patients whose tumors had low NEAT1 expression. Further, NEAT1 significantly accelerates NSCLC cell growth and metastasis in vitro and tumor growth in vivo. Additionally, by using bioinformatics study and RNA pull down combined with luciferase reporter assays, we demonstrated that NEAT1 functioned as a competing endogenous RNA (ceRNA) for has-miR-377-3p, antagonized its functions and led to the de-repression of its endogenous targets E2F3, which was a core oncogene in promoting NSCLC progression. Taken together, these observations imply that the NEAT1 modulated the expression of E2F3 gene by acting as a competing endogenous RNA, which may build up the missing link between the regulatory miRNA network and NSCLC progression. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=long%20non-coding%20RNA%20NEAT1" title="long non-coding RNA NEAT1">long non-coding RNA NEAT1</a>, <a href="https://publications.waset.org/abstracts/search?q=hsa-miRNA-377-3p" title=" hsa-miRNA-377-3p"> hsa-miRNA-377-3p</a>, <a href="https://publications.waset.org/abstracts/search?q=E2F3" title=" E2F3"> E2F3</a>, <a href="https://publications.waset.org/abstracts/search?q=non-small%20cell%20lung%20cancer" title=" non-small cell lung cancer"> non-small cell lung cancer</a>, <a href="https://publications.waset.org/abstracts/search?q=tumorigenesis" title=" tumorigenesis"> tumorigenesis</a> </p> <a href="https://publications.waset.org/abstracts/41377/lncrna-neat1-promotes-nsclc-progression-through-acting-as-a-cerna-of-mir-377-3p" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/41377.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">369</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">6</span> Sirt1 Promotes C2C12 Myoblast Cell Proliferation by Myostatin Signaling Pathway</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang">Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun"> Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Ruilin%20Xue"> Ruilin Xue</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Backgrounds: Previous studies showed that Sirt1 plays an important role in C2C12 myoblast cell proliferation, but the mechanism(s) involved in this process remains unclear. This work was undertaken to determine if Myostatin participates in the regulation of C2C12 proliferation by Sirt1. Methods: We administrated the Sirt1 activator resveratrol, inhibitor Nicotinamide (NAM) and Myostatin inhibitor SB431542 on C2C12 myoblast cells. Cell viability was evaluated by CCK8 assay. The expression of Sirt1 and MyoD were detected by qRT-PCR. Utilizing western blot to determinate the expression of myostatin, P107 and p-P107. Results: Our results showed that resveratrol promoted the proliferation of C2C12 myoblast cells, while NAM suppressed the proliferation of C2C12 myoblast cells; SB431542 promoted the proliferation of C2C12 myoblast cells and attenuated the inhibition effect of NAM on C2C12 myoblast cells proliferation; Resveratrol can significantly increase the expression of Sirt1 and MyoD, decrease the expression of Myostatin, while NAM can significantly down-regulate the expression of Sirt1, MyoD and the phosphorylation of P107(p-P107), but up-regulate the expression of Myostatin and the protein P107; SB431542 can significantly mitigate the effect of NAM on the expression of MyoD, P107, and p-P107. Conclusions: Taken together, these results indicate that Sirt1 promotes the proliferation of C2C12 myoblast cells via Myostatin signaling pathway. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sirt1" title="Sirt1">Sirt1</a>, <a href="https://publications.waset.org/abstracts/search?q=C2C12%20cells" title=" C2C12 cells"> C2C12 cells</a>, <a href="https://publications.waset.org/abstracts/search?q=proliferation" title=" proliferation"> proliferation</a>, <a href="https://publications.waset.org/abstracts/search?q=myostatin%20signaling%20pathway" title=" myostatin signaling pathway "> myostatin signaling pathway </a> </p> <a href="https://publications.waset.org/abstracts/21780/sirt1-promotes-c2c12-myoblast-cell-proliferation-by-myostatin-signaling-pathway" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/21780.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">450</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">5</span> Hsa-miR-329 Functions as a Tumor Suppressor through Targeting MET in Non-Small Cell Lung Cancer</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Cheng-Cao%20Sun">Cheng-Cao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Shu-Jun%20Li"> Shu-Jun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Feng%20Zhang"> Feng Zhang</a>, <a href="https://publications.waset.org/abstracts/search?q=De-Jia%20Li"> De-Jia Li </a> </p> <p class="card-text"><strong>Abstract:</strong></p> MicroRNAs (miRNAs) act as key regulators of multiple cancers. Hsa-miR-329 (miR-329) functions as a tumor suppressor in some malignancies. However, its role on lung cancer remains poorly understood. In this study, we investigated the role of miR-329 on the development of lung cancer. The results indicated that miR-329 was decreased in primary lung cancer tissues compared with matched adjacent normal lung tissues and very low levels were found in a non-small cell lung cancer (NSCLC) cell lines. Ectopic expression of miR-329 in lung cancer cell lines substantially repressed cell growth as evidenced by cell viability assay, colony formation assay and BrdU staining, through inhibiting cyclin D1, cyclin D2, and up-regulatiing p57(Kip2) and p21(WAF1/CIP1). In addition, miR-329 promoted NSCLC cell apoptosis, as indicated by up-regulation of key apoptosis gene cleaved caspase-3, and down-regulation of anti-apoptosis gene Bcl2. Moreover, miR-329 inhibited cellular migration and invasiveness through inhibiting matrix metalloproteinases (MMP)-7 and MMP-9. Further, oncogene MET was revealed to be a putative target of miR-329, which was inversely correlated with miR-329 expression. Furthermore, down-regulation of MET by siRNA performed similar effects to over-expression of miR-329. Collectively, our results demonstrated that miR-329 played a pivotal role in lung cancer through inhibiting cell proliferation, migration, invasion, and promoting apoptosis by targeting oncogenic MET. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=hsa-miRNA-329%28miR-329%29" title="hsa-miRNA-329(miR-329)">hsa-miRNA-329(miR-329)</a>, <a href="https://publications.waset.org/abstracts/search?q=MET" title=" MET"> MET</a>, <a href="https://publications.waset.org/abstracts/search?q=non-small%20cell%20lung%20cancer%20%28NSCLC%29" title="non-small cell lung cancer (NSCLC)">non-small cell lung cancer (NSCLC)</a>, <a href="https://publications.waset.org/abstracts/search?q=proliferation" title=" proliferation"> proliferation</a>, <a href="https://publications.waset.org/abstracts/search?q=apoptosis" title=" apoptosis"> apoptosis</a> </p> <a href="https://publications.waset.org/abstracts/41379/hsa-mir-329-functions-as-a-tumor-suppressor-through-targeting-met-in-non-small-cell-lung-cancer" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/41379.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">409</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4</span> Advancement in Adhesion and Osteogenesis of Stem Cells with Histatin Coated 3D-Printed Bio-Ceramics</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Haiyan%20Wang">Haiyan Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Dongyun%20Wang"> Dongyun Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Yan"> Yongyong Yan</a>, <a href="https://publications.waset.org/abstracts/search?q=Richard%20T.%20Jaspers"> Richard T. Jaspers</a>, <a href="https://publications.waset.org/abstracts/search?q=Gang%20Wu"> Gang Wu</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Mesenchymal stem cell and 3D printing-based bone tissue engineering present a promising technique to repair large-volume bone defects. Its success is highly dependent on cell attachment, spreading, osteogenic differentiation, and in vivo survival of stem cells on 3D-printed scaffolds. In this study, human salivary histatin-1 (Hst1) was utilized to enhance the interactions between human adipose-derived stem cells (hASCs) and 3D-printed 尾-tricalcium phosphate (尾-TCP) bioceramic scaffolds. Fluorescent images showed that Hst1 significantly enhanced the adhesion of hASCs to both bioinert glass and 3D-printed 尾-TCP scaffold. In addition, Hst1 was associated with significantly higher proliferation and osteogenic differentiation of hASCs on 3D-printed 尾-TCP scaffolds. Moreover, coating 3D-printed 尾-TCP scaffolds with histatin significantly promotes the survival of hASCs in vivo. The ERK and p38 but not JNK signaling was found to be involved in the superior adhesion of hASCs to 尾-TCP scaffolds with the aid of Hst1. In conclusion, Hst1 could significantly promote the adhesion, spreading, osteogenic differentiation, and in vivo survival of hASCs on 3D-printed 尾-TCP scaffolds, bearing a promising application in stem cell/3D printing-based constructs for bone tissue engineering. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=3d%20printing" title="3d printing">3d printing</a>, <a href="https://publications.waset.org/abstracts/search?q=adipose-derived%20stem%20cells" title=" adipose-derived stem cells"> adipose-derived stem cells</a>, <a href="https://publications.waset.org/abstracts/search?q=bone%20tissue%20engineering" title=" bone tissue engineering"> bone tissue engineering</a>, <a href="https://publications.waset.org/abstracts/search?q=histatin-1" title=" histatin-1"> histatin-1</a>, <a href="https://publications.waset.org/abstracts/search?q=osteogenesis" title=" osteogenesis"> osteogenesis</a> </p> <a href="https://publications.waset.org/abstracts/183798/advancement-in-adhesion-and-osteogenesis-of-stem-cells-with-histatin-coated-3d-printed-bio-ceramics" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/183798.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">63</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3</span> Sulforaphane Attenuates Fibrosis of Dystrophic Muscle in Mdx Mice via Nrf2-Mediated Inhibition of TGF-尾/Smad Signaling</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun">Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Ruilin%20Xue"> Ruilin Xue</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Backgrounds: A few lines of evidence show that Sulforaphane (SFN) has anti-fibrosis effect in liver tissue via Nrf2-mediated inhibition of TGF-尾/Smad signaling. However, its effects on muscular dystrophic fibrosis remain unknown. This work was undertaken to evaluate the effects of SFN on fibrosis in dystrophic muscle. Methods: 3-month-old male mdx mice were treated with SFN by gavage (2 mg/kg body weight per day) for 3 months. Gastrocnemius, tibial anterior and triceps brachii muscles were collected for related analysis. Fibrosis in skeletal muscles was analyzed by Sirius red staining. Histology and morphology of skeletal muscles were investigated by H&E staining. Moreover, the expressions of Nrf2, NQO1, HO-1, and TGF-尾/Smad signaling pathway were detected by western blot, qRT-PCR, immunohistochemistry and immunofluorescence assays. Results: Our results demonstrated that SFN treatment significantly decreased and improved morphological features in mdx muscles. Moreover, SFN increased the expression of muscle phase II enzymes NQO1 and HO-1 and significantly decreased the expression of TGF-尾1锛宲-smad2, p-smad3, 伪-SMA, fibronectin, collagen I, PAI-1, and TIMP-1 in Nrf2 dependent manner. Additionally, SFN significantly decreased the expression of CD45 and TNF-伪. Conclusions: Collectively, these results show that SFN can ameliorate muscle fibrosis in mdx mice by Nrf2-induced inhibition of TGF-尾/Smad signaling pathway, which indicate Nrf2 may be useful for the treatment of muscular dystrophy. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=sulforaphane" title="sulforaphane">sulforaphane</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2" title=" Nrf2"> Nrf2</a>, <a href="https://publications.waset.org/abstracts/search?q=TGF-%CE%B2%2Fsmad%20signaling" title=" TGF-尾/smad signaling"> TGF-尾/smad signaling</a>, <a href="https://publications.waset.org/abstracts/search?q=duchenne%20muscular%20dystrophy" title=" duchenne muscular dystrophy"> duchenne muscular dystrophy</a>, <a href="https://publications.waset.org/abstracts/search?q=fibrosis" title=" fibrosis"> fibrosis</a> </p> <a href="https://publications.waset.org/abstracts/19674/sulforaphane-attenuates-fibrosis-of-dystrophic-muscle-in-mdx-mice-via-nrf2-mediated-inhibition-of-tgf-vsmad-signaling" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/19674.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">441</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">2</span> Sulforaphane Attenuates Muscle Inflammation in Dystrophin-Deficient Mdx Mice via Nrf2/HO-1 Signaling Pathway</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun">Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Ruilin%20Xue"> Ruilin Xue</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Backgrounds: Inflammation is widely distributed in patients with Duchenne muscular dystrophy (DMD), and ultimately leads to progressive deterioration of muscle function with the co-effects of chronic muscle damage, oxidative stress, and reduced oxidative capacity. NF-E2-related factor 2 (Nrf2) plays a critical role in defending against inflammation in different tissues via activation of phase II enzymes, heme oxygenase-1 (HO-1). However, whether Nrf2/HO-1 pathway can attenuate muscle inflammation on DMD remains unknown. The purpose of this study was to determine the anti-inflammatory effects of Sulforaphane (SFN) on DMD. Methods: 4-week-old male mdx mice were treated with SFN by gavage (2 mg/kg body weight per day) for 4 weeks. Gastrocnemius, tibial anterior and triceps brachii muscles were collected for related analysis. Immune cell infiltration in skeletal muscles was analyzed by H&E staining and immuno-histochemistry. Moreover, the expressions of inflammatory cytokines,pro-inflammatory cytokines and Nrf2/HO-1 pathway were detected by western blot, qRT-PCR, immunohistochemistry and immunofluorescence assays. Results: Our results demonstrated that SFN treatment increased the expression of muscle phase II enzymes HO-1 in Nrf2 dependent manner. Inflammation in mdx skeletal muscles was reduced by SFN treatment as indicated by decreased immune cell infiltration and lower expressions of the inflammatory cytokines CD45, pro-inflammatory cytokines tumour necrosis factor-伪 and interleukin-6 in the skeletal muscles of mdx mice. Conclusions: Collectively, these results show that SFN can ameliorate muscle inflammation in mdx mice by Nrf2/HO-1 pathway, which indicates Nrf2/HO-1 pathway may represent a new therapeutic target for DMD. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=sulforaphane" title="sulforaphane">sulforaphane</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2" title=" Nrf2"> Nrf2</a>, <a href="https://publications.waset.org/abstracts/search?q=HO-1" title=" HO-1"> HO-1</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a> </p> <a href="https://publications.waset.org/abstracts/19664/sulforaphane-attenuates-muscle-inflammation-in-dystrophin-deficient-mdx-mice-via-nrf2ho-1-signaling-pathway" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/19664.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">334</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">1</span> Sulforaphane Alleviates Muscular Dystrophy in Mdx Mice by Activation of Nrf2</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Chengcao%20Sun">Chengcao Sun</a>, <a href="https://publications.waset.org/abstracts/search?q=Cuili%20Yang"> Cuili Yang</a>, <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Ruilin%20Xue"> Ruilin Xue</a>, <a href="https://publications.waset.org/abstracts/search?q=Liang%20Wang"> Liang Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Yongyong%20Xi"> Yongyong Xi</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Backgrounds: Sulforaphane, one of the most important isothiocyanates in the human diet, is known to have chemopreventive and antioxidant activities in different tissues via activation of NF-E2-related factor 2 (Nrf2)-mediated induction of antioxidant/phase II enzymes, such as heme oxygenase-1 (HO-1) and NAD(P)H quinone oxidoreductase 1 (NQO1). However, its effects on muscular dystrophy remain unknown. This work was undertaken to evaluate the effects of Sulforaphane on Duchenne muscular dystrophy (DMD). Methods: 4-week-old mdx mice were treated with SFN by gavage (2 mg/kg body weight per day) for 8 weeks. Blood was collected from eye socket every week, and tibial anterior, extensor digitorum longus, gastrocnemius, soleus, triceps brachii muscles and heart samples were collected after 8-week gavage. Force measurements and mice exercise capacity assays were detected. GSH/GSSG ratio, TBARS, CK and LDH levels were analyzed by spectrophotometric methods. H&E staining was used to analyze histological and morphometric of skeletal muscles of mdx mice, and Evas blue dye staining was made to detect sarcolemmal integrity of mdx mice. Further, the role of Sulforaphane on Nrf2/ARE signaling pathway was analyzed by ELISA, western blot and qRT-PCR. Results: Our results demonstrated that SFN treatment increased the expression and activity of muscle phase II enzymes NQO1 and HO-1 with Nrf2 dependent manner. SFN significantly increased skeletal muscle mass, muscle force (~30%), running distance (~20%) and GSH/GSSG ratio (~3.2 folds) of mdx mice, and decreased the activities of plasma creatine phosphokinase (CK) (~45%) and lactate dehydrogenase (LDH) (~40%), gastrocnemius hypertrophy (~25%), myocardial hypertrophy (~20%) and MDA levels (~60%). Further, SFN treatment also reduced the central nucleation (~40%), fiber size variability, inflammation and improved the sarcolemmal integrity of mdx mice. Conclusions: Collectively, these results show that SFN can improve muscle function, pathology and protect dystrophic muscle from oxidative damage in mdx mice through Nrf2 signaling pathway, which indicate Nrf2 may have clinical implications for the treatment of patients with muscular dystrophy. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=sulforaphane" title="sulforaphane">sulforaphane</a>, <a href="https://publications.waset.org/abstracts/search?q=duchenne%20muscular%20dystrophy" title=" duchenne muscular dystrophy"> duchenne muscular dystrophy</a>, <a href="https://publications.waset.org/abstracts/search?q=Nrf2" title=" Nrf2"> Nrf2</a>, <a href="https://publications.waset.org/abstracts/search?q=oxidative%20stress" title=" oxidative stress"> oxidative stress</a> </p> <a href="https://publications.waset.org/abstracts/19659/sulforaphane-alleviates-muscular-dystrophy-in-mdx-mice-by-activation-of-nrf2" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/19659.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">322</span> </span> </div> </div> </div> </main> <footer> <div id="infolinks" class="pt-3 pb-2"> <div class="container"> <div style="background-color:#f5f5f5;" class="p-3"> <div class="row"> <div class="col-md-2"> <ul class="list-unstyled"> About <li><a href="https://waset.org/page/support">About Us</a></li> <li><a href="https://waset.org/page/support#legal-information">Legal</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/WASET-16th-foundational-anniversary.pdf">WASET celebrates its 16th foundational anniversary</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Account <li><a href="https://waset.org/profile">My Account</a></li> </ul> </div> <div class="col-md-2"> <ul 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