Article Publish Status: FREE
Abstract Title:

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

Abstract Source:

Food Sci Nutr. 2019 Dec ;7(12):3873-3882. Epub 2019 Nov 19. PMID: 31890165

Abstract Author(s):

Juan Wen, Israr Khan, Anping Li, Xinjun Chen, Pingrong Yang, Pingshun Song, Yaping Jing, Junshu Wei, Tuanjie Che, Chunjiang Zhang

Article Affiliation:

Juan Wen


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 protectiveeffects against the TNBS-induced colitis via the Th1/Th2/Th17 pathway.

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