Cis-Nerolidol Inhibits MAP Kinase and NF-κB Signaling Pathways and Prevents Epithelial Tight Junction Dysfunction in Colon Inflammation: In Vivo and In Vitro Studies

• Published in: Molecules (Basel, Switzerland) Vol. 28; no. 7; p. 2982
• Main Authors: Raj, Vishnu, Venkataraman, Balaji, Ojha, Shreesh K., Almarzooqi, Saeeda, Subramanian, Veedamali S., Al-Ramadi, Basel K., Adrian, Thomas E., Subramanya, Sandeep B.
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 27.03.2023; MDPI
• Subjects: Adalimumab; Analysis; Antioxidants; Caco-2 Cells; Chemokines; Colitis - chemically induced; Colitis - drug therapy; Colitis - metabolism; Colon; Crohn's disease; Cytokines; Cytokines - metabolism; Cytotoxicity; Dextran; Dextran Sulfate - adverse effects; DSS colitis; epithelial tight junction; Ethical aspects; Gastrointestinal system; Humans; Inflammation; Inflammation - drug therapy; Inflammation - metabolism; Inflammatory bowel disease; Intestinal Mucosa - metabolism; Investigations; Kinases; Lipopolysaccharides - pharmacology; Macrophages; MAPK; Mitogen-Activated Protein Kinases - metabolism; Morphology; nerolidol; NF-kappa B - metabolism; Permeability; Phosphorylation; Physiological aspects; Protein expression; Proteins; RAW macrophages; Sesquiterpenes - pharmacology; Signal Transduction; Tight Junction Proteins - metabolism; Tight Junctions - metabolism; Ulcerative colitis; United States; Illinois; United Arab Emirates; nerolidol; Caco-2 cells; DSS colitis; MAPK; epithelial tight junction; RAW macrophages

Inflammation of the GI tract leads to compromised epithelial barrier integrity, which increases intestine permeability. A compromised intestinal barrier is a critical event that leads to microbe entry and promotes inflammatory responses. Inflammatory bowel diseases that comprise Crohn’s disease (CD)...