{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,16]],"date-time":"2026-02-16T10:14:32Z","timestamp":1771236872176,"version":"3.50.1"},"reference-count":27,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2021,11,18]],"date-time":"2021-11-18T00:00:00Z","timestamp":1637193600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["aspenjournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Parenter Enteral Nutr"],"published-print":{"date-parts":[[2022,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Background<\/jats:title><jats:p>Acute liver injury (ALI) is an essential component of sepsis associated with poor outcomes. Octanoic acid (OA), a medium\u2010chain fatty acid, has a protective effect on sepsis\u2010induced organ damage, and autophagy is an adaptive response to sepsis. However, the underlying mechanism by which OA prevents ALI remains unknown. Therefore, we investigated whether OA\u2010rich enteral nutrition (EN) prevented lipopolysaccharide (LPS)\u2010induced ALI through the c\u2010Jun N\u2010terminal kinase (JNK)\u2010dependent autophagy.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Firstly, Sprague Dawley rats were randomly divided into four groups (sham, LPS, LPS + EN, and LPS + EN + OA) to detect the effect of OA\u2010rich EN on LPS\u2010induced ALI. Then, rats were randomly divided into five groups (sham, LPS, LPS + EN + OA, LPS + EN + OA + anisomycin (AN), and LPS + SP600125) to explore the mechanism by which OA\u2010rich EN prevented ALI. EN and OA\u2010rich EN were conducted through gastric tubes for 3 days. The liver protective effects were measured by liver histopathological changes, enzymes, inflammatory cytokines of serum and liver, the levels of autophagy, and JNK activity.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>OA\u2010rich EN inhibited JNK activity, up\u2010regulated autophagy and prevented LPS\u2010induced ALI. Inhibition of JNK activity conferred by SP promoted autophagy and prevented LPS\u2010induced ALI. Moreover, the protective effect of autophagy and inhibition of JNK activity conferred by OA\u2010rich EN on ALI was counteracted by AN.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>OA\u2010rich EN prevented LPS\u2010induced ALI through JNK\u2010dependent autophagy. This result suggested that OA\u2010rich EN may be a therapeutic potential for ALI in patients with sepsis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jpen.2297","type":"journal-article","created":{"date-parts":[[2021,11,1]],"date-time":"2021-11-01T02:43:20Z","timestamp":1635734600000},"page":"1353-1360","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Octanoic acid\u2013rich enteral nutrition prevented lipopolysaccharide\u2010induced acute liver injury through c\u2010Jun N\u2010terminal kinase\u2013dependent autophagy"],"prefix":"10.1002","volume":"46","author":[{"given":"Kaiming","family":"He","sequence":"first","affiliation":[{"name":"Department of General Surgery the Second Affiliated Hospital of Soochow University  Suzhou China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chun","family":"Cao","sequence":"additional","affiliation":[{"name":"Department of General Surgery the Second Affiliated 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