Promotion of wound healing by acetate in murine colonic epithelial cell via c-Jun N-terminal kinase activation

Takahiro Nakano, Kazuhiko Uchiyama, Chihiro Ushiroda, Saori Kashiwagi, Yuki Toyokawa, Katsura Mizushima, Ken Inoue, Osamu Dohi, Tetsuya Okayama, Naohisa Yoshida, Kazuhiro Katada, Kazuhiro Kamada, Osamu Handa, Takeshi Ishikawa, Tomohisa Takagi, Hideyuki Konishi, Yuji Naito, Yoshito Itoh

Research output: Contribution to journalArticlepeer-review

7 Citations (Scopus)


Background and Aim: Mucosal healing is an important clinical goal in patients with inflammatory bowel disease. Recently, short-chain fatty acids (SCFAs) have been reported to have multifaceted effects to host. However, the effects of SCFAs on wound healing in intestinal epithelial cells are unclear. In the present study, we investigated the effects of acetate, one of the major SCFAs, on the wound healing of murine colonic epithelial cells. Methods: Young adult mouse colonic epithelial cells were used to determine the effect of acetate using wound healing assay. Mitogen-activated protein kinase and Rho kinase inhibitor were used to elucidate intracellular signal of wound healing treated with acetate. Meanwhile, Rho activation assays were utilized to measure Rho activation levels. To assess in vivo effects, C57B6 mice with dextran sodium sulfate for 7 days were treated with enema administration of acetate for 7 days. Body weight, disease activity index, colon length, and mucosal break ratio in histology were examined. Results: Acetate enhanced wound healing and fluorescence intensity of actin stress fiber compared with control. These effects were canceled with pretreatment of c-Jun N-terminal kinase (JNK) inhibitor or Rho kinase inhibitor. Furthermore, JNK inhibitor reduced the activation of Rho induced by acetate. In the dextran sodium sulfate-induced colitis model, the mice with enema treatment of acetate significantly exhibited recovery. Conclusions: In this study, we demonstrated that acetate promoted murine colonic epithelial cell wound healing via activation of JNK and Rho signaling pathways. These findings suggested that acetate could have applications as a therapeutic agent for patients with intestinal mucosal damage, such as inflammatory bowel disease.

Original languageEnglish
Pages (from-to)1171-1179
Number of pages9
JournalJournal of Gastroenterology and Hepatology (Australia)
Issue number7
Publication statusPublished - 01-07-2020
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Hepatology
  • Gastroenterology


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