Caffeine Pre-treatment Mitigates Lipopolysaccharide-Induced Oxidative Stress and Lipid Peroxidation in Rat Lung Tissue

Background: Lipopolysaccharide (LPS) induces acute lung injury (ALI), which is mechanistically linked to severe oxidative stress and disruption of the antioxidant defense system. This study evaluates the capacity of caffeine pre-treatment to mitigate LPS-induced oxidative damage in rat lung tissue, specifically focusing on key antioxidant markers. Methods: Thirty-five male Wistar rats were divided into five groups: Control (without any drug intervention), LPS-only (۱۰ mg/kg i.p.), LPS + Dexamethasone (۲.۵ mg/kg i.p.), and LPS + Low-dose caffeine (۱۰ mg/kg oral gavage) or High-dose caffeine (۵۰ mg/kg oral gavage) pre-treatment for ۱۴ days. Oxidative stress status was assessed in lung homogenates by measuring lipid peroxidation using Malondialdehyde (MDA) levels and evaluating antioxidant capacity through Total Antioxidant Capacity (TAC) and Catalase (CAT) activity via colorimetric assays. Results: LPS administration significantly increased lipid peroxidation, evidenced by elevated MDA levels (p>۰.۰۰۵), and concurrently depleted the lung's defense capacity, shown by a reduction in TAC and CAT activity. Pre-treatment with both low- and high-dose caffeine significantly reversed this damage. Caffeine effectively reduced MDA levels (p>۰.۰۰۵ for low-dose; p>۰.۰۰۶ for high-dose) and demonstrated a trend toward restoring TAC and CAT activity compared to the LPS-only group, indicating significant mitigation of oxidative damage. Conclusion: Caffeine pre-treatment successfully alleviates LPS-induced oxidative stress in rat lung tissue by reducing lipid peroxidation (MDA) and supporting the intrinsic antioxidant system (TAC and CAT). These findings suggest that caffeine acts as a potent antioxidant agent, contributing to its overall protective effect against ALI.

کلیدواژه ها:

Caffeine ، Acute Lung Injury ، Malondialdehyde ، Total Antioxidant Capacity ، Catalase