Details

Autor(en) / Beteiligte

• Horii, Yusuke
• Uchiyama, Kazuhiko
• Yasukawa, Zenta
• Tokunaga, Makoto
• Okubo, Tsutomu
• Mizushima, Katsura
• Hotta, Yuma
• Tanaka, Makoto
• Katada, Kazuhiro
• Kamada, Kazuhiro
• Handa, Osamu
• Takagi, Tomohisa
• Naito, Yuji

Titel

Dietary Fiber Enhances Intestinal Epithelial Wound Healing Via Activation of ERK and Rho Kinase

Ist Teil von

• Digestive diseases and sciences, 2022-05, Vol.60 (9), p.2564

Ort / Verlag

Springer

Erscheinungsjahr

2022

Link zum Volltext

Quelle

2022 ECC(Springer)

Beschreibungen/Notizen

• Background and Aim: Mucosal healing is an important therapeutic end point in clinical trials and clinical practice for inflammatory bowel disease (IBD). Partially hydrolyzed dietary fiber (partially hydrolyzed guar gum (PHGG)) has been reported to improve mice DSS colitis model via regulation of colonic inflammation. But its role for colonic epithelial mucosal healing has not been reported. In this study, we investigated the role of PHGG to enhance colonic epithelial cell restitution. Materials and Methods: Mouse colonic epithelial cells (YAMC: Young Adult Mouse Colonic epithelial cells) were treated with PHGG (10 mg/ml). Cellular restitution was measured by wound healing assay as follows: Cells were scraped with a 10 [micro]l extra long micropipette tip, denuding a strip of the monolayer approximately 500 [micro]l in diameter. After incubation, the cells were photographed with a digital camera, and the migrated area was measured by Image J software. Y-27632, a selective Rho-kinase inhibitor was used to block Rho kinase activity. The activation of Rho kinase was measured by Rho activation assay. To reveal the intracellular pathway of wound healing inducing by PHGG, we checked MAPK activation. Results: PHGG treatment significantly enhanced the wound healing of YAMC compared with control (PHGG: 18.5 [+ or -] 2.1 %, control: 42.2 [+ or -] 1.5 % of wound remaining) 24 h after wounding. Rho activity was enhanced with the treatment of PHGG and Y-27632 treatment canceled the enhancement of wound healing by PHGG. ERK was phosphorylated by PHGG and U0126, ERK inhibitor, decreased Rho activity induced by PHGG. Conclusions: PHGG enhanced colonic epithelial cell restitution via activation of ERK and Rho kinase.