Feeding with olive oil attenuates inflammation in dextran sulfate sodium-induced colitis in rat.
Chronic inflammation of long-term ulcerative colitis contributes to an increased risk of colon cancer. Few studies address whether extra-virgin olive oil (EVOO) intake suppresses inflammation, cell proliferation and signal transducers and activators of transcription (STAT) in the experimental colitis model. The aim of this study was to assess whether a 5% EVOO suppressed inflammation, increased cell proliferation and the expressions of STAT3 and STAT3 phosphorylation (pSTAT3) in dextran sulfate sodium (DSS)-induced colitis. Rats were administered DSS via drinking water (weight percentage: 4%) for 1 week with a 1-week recovery period for three cycles. Rats were divided into three groups: control group, standard diet without DSS; DSS group, standard diet+DSS; and DSS+EVOO group, EVOO diet (weight percentage: 5%)+DSS. Rats were sacrificed 5 weeks after DSS was first administered, and colonic damage was histologically and biochemically evaluated. As a result, chronic feeding of 5% EVOO attenuated inflammation. This was evaluated using a disease activity index, body weight loss and a histological score. Enhanced expressions of STAT3, pSTAT3, COX-2 and iNOS by DSS was attenuated by EVOO. In addition, EVOO attenuated increases in cell proliferation (PCNA) caused by DSS and recovered decreases in apoptosis (cleaved caspase-3). In conclusion, the study indicated that chronic feeding of 5% EVOO inhibited chronic inflammation in DSS-induced colitis in rats and also attenuated cell proliferation and recovered apoptosis in DSS colitis.
Department of Internal Medicine and Gastrointestinal Endoscopy, Saga Medical School, Saga 849-8501, Japan; Basic Science of Nursing, Saga Medical School, Saga 849-8501, Japan.
Toru
T
Takashima
Department of Internal Medicine and Gastrointestinal Endoscopy, Saga Medical School, Saga 849-8501, Japan.
Yasuhisa
Y
Sakata
Department of Internal Medicine and Gastrointestinal Endoscopy, Saga Medical School, Saga 849-8501, Japan.
Ryuichi
R
Iwakiri
Department of Internal Medicine and Gastrointestinal Endoscopy, Saga Medical School, Saga 849-8501, Japan.
Ryosuke
R
Shiraishi
Department of Internal Medicine and Gastrointestinal Endoscopy, Saga Medical School, Saga 849-8501, Japan.
Yasutomo
Y
Oda
Basic Science of Nursing, Saga Medical School, Saga 849-8501, Japan.
Norie
N
Inoue
Department of Pathology and Biodefense, Saga Medical School, Saga 849-8501, Japan.
Atsushi
A
Nakayama
Department of Pathology and Biodefense, Saga Medical School, Saga 849-8501, Japan.
Shuji
S
Toda
Department of Internal Medicine and Gastrointestinal Endoscopy, Saga Medical School, Saga 849-8501, Japan. Electronic address: fujimoto@med.saga-u.ac.jp.
Kazuma
K
Fujimoto
D000818:Animals; D003092:Colitis / Q000139:chemically induced* / Q000378:metabolism / Q000517:prevention & control; D051546:Cyclooxygenase 2 / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D016264:Dextran Sulfate / Q000009:adverse effects*; D008297:Male; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D000069463:Olive Oil; D010938:Plant Oils / Q000008:administration & dosage*; D051381:Rats; D017207:Rats, Sprague-Dawley
D016207:Cytokines; D000069463:Olive Oil; D010938:Plant Oils; D016264:Dextran Sulfate; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2
Apoptosis; Colon cancer; Inflammatory bowel disease; STAT3; Ulcerative colitis; pSTAT3