{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T19:32:56Z","timestamp":1790623976453,"version":"4.1.0"},"reference-count":42,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2019,9,29]],"date-time":"2019-09-29T00:00:00Z","timestamp":1569715200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81600322"],"award-info":[{"award-number":["81600322"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81770707"],"award-info":[{"award-number":["81770707"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002402","name":"Sun Yat-sen University","doi-asserted-by":"publisher","award":["16ykpy47"],"award-info":[{"award-number":["16ykpy47"]}],"id":[{"id":"10.13039\/501100002402","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Sodium butyrate (NaBu) is reported to play important roles in a number of chronic diseases. The present work is aimed to investigate the effect of NaBu on angiotensin II (Ang II)\u2010induced cardiac hypertrophy and the underlying mechanism in in vivo and in vitro models. Sprague Dawley rats were infused with vehicle or Ang II (200\u00a0ng\/kg\/min) and orally administrated with or without NaBu (1\u00a0g\/kg\/d) for two weeks. Cardiac hypertrophy parameters and COX2\/PGE2 pathway were analysed by real\u2010time PCR, ELISA, immunostaining and Western blot. The cardiomyocytes H9C2 cells were used as in vitro model to investigate the role of NaBu (2\u00a0mmol\/L) in inhibition of Ang II\u2010induced cardiac hypertrophy. NaBu significantly attenuated Ang II\u2010induced increase in the mean arterial pressure. Ang II treatment remarkably increased cardiac hypertrophy as indicated by increased ratio of heart weight\/body weight and enlarged cardiomyocyte size, extensive fibrosis and inflammation, as well as enhanced expression of hypertrophic markers, whereas hearts from NaBu\u2010treated rats exhibited a significant reduction in these hypertrophic responses. Mechanistically, NaBu inhibited the expression of COX2\/PGE2 along with production of ANP and phosphorylated ERK (pERK) stimulated by Ang II in in vivo and in vitro, which was accompanied by the suppression of HDAC5 and HDAC6 activities. Additionally, knocking down the expression of HDAC5 and HDAC6 via gene\u2010editing strategy dramatically blocked Ang II\u2010induced hypertrophic responses through COX2\/PGE2 pathway. These results provide solid evidence that NaBu attenuates Ang II\u2010induced cardiac hypertrophy by inhibiting the activation of COX2\/PGE2 pathway in a HDAC5\/HDAC6\u2010dependent manner.<\/jats:p>","DOI":"10.1111\/jcmm.14684","type":"journal-article","created":{"date-parts":[[2019,9,30]],"date-time":"2019-09-30T21:50:26Z","timestamp":1569880226000},"page":"8139-8150","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":92,"title":["Sodium butyrate attenuates angiotensin II\u2010induced cardiac hypertrophy by inhibiting COX2\/PGE2 pathway via a HDAC5\/HDAC6\u2010dependent mechanism"],"prefix":"10.1111","volume":"23","author":[{"given":"Linlin","family":"Zhang","sequence":"first","affiliation":[{"name":"Institue of Hypertension Sun Yat\u2010sen University School of Medicine Guangzhou 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