Modulation of Inflammatory and Apoptotic Pathways by Tamarix Aphylla Essential Oil in TNBS-Induced Colitis: A Focus on Cytokine Balancing, NF-κB, p38 MAPK, and Nrf2 Activation.

Inflammatory Bowel Disease (IBD) refers to the inflammatory disorders of the colon and small intestine. The effect of the essential oil from Tamarix aphylla (TAEO) on inflammation and apoptosis has been investigated using a rat TNBS-induced colitis model. The study utilized macroscopic and histopathological evaluations, cytokine profiling by ELISA, and protein expression assays to assess the effects of TAEO on ulceration, cytokine levels, apoptotic proteins, and anti-apoptotic proteins. Sound experimental groups received several dosages of TAEO (10, 30, and hundred mg/kg) and dexamethasone serving as a comparative control. TAEO significantly reduced mucosal damage in a dose-dependent manner, with dosages of 30 and 100 mg/kg effectively decreasing the ulcer index compared to controls (p < 0.001). It also modulated cytokine profiles, notably reducing TNF-α (p < 0.05 for 30 mg/kg; p < 0.001 for 100 mg/kg), IL-1β, and TGF-β (p < 0.05 for 30 mg/kg; p < 0.001 for 100 mg/kg), while increasing IL-10 at higher doses (p < 0.01 for 30 mg/kg; p < 0.001 for 100 mg/kg). Furthermore, TAEO reduced the expression of pro-apoptotic proteins Bax and caspase-3 (p < 0.001 for both at 100 mg/kg), and enhanced the anti-apoptotic protein Bcl-2. Reductions in NF-κB and p38 MAPK activation were also significant (p < 0.01 and p < 0.001, respectively, for 100 mg/kg). Notably, high-dose TAEO (100 mg/kg) significantly activated the Nrf2 pathway more than dexamethasone (p < 0.001), promoting antioxidant defenses. Histopathological assessments confirmed these findings, showing substantial improvements in tissue architecture and reductions in inflammatory markers. TAEO possesses strong anti-inflammatory, anti-apoptotic, and antioxidant actions in TNBS-induced colitis with high therapeutic potential against IBD. The effects are specific towards higher doses, suggesting a dose-dependent mechanism of action, and justifying further testing.