Tea Tree Oil Terpinen-4-ol Protects Gut Barrier Integrity by Upregulation of Tight Junction Proteins via the ERK1/2-Signaling Pathway

Yanhong Yong; Biao Fang; Yingxin Huang; Junyu Li; Tianyue Yu; Lianyun Wu; Canying Hu; Xiaoxi Liu; Zhichao Yu; Xingbin Ma; Ravi Gooneratne; Sidong Li; A M Abd El-Aty; Xianghong Ju

doi:10.3389/fnut.2021.805612

Tea Tree Oil Terpinen-4-ol Protects Gut Barrier Integrity by Upregulation of Tight Junction Proteins via the ERK1/2-Signaling Pathway

Front Nutr. 2022 Jan 27:8:805612. doi: 10.3389/fnut.2021.805612. eCollection 2021.

Authors

Yanhong Yong^{1

2}, Biao Fang², Yingxin Huang², Junyu Li³, Tianyue Yu³, Lianyun Wu³, Canying Hu³, Xiaoxi Liu¹, Zhichao Yu², Xingbin Ma², Ravi Gooneratne⁴, Sidong Li⁵, A M Abd El-Aty^{6

7}, Xianghong Ju^{1

2}

Affiliations

¹ Shenzhen Institute of Guangdong Ocean University, Shenzhen, China.
² Department of Veterinary Medicine, College of Agricultural Sciences, Guangdong Ocean University, Zhanjiang, China.
³ Department of Animal Science, College of Agricultural Sciences, Guangdong Ocean University, Zhanjiang, China.
⁴ Department of Wine, Food and Molecular Biosciences, Faculty of Agriculture and Life Sciences, Lincoln University, Lincoln, New Zealand.
⁵ College of Chemistry and Environment, Guangdong Ocean University, Zhanjiang, China.
⁶ Department of Pharmacology, Faculty of Veterinary Medicine, Cairo University, Giza, Egypt.
⁷ Department of Medical Pharmacology, Medical Faculty, Ataturk University, Erzurum, Turkey.

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.

Keywords: ERK1/2-signaling pathway; inflammatory bowel disease; mouse model; terpinen 4-ol; tight junction (TJ) proteins.