Alpha‐linolenic acid given as an anti‐inflammatory agent in a mouse model of colonic inflammation

• Published in: Food science & nutrition Vol. 7; no. 12; pp. 3873 - 3882
• Main Authors: Wen, Juan, Khan, Israr, Li, Anping, Chen, Xinjun, Yang, Pingrong, Song, Pingshun, Jing, Yaping, Wei, Junshu, Che, Tuanjie, Zhang, Chunjiang
• Format: Journal Article
• Language: English
• Published: United States John Wiley & Sons, Inc 01-12-2019; John Wiley and Sons Inc
• Subjects: Body weight; Body weight loss; Cardiovascular disease; Cholesterol; Colitis; Colon; Cytokines; Damage; Diet; Experiments; Fatty acids; Fish oils; Food; Helper cells; High density lipoprotein; High fat diet; Hyperlipidemia; Immune system; Inflammation; Inflammatory bowel disease; Interferon; Linolenic acid; Lipids; Lymphocytes T; Metabolism; Metabolites; Original Research; Researchers; Signs and symptoms; Spleen; Sulfonic acid; Triglycerides; T‐cell‐related cytokines; Weight loss; α‐linolenic acid; α‐linolenic acid; T‐cell‐related cytokines; inflammatory bowel disease
• ISSN: 2048-7177; 2048-7177
• DOI: 10.1002/fsn3.1225

This study examined the relationship between the high‐fat, high‐sugar diet (HFHSD) and trinitrobenzene sulfonic acid (TNBS) induced mouse colitis, the therapeutic effect of alpha‐linolenic acid (ALA) on mouse colitis, and the relationship between HFHSD and hyperlipidemia. We also examined the possible underlying mechanisms behind their interactions. Female BABL/c mice were fed with HFHSD for the 9 weeks. At the same time, ALA treatment (150 or 300 mg/kg) was administered on a daily basis. At the end of the 9 weeks, experimental colitis was induced by the intra‐colonic administration of TNBS. Body weight, spleen weight, disease activity index (DAI), histological changes, T‐cell‐related cytokine level, and lipid profiles were measured after treatment. TNBS induced severe clinical manifestations of colitis and histological damage. Low‐ALA (150 mg/kg) administration profoundly ameliorated TNBS‐induced clinical manifestations, body weight loss, spleen weight loss, and histological damage. On the contrary, the high‐ALA (300 mg/kg) administration did not ameliorate colitis and even exacerbated the symptoms. HFHSD consumption assisted TNBS in changing IL‐12, IFN‐γ, IL‐2, and IL‐17A in the liver. As expected, these changes were recovered through low‐ALA. In addition, HFHSD had a significant impact on the total cholesterol (TC), high‐density lipoprotein cholesterol (HDL‐C), and triglyceride (TG), which related to the increased risk of hyperlipidemia. In summation, HFHSD exacerbated the TNBS‐induced colitis via the Th1/Th17 pathway. The Low‐ALA (150 mg/kg) exhibited protective effects against the TNBS‐induced colitis via the Th1/Th2/Th17 pathway.
High‐fat, high‐sugar diet (HFHSD) exacerbated the trinitrobenzene sulfonic acid (TNBS)‐induced colitis via the Th1/Th17 pathway activation. The Low‐alpha‐linolenic acid (ALA) exhibited protective effects against the TNBS‐induced colitis via the Th1/Th2/Th17 pathway suppression.