Grape seed proanthocyanidin improves intestinal inflammation in canine through regulating gut microbiota and bile acid compositions.

Although certain progress has been made in treating canine inflammatory bowel disease (IBD), a large proportion of dogs have a poor prognosis and may develop resistance and side effects. Therefore, it is of great significance to prevent or alleviate canine IBD through nutritional intervention. Plant polyphenol can interact with intestinal bacteria and has important prospects in the intestinal health improvement. This study evaluated the effect of grape seed proanthocyanidin (GSP), a plant-derived natural polyphenol, on Labrador Retrievers with mild IBD. In Experiment 1 of this study, GSP alleviated persistent intestinal inflammation in canines by improving inflammatory indexes and reducing intestinal permeability. Moreover, GSP treatment increased the abundance of bacteria with potential anti-inflammatory properties and engaging bile acid metabolism, including Ruminococcaceae, Faecalibacterium, Ruminococcus_torques_group, and Lachnospiraceae_NK4A136_group. Notably, targeted metabolomic analysis identified elevated productions of fecal chenodeoxycholic acid and its microbial transformation product lithocholic acid, which might contribute to relieving canine intestinal inflammation. Further, in Experiment 2, fecal microbiota transplantation was used to determine whether gut microbiota is a potential mechanism for GSP efficacy. Dogs with mild IBD received the fecal microbiota from the group administered GSP and mirrored the improvement effects of GSP, which results verified that gut microbial alteration could be an underlying mechanism for GSP efficiency on canine IBD. Our findings highlight that the mechanism of the GSP function on canine IBD is mediated by altering gut microbial composition and improving bile acid metabolism. This study proposes a natural polyphenol-based dietary strategy for improving canine intestinal health.

Effects of Avenanthramide on the Small Intestinal Damage through Hsp70-NF-κB Signaling in an Ovalbumin-Induced Food Allergy Model.

A food allergy is caused by an abnormal immune reaction and can induce serious intestinal inflammation and tissue damage. Currently, the avoidance of food allergens is still the most effective way to prevent or reduce allergic symptoms, so the development of new strategies to treat allergies is important. Avenanthramide (AVA) is a bioactive polyphenol derived from oats with a wide range of biological activities; however, it is still not clear whether or how AVA alleviates intestinal damage under allergic situations. The aim of this study was to explore the effect of AVA on the small intestinal damage in an ovalbumin (OVA)-induced food allergy model and its mechanism. In experiment 1, 10 mg/kg bw and 20 mg/kg bw doses of AVA both decreased the serum levels of OVA-specific IgE, histamine, and prostaglandin D induced by OVA. The AVA administration relieved inflammation indicated by the lower serum concentrations of pro-inflammatory cytokines including interleukin-1ß, IL-6, and tumor necrosis factor-α. The levels of tight junction proteins including Claudin-1, ZO-1, and Occludin in the jejunum were elevated after AVA administration, accompanied by the improved intestinal morphology. Furthermore, AVA elevated the protein expression of heat shock protein 70 (Hsp70) and inhibited the phosphorylation of nuclear factor kappa-B (NF-κB), thus the apoptozole, which a Hsp70 inhibitor, was applied in experiment 2 to assess the contribution of Hsp70-NF-κB signaling to the effects of AVA. In the experiment 2, the inhibition of Hsp70 signaling treatment abolished the beneficial effects of AVA on the small intestinal damage and other allergic symptoms in mice challenged with OVA. Taken together, our results indicated that AVA exerted an intestinal protection role in the OVA-induced allergy, the mechanism of which was partly mediated by the Hsp70-NF-κB signaling.