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

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.

Anti-inflammatory effect of Perilla frutescens seed oil rich in omega-3 fatty acid on dextran sodium sulfate-induced colitis in mice

“…Wen et al . found that the protective effects of given ALA (150 mg/kg) dose on mouse colitis induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) and suggested its possible underlying mechanisms of the interactions via the Th1/Th2/Th17 pathway ( 28 ). ALA from the diet could be incorporated into tissue membrane phospholipids or enzymatic conversion to EPA and DHA ( 29 ).…”

Walnut Oil Alleviates Intestinal Inflammation and Restores Intestinal Barrier Function in Mice

“…This fatty acid disrupts the Th1/Th2/Th17 pathways involved in inflammatory bowel disease (IBD) pathogenesis and activates the Treg pathway. It is proven that the predominant cytokine involved in the Treg pathway, Il-10, acts as an anti-inflammatory factor [39]. Another proposed mechanism assumed that the omega fatty acids, as precursors for eicosanoids, modulate the inflammatory response.…”

Pterocarpus mildbraedii(Harms) extract resolves propanil‐induced hepatic injury via repression of inflammatory stress responses in Wistar rats

“…Furthermore, the hepatoprotective effects of the ethanolic extract of Vitis vinifera seeds in diabetic rats have been attributed to the presence of fatty acids such as hexadecanoic, octadecadienoic, and octadecanoic acids (Giribabu et al., 2018). The potential of PME as a functional food is boosted by the presence of α‐linolenic acid, an omega‐3‐fatty acid that has been reported to possess anti‐inflammatory activity (Ros et al., 2018; Wen et al., 2019). However, additional characterization studies are necessary to delineate the specific active principles responsible for the pharmacological action of Pterocarpus mildbraedii .…”