Abstract
Tea tree oil (TTO) exhibits a potent antioxidant, antibacterial, and anti-inflammatory activity and is commonly used in skincare products. However, it is not clear whether TTO can protect gut barrier damage in inflammatory bowel disease (IBD) patients. Herein, we report the impact of terpinen-4-ol (TER, the primary constituent of TTO), on lipopolysaccharide (LPS)-induced intestinal epithelial cell barrier function impairment in intestinal porcine epithelial cell lines (IPEC-J2) and dextran sulfate sodium (DSS)-induced IBD in mice. TER protected against LPS-induced damage in IPEC-J2 cells in vitro and attenuated DSS-induced colitis in vivo. Added TER promoted the tight junction (TJ) proteins expressing in vitro and in vivo and attenuated the LPS-induced upregulation of ERK phosphorylation in IPEC-J2 cells. However, when an inhibitor of ERK phosphorylation was added, TER did not promote the expression of TJ protein, denoting that the ERK signaling pathway mediates the upregulation of TJ proteins. Our data may propose the potential application of TER in treating IBD.
Highlights
Inflammatory bowel disease (IBDs) is a chronic inflammatory disease of the gastrointestinal tract, which comprises Crohn’s disease (CD), ulcerative colitis (UC), and indeterminate colitis [1]
The spectral results were similar to the TER structure reported in previous studies [24, 25]
Our study showed that TER protected IPEC-J2 cells against LPS-induced inflammation and dextran sulfate sodium (DSS)-induced colitis
Summary
Inflammatory bowel disease (IBDs) is a chronic inflammatory disease of the gastrointestinal tract, which comprises Crohn’s disease (CD), ulcerative colitis (UC), and indeterminate colitis [1]. This disease affects all ages, and the clinical features primarily include fever, weight loss, diarrhea, and blood in stool [2]. The lesions of IBD patients are mainly confined to the colorectal mucosa and submucosa They are characterized by mucosal barrier damage and impaired tight junction (TJ) functions, resulting in a loss in gut barrier integrity [4]. Tight junctions between epithelial cells play a role in maintaining the permeability and integrity of the intestinal mucosal barrier. The upregulation of both ZO-1 and occludin expression significantly improves the integrity, reduces the intestinal mucosal barrier permeability, and prevents the infiltration of harmful substances in IBD patients [7, 8]
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