Abstract
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.
Highlights
Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is chronic a remittent or progressive intestinal inflammatory conditions featuring by over‐expression of pro‐ inflammatory cytokines and decreased levels of immunosuppressive cytokines (Kaser, Zeissig, & Blumberg, 2009; Niessner & Volk, 1995)
We investigate the effects of HFHSD and alpha‐linolenic acid (ALA) supplement to trinitrobenzene sulfonic acid (TNBS)‐induced mouse colitis by a dietary intervention strategy, which is consistent with the current popular Western food
These experiments suggest that consuming a low dose of ALA daily could significantly prevent the incidence of colitis by the capacity of ALA and its metabolites to adjust the expression of T helper (Th) cell‐related cytokines in the colon
Summary
Inflammatory bowel disease (IBD), including ulcerative colitis (UC) and Crohn's disease (CD), is chronic a remittent or progressive intestinal inflammatory conditions featuring by over‐expression of pro‐ inflammatory cytokines and decreased levels of immunosuppressive cytokines (Kaser, Zeissig, & Blumberg, 2009; Niessner & Volk, 1995). We investigate the effects of HFHSD and ALA supplement to trinitrobenzene sulfonic acid (TNBS)‐induced mouse colitis by a dietary intervention strategy, which is consistent with the current popular Western food. These experiments suggest that consuming a low dose of ALA daily could significantly prevent the incidence of colitis by the capacity of ALA and its metabolites to adjust the expression of T helper (Th) cell‐related cytokines in the colon. Over‐increasing n‐3/n‐6 PUFAs ratio did not protect mice from TNBS‐induced colitis and could even exacerbate the symptoms
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