Chamomile tea as a supplement therapy relieves thinner induced-lung injury in rats through inhibiting inflammation, oxidative stress and P53-dependant apoptotic pathways

Abstract Background Lung injury is a frequent adverse effect of chronic thinner exposure. The purpose of this research was to assess whether or not chamomile tea may protect against thinner-induced lung damage and its potential mechanisms. Thirty adult male Wistar rats were randomly assigned into five equal groups; the first three were control, vehicle, and chamomile tea (400 mg/kg bw), while the last two groups were inhaled thinner at a dosage of 4500 ppm, four hours/day, six days/week, with or without chamomile tea, daily for eight weeks. Lung tissues were taken for biochemical and immunohistochemical investigations at the end of intervention period. Results Thinner exposure resulted in significant increases in inflammatory cytokines (TNF- α , IL-1, IL-6), inflammatory mediators (COX2,NF- κβ ), adhesion molecules (ICAM-1, VCAM-1), lipid peroxidation product 4-HNE, and nitric oxide bioavailability, accompanied by depletion of the anti-inflammatory cytokine IL-10, GSH content, GPX activity, and total antioxidant capacity within lung tissue. Thinner exposure also resulted in cell cycle arrest, appeared at the S and G 2/ M phases, decline in the anti-apoptotic BCL2 and increases in Bax, cytochrome-c, Bax/Bcl2 ratio, expression of P53 and caspase-3, and the proportions of annexin V/PI positive cells, indicating heightened apoptosis. Nevertheless, a higher reduction in lung inflammation, oxidative damage, and apoptosis were prominently observed following administration of chamomile tea to the thinner group. Conclusion Findings could verify the safety and efficacy of chamomile tea as a natural medication for thinner toxicity and related pulmonary damage.