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We are analyzing https://link.springer.com/article/10.1007/s13105-021-00854-5.

Title:
Procyanidin A1 alleviates DSS-induced ulcerative colitis via regulating AMPK/mTOR/p70S6K-mediated autophagy | Journal of Physiology and Biochemistry
Description:
Ulcerative colitis (UC) is a recurrent chronic inflammatory disease. The symptom of UC is mainly diarrhea including bloody stools. Increasing evidence has suggested that procyanidin A1 (PCA1) exerts an anti-inflammatory effect in several diseases. However, the role of PCA1 in UC is still a mystery. In our study, we explored the effect of PCA1 in dextran sulfate sodium (DSS)–induced UC mice and lipopolysaccharide (LPS)-stimulated HT-29 and IEC-6 cells. Then, cell proliferation, apoptosis, the production of proinflammatory cytokines, and autophagy-related markers were determined. Furthermore, the AMPK/mTOR/p70S6K signaling pathway was assayed by Western blot assay. In in vivo study, we found that PCA1 administration alleviated DSS-induced UC, as evidenced by reducing weight loss, clinical scores, colon weight/length ratio, histological damage, proinflammatory cytokines, and apoptosis. Moreover, we showed that the expression of Beclin-1 and LC3II/I ratio was increased, whereas the level of p62 was decreased after PCA1 treatment in vivo. Meanwhile, the reduced AMP/ATP ratio, enhanced expression of p-AMPK, and decreased p-p70S6K and p-mTOR levels indicate the activation of AMPK/mTOR/p70S6K signaling pathway. In in vitro study, PCA1 promoted cell proliferation and inhibited cell apoptosis in LPS-stimulated HT-29 and IEC-6 cells. Pro-inflammatory cytokines and autophagy-related factors exhibited the same trend as in in vivo results. Mechanically, PCA1 activated the AMPK/mTOR/p70S6K signaling pathway. The treatment with an AMPK inhibitor compound C significantly reversed the anti-inflammatory effect of PCA1 in LPS-stimulated cells. Taken together, these data indicated that PCA1 alleviated UC through induction of AMPK/mTOR/p70S6K-mediated autophagy.
Website Age:
28 years and 1 months (reg. 1997-05-29).

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  • Education
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What CMS is link.springer.com built with?

Custom-built

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🌠 Phenomenal Traffic: 5M - 10M visitors per month


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How Does Link.springer.com Make Money? {šŸ’ø}

We're unsure how the site profits.

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Keywords {šŸ”}

article, pubmed, google, scholar, cas, colitis, autophagy, ulcerative, hebei, procyanidin, central, pca, dssinduced, inflammatory, disease, cells, cell, pathway, zhang, dextran, mice, httpsdoiorgs, science, data, signaling, university, privacy, cookies, content, journal, alleviates, regulating, lang, liu, qiumei, shi, study, sulfate, sodium, apoptosis, vitro, rev, bowel, province, technology, information, publish, search, ampkmtorpskmediated, january,

Topics {āœ’ļø}

regulating ampk/mtor/p70s6k-mediated autophagy ampk/mtor/p70s6k-mediated autophagy ampk-mtor-p70s6k-mediated autophagy ampk/mtor/p70s6k signaling pathway month download article/chapter ampk/mtor/p70s6k pathway dss-induced ulcerative colitis grape-seed procyanidins act pi3k/akt/mtor inhibition autophagy-related factors exhibited genome-wide association scan nf-Īŗb colon weight/length ratio dextran sulfate sodium reduced amp/atp ratio full article pdf qiumei shi revised qiumei shi designed intestinal metrnl deficiency qinghui jia article zhang related subjects autophagy-related markers privacy choices/manage cookies inflammatory bowel disease murthy sn de koning ma ampk inhibitor compound top talent project induced uc mice inhibiting inflammatory responses procyanidin a1 shao bz published maps p-mtor levels inflammatory bowel diseases induced colitis lps-stimulated ht-29 decreased p-p70s6k regulating macrophage polarization han bz jiangsong bai analyzed qiumei shi lps-stimulated cells pro-inflammatory cytokines anti-inflammatory effect reducing weight loss wuying lang performed inhibiting nlrp3 inflammasome fur animal breeding

Schema {šŸ—ŗļø}

WebPage:
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         headline:Procyanidin A1 alleviates DSS-induced ulcerative colitis via regulating AMPK/mTOR/p70S6K-mediated autophagy
         description:Ulcerative colitis (UC) is a recurrent chronic inflammatory disease. The symptom of UC is mainly diarrhea including bloody stools. Increasing evidence has suggested that procyanidin A1 (PCA1) exerts an anti-inflammatory effect in several diseases. However, the role of PCA1 in UC is still a mystery. In our study, we explored the effect of PCA1 in dextran sulfate sodium (DSS)–induced UC mice and lipopolysaccharide (LPS)-stimulated HT-29 and IEC-6 cells. Then, cell proliferation, apoptosis, the production of proinflammatory cytokines, and autophagy-related markers were determined. Furthermore, the AMPK/mTOR/p70S6K signaling pathway was assayed by Western blot assay. In in vivo study, we found that PCA1 administration alleviated DSS-induced UC, as evidenced by reducing weight loss, clinical scores, colon weight/length ratio, histological damage, proinflammatory cytokines, and apoptosis. Moreover, we showed that the expression of Beclin-1 and LC3II/I ratio was increased, whereas the level of p62 was decreased after PCA1 treatment in vivo. Meanwhile, the reduced AMP/ATP ratio, enhanced expression of p-AMPK, and decreased p-p70S6K and p-mTOR levels indicate the activation of AMPK/mTOR/p70S6K signaling pathway. In in vitro study, PCA1 promoted cell proliferation and inhibited cell apoptosis in LPS-stimulated HT-29 and IEC-6 cells. Pro-inflammatory cytokines and autophagy-related factors exhibited the same trend as in in vivo results. Mechanically, PCA1 activated the AMPK/mTOR/p70S6K signaling pathway. The treatment with an AMPK inhibitor compound C significantly reversed the anti-inflammatory effect of PCA1 in LPS-stimulated cells. Taken together, these data indicated that PCA1 alleviated UC through induction of AMPK/mTOR/p70S6K-mediated autophagy.
         datePublished:2022-01-10T00:00:00Z
         dateModified:2022-01-10T00:00:00Z
         pageStart:213
         pageEnd:227
         sameAs:https://doi.org/10.1007/s13105-021-00854-5
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            Ulcerative colitis (UC)
            Inflammatory bowel disease (IBD)
            Procyanidin A1 (PCA1)
            Autophagy
            Biomedicine
            general
            Human Physiology
            Animal Physiology
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      headline:Procyanidin A1 alleviates DSS-induced ulcerative colitis via regulating AMPK/mTOR/p70S6K-mediated autophagy
      description:Ulcerative colitis (UC) is a recurrent chronic inflammatory disease. The symptom of UC is mainly diarrhea including bloody stools. Increasing evidence has suggested that procyanidin A1 (PCA1) exerts an anti-inflammatory effect in several diseases. However, the role of PCA1 in UC is still a mystery. In our study, we explored the effect of PCA1 in dextran sulfate sodium (DSS)–induced UC mice and lipopolysaccharide (LPS)-stimulated HT-29 and IEC-6 cells. Then, cell proliferation, apoptosis, the production of proinflammatory cytokines, and autophagy-related markers were determined. Furthermore, the AMPK/mTOR/p70S6K signaling pathway was assayed by Western blot assay. In in vivo study, we found that PCA1 administration alleviated DSS-induced UC, as evidenced by reducing weight loss, clinical scores, colon weight/length ratio, histological damage, proinflammatory cytokines, and apoptosis. Moreover, we showed that the expression of Beclin-1 and LC3II/I ratio was increased, whereas the level of p62 was decreased after PCA1 treatment in vivo. Meanwhile, the reduced AMP/ATP ratio, enhanced expression of p-AMPK, and decreased p-p70S6K and p-mTOR levels indicate the activation of AMPK/mTOR/p70S6K signaling pathway. In in vitro study, PCA1 promoted cell proliferation and inhibited cell apoptosis in LPS-stimulated HT-29 and IEC-6 cells. Pro-inflammatory cytokines and autophagy-related factors exhibited the same trend as in in vivo results. Mechanically, PCA1 activated the AMPK/mTOR/p70S6K signaling pathway. The treatment with an AMPK inhibitor compound C significantly reversed the anti-inflammatory effect of PCA1 in LPS-stimulated cells. Taken together, these data indicated that PCA1 alleviated UC through induction of AMPK/mTOR/p70S6K-mediated autophagy.
      datePublished:2022-01-10T00:00:00Z
      dateModified:2022-01-10T00:00:00Z
      pageStart:213
      pageEnd:227
      sameAs:https://doi.org/10.1007/s13105-021-00854-5
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         Ulcerative colitis (UC)
         Inflammatory bowel disease (IBD)
         Procyanidin A1 (PCA1)
         Autophagy
         Biomedicine
         general
         Human Physiology
         Animal Physiology
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                     type:PostalAddress
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            name:Wuying Lang
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                  name:Shangluo University
                  address:
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                  name:Hebei Normal University of Science and Technology
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                     name:Hebei Key Laboratory of Specialty Animal Germplasm Resources Exploration and Innovation (Under Planning), Hebei Normal University of Science and Technology, Qinhuangdao, People’s Republic of China
                     type:PostalAddress
                  type:Organization
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            name:Jiangsong Bai
            affiliation:
                  name:Technological Innovation Center for Fur Animal Breeding of Hebei Province
                  address:
                     name:Technological Innovation Center for Fur Animal Breeding of Hebei Province, Shijiazhuang, People’s Republic of China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Qinghui Jia
            affiliation:
                  name:Hebei Normal University of Science and Technology
                  address:
                     name:Hebei Key Laboratory of Preventive Veterinary Medicine, Hebei Normal University of Science and Technology, Qinhuangdao, People’s Republic of China
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Qiumei Shi
            url:http://orcid.org/0000-0002-4882-6309
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                  name:Hebei Normal University of Science and Technology
                  address:
                     name:Hebei Key Laboratory of Preventive Veterinary Medicine, Hebei Normal University of Science and Technology, Qinhuangdao, People’s Republic of China
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      name:Xin Liu
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            name:Hebei Normal University of Science and Technology
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               name:Technological Innovation Center for Fur Animal Breeding of Hebei Province, Shijiazhuang, People’s Republic of China
               type:PostalAddress
            type:Organization
      name:Qinghui Jia
      affiliation:
            name:Hebei Normal University of Science and Technology
            address:
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