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Li</title> <meta name="description" content="Search results for: Shu-Jun Li"> <meta name="keywords" content="Shu-Jun Li"> <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="Shu-Jun Li"> <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> 7</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: Shu-Jun Li</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">7</span> Role of Sulforaphane on Alleviating Duchenne Muscular Dystrophy(DMD) through 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=Shujun%20Li"> Shujun Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Dejia%20Li"> Dejia Li</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Sulforaphane (SFN) possesses powerful chemo-preventive effects and plays a crucial role on oxidative stress and inflammatory. In our recent study, SFN treatment could relieve muscular dystrophy in mdx mice by activating Nrf2 (NF-E2 related factor 2). Moreover, our findings indicated that SFN-activated Nrf2 alleviated muscle inflammation in dystrophin-deficient mdx mice through suppressing NF-魏B signaling pathway. Collectively, SFN-induced Nrf2 molecular pathway might be a promising approach for treatment of the patients with Duchenne 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=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=fibrosis" title=" fibrosis"> fibrosis</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/41533/role-of-sulforaphane-on-alleviating-duchenne-muscular-dystrophydmd-through-activation-of-nrf2" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/41533.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">214</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> 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">5</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">4</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">3</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">2</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">323</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> The Second Generation of Tyrosine Kinase Inhibitor Afatinib Controls Inflammation by Regulating NLRP3 Inflammasome Activation</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Shujun%20Xie">Shujun Xie</a>, <a href="https://publications.waset.org/abstracts/search?q=Shirong%20Zhang"> Shirong Zhang</a>, <a href="https://publications.waset.org/abstracts/search?q=Shenglin%20Ma"> Shenglin Ma</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Chronic inflammation might lead to many malignancies, and inadequate resolution could play a crucial role in tumor invasion, progression, and metastases. A randomised, double-blind, placebo-controlled trial shows that IL-1尾 inhibition with canakinumab could reduce incident lung cancer and lung cancer mortality in patients with atherosclerosis. The process and secretion of proinflammatory cytokine IL-1尾 are controlled by the inflammasome. Here we showed the correlation of the innate immune system and afatinib, a tyrosine kinase inhibitor targeting epidermal growth factor receptor (EGFR) in non-small cell lung cancer. Methods: Murine Bone marrow derived macrophages (BMDMs), peritoneal macrophages (PMs) and THP-1 were used to check the effect of afatinib on the activation of NLRP3 inflammasome. The assembly of NLRP3 inflammasome was check by co-immunoprecipitation of NLRP3 and apoptosis-associated speck-like protein containing CARD (ASC), disuccinimidyl suberate (DSS)-cross link of ASC. Lipopolysaccharide (LPS)-induced sepsis and Alum-induced peritonitis were conducted to confirm that afatinib could inhibit the activation of NLRP3 in vivo. Peripheral blood mononuclear cells (PBMCs) from non-small cell lung cancer (NSCLC) patients before or after taking afatinib were used to check that afatinib inhibits inflammation in NSCLC therapy. Results: Our data showed that afatinib could inhibit the secretion of IL-1尾 in a dose-dependent manner in macrophage. Moreover, afatinib could inhibit the maturation of IL-1尾 and caspase-1 without affecting the precursors of IL-1尾 and caspase-1. Next, we found that afatinib could block the assembly of NLRP3 inflammasome and the ASC speck by blocking the interaction of the sensor protein NLRP3 and the adaptor protein ASC. We also found that afatinib was able to alleviate the LPS-induced sepsis in vivo. Conclusion: Our study found that afatinib could inhibit the activation of NLRP3 inflammasome in macrophage, providing new evidence that afatinib could target the innate immune system to control chronic inflammation. These investigations will provide significant experimental evidence in afatinib as therapeutic drug for non-small cell lung cancer or other tumors and NLRP3-related diseases and will explore new targets for afatinib. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=inflammasome" title="inflammasome">inflammasome</a>, <a href="https://publications.waset.org/abstracts/search?q=afatinib" title=" afatinib"> afatinib</a>, <a href="https://publications.waset.org/abstracts/search?q=inflammation" title=" inflammation"> inflammation</a>, <a href="https://publications.waset.org/abstracts/search?q=tyrosine%20kinase%20inhibitor" title=" tyrosine kinase inhibitor"> tyrosine kinase inhibitor</a> </p> <a href="https://publications.waset.org/abstracts/109769/the-second-generation-of-tyrosine-kinase-inhibitor-afatinib-controls-inflammation-by-regulating-nlrp3-inflammasome-activation" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/109769.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">118</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 class="list-unstyled"> Explore <li><a href="https://waset.org/disciplines">Disciplines</a></li> <li><a href="https://waset.org/conferences">Conferences</a></li> <li><a href="https://waset.org/conference-programs">Conference Program</a></li> <li><a href="https://waset.org/committees">Committees</a></li> <li><a href="https://publications.waset.org">Publications</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Research <li><a href="https://publications.waset.org/abstracts">Abstracts</a></li> <li><a href="https://publications.waset.org">Periodicals</a></li> <li><a href="https://publications.waset.org/archive">Archive</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Open Science <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Science-Philosophy.pdf">Open Science Philosophy</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Science-Award.pdf">Open Science Award</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Open-Society-Open-Science-and-Open-Innovation.pdf">Open Innovation</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Postdoctoral-Fellowship-Award.pdf">Postdoctoral Fellowship Award</a></li> <li><a target="_blank" rel="nofollow" href="https://publications.waset.org/static/files/Scholarly-Research-Review.pdf">Scholarly Research Review</a></li> </ul> </div> <div class="col-md-2"> <ul class="list-unstyled"> Support <li><a href="https://waset.org/page/support">Support</a></li> <li><a href="https://waset.org/profile/messages/create">Contact Us</a></li> <li><a href="https://waset.org/profile/messages/create">Report Abuse</a></li> </ul> </div> </div> </div> </div> </div> <div class="container text-center"> <hr style="margin-top:0;margin-bottom:.3rem;"> <a href="https://creativecommons.org/licenses/by/4.0/" target="_blank" class="text-muted small">Creative Commons Attribution 4.0 International License</a> <div id="copy" class="mt-2">© 2024 World Academy of Science, Engineering and Technology</div> </div> </footer> <a href="javascript:" id="return-to-top"><i class="fas fa-arrow-up"></i></a> <div class="modal" id="modal-template"> <div class="modal-dialog"> <div class="modal-content"> <div class="row m-0 mt-1"> <div class="col-md-12"> <button type="button" class="close" data-dismiss="modal" aria-label="Close"><span aria-hidden="true">×</span></button> </div> </div> <div class="modal-body"></div> </div> </div> </div> <script src="https://cdn.waset.org/static/plugins/jquery-3.3.1.min.js"></script> <script src="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/js/bootstrap.bundle.min.js"></script> <script src="https://cdn.waset.org/static/js/site.js?v=150220211556"></script> <script> jQuery(document).ready(function() { /*jQuery.get("https://publications.waset.org/xhr/user-menu", function (response) { jQuery('#mainNavMenu').append(response); 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