Veterinary Research Forum

Abstract Micromeria congesta (MC) is a medicinal plant traditionally used in the Şanlıurfa, Adıyaman, and Gaziantep provinces of Türkiye for treating respiratory disorders. Despite its ethnobotanical relevance, its pharmacological effects on lung inflammation remain unclear. This study evaluated the protective effects of MC essential oil (MCEO) against lipopolysaccharide (LPS)-induced acute lung injury in rats, with a focus on inflammation and tissue damage. The MC was collected from its natural habitat, and its EO was extracted by hydro-distillation using a Clevenger-type apparatus. The Gas chromatography-mass spectrometry analysis revealed 28 compounds, with piperitenone oxide (33.97%) and pulegone (22.30%) as the main constituents. Thirty-six Wistar albino rats were randomly assigned into six groups, including three MCEO-treated (12.50, 25.00, and 50.00 mg kg^-1), dexamethasone, LPS-only, and control groups. The MCEO was administered by gavage for seven days, followed by intra-venous LPS on day eight (except for the control group). Blood and lung tissues were collected 6 hr later for biochemical, histopathological, and molecular analyses. The MCEO treatment significantly lowered blood glucose and urea levels compared to the LPS group. It also modulated NLRP3, caspase-3, and tumor necrosis factor alpha genes expressions, as determined by RT-PCR analysis, indicating anti-inflammatory effects. Histopathological findings confirmed a dose-dependent reduction in lung inflammation and tissue damage. The MCEO administration alleviated LPS-induced acute lung injury in rats through anti-inflammatory and protective effects, as confirmed by molecular (NLRP3, caspase-3, and tumor necrosis factor alpha) and histopathological analyses. Additionally, MCEO reduced blood glucose and urea levels, supporting its systemic protective role against endotoxin-induced inflammation.

Abstract Intense exercise is known to induce oxidative stress and inflammation, potentially leading to liver damage. This study examined the potential protective effects of apilarnil (AP), a natural bioactive compound with antioxidant and anti-inflammatory properties, against exercise-induced liver injury. Thirty-five male Wistar albino rats were allocated into five groups: Control, non-exercise (NEX), exercise (EX), EX + AP1 (0.20 g kg^-1) and EX + AP2 (0.40 g kg^-1). At the end of the 14-day experiment, serum and liver tissue samples were collected for the analysis of histopathological changes, oxidative stress markers, inflammatory cytokines and serum biochemical parameters. Histopathological evaluations revealed substantial liver damage in the EX group. However, in the EX + AP1 and EX + AP2 groups, the severity of these lesions was significantly attenuated. Biochemical analyses demonstrated elevated levels of tumor necrosis factor-alpha, interleukin-1 beta and interleukin-6 in the NEX group were markedly reduced by AP supplementation. Similarly, malondialdehyde levels were increased, while the activities of antioxidant enzymes - catalase, superoxide dismutase and glutathione peroxidase were declined in the NEX group. AP supplementation reversed these effects by lowering malondialdehyde levels and enhancing antioxidant enzyme activities in the EX + AP1 and EX + AP2 groups. Additionally, serum biochemical analyses indicated improved lipid profiles and liver function parameters in the AP -treated groups compared to the NEX group. In conclusion, histopathological and biochemical findings indicated that AP supplementation mitigated exercise-induced liver damage by reducing oxidative stress and inflammation, while enhancing antioxidant defenses.