Abstract
Sea bass (Lateolabrax maculatus) is a kind of food material commonly consumed in daily life. In traditional Chinese medicinal books, it has been indicated that sea bass can be applied for managing many inflammation-associated conditions. However, the studies on the pharmacological mechanisms of inflammation of sea bass remain scarce. Hence, this study aims to investigate the molecular mechanisms of the anti-inflammatory activity of sea bass. Anti-inflammatory activities of sea bass were assessed using dextran sulfate sodium (DSS)-induced colitis in a mice model and lipopolysaccharide (LPS)-activated macrophages model. Low body weight and short colon length were observed in DSS-fed mice that were significantly recovered upon sea bass treatments. Moreover, the colon histopathology score showed that sea bass-treated mice had decreased crypt damage, focal inflammation infiltration and the extent of inflammation, suggesting that treatment with sea bass could attenuate intestinal inflammation. In addition, the in-vitro study conjointly indicated that sea bass could suppress the inflammatory mediators in LPS-activated macrophage by inhibiting the TLR4-linked pathway. The present findings demonstrated that sea bass has an inhibitory effect on TLR4 signaling; thus, it could be a promising candidate for treating inflammation-associated conditions. A further justification for the clinical application of sea bass in treating inflammation-associated conditions is necessary.
Highlights
Inflammatory bowel disease (IBD) is principally outlined as Crohn’s disease and ulcerative colitis (UC)
The current results clearly indicate that aqueous extract of sea bass (ASB) possesses potential anti-inflammation therapeutic efficacy through inhibiting the activation of Toll-like receptor 4 (TLR4) signaling against dextran sulfate sodium (DSS)-induced colitis and LPS-activated macrophages
According to the in vivo and in vitro studies, the activation of TLR4 signaling was significantly inhibited upon ASB treatments
Summary
Inflammatory bowel disease (IBD) is principally outlined as Crohn’s disease and ulcerative colitis (UC). Ulcerative colitis (UC) mainly presents in the rectal and colonic mucosa and is accompanied by weight loss, diarrhea, abdominal pain, and rectal bleeding This kind of uncontrolled gut inflammation affects millions of individuals in the world [1,2]. Colitis is induced chemically in this model by adding DSS to the drinking water of mice It mainly affects the distal colon; some inflammatory responses appeared even in the proximal colon and caecum. Toll-like receptor 4 (TLR4) signaling is one of the important mechanisms for inflammation-related studies and it is a key receptor for commensal recognition in gut innate immunity [12] It was the subject of target inhibition in ulcerative colitis (UC) [12,13]. It is necessary to evaluate the effects of TLR4 signaling in DSS-induced colitis for studying UC in detail
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