Pycnogenol mitigates obesity-associated liver injury via Nrf2/HO-1 activation and NF-κB restraint in rats

Obesity is a major determinant of metabolic dysfunction, characterized by insulin resistance, dyslipidemia, and low-grade chronic inflammation, and most commonly manifests as steatotic liver disease. This study investigated the effects of Pycnogenol® (Pinus pinaster bark extract) on obesity-induced hepatic injury at histological and molecular levels. A total of 28 male Sprague Dawley rats were fed either a standard diet or a high-fat diet (30 days) and allocated into control, Pycnogenol, obesity, and obesity + Pycnogenol groups. Pycnogenol was administered orally at 30 mg/kg for 15 days. At the end of the experiment, liver tissues were collected for histopathological evaluation and Western blot analysis. In the obesity group, marked macrovesicular steatosis, lobular inflammation, and hepatocellular ballooning were observed, with significantly increased Nonalcoholic Fatty Liver Disease Activity Score (NAS) scores. Pycnogenol administration significantly reduced NAS scores and partially restored hepatic architecture. At the molecular level, elevated Caspase-3 and nuclear factor kappa B (NF-κB) expression in the obesity group were significantly suppressed by Pycnogenol, while decreased Bcl-2, Nuclear factor–erythroid 2–related factor 2 (Nrf2), and (Heme oxygenase-1) HO-1 levels were restored toward control values. Pycnogenol alone did not produce significant alterations compared with the control group. In conclusion, Pycnogenol attenuated obesity-induced liver injury by reduced histopathological severity, suppressing inflammatory/apoptotic signaling, and reactivating antioxidant defenses. These findings suggest that Pycnogenol may serve as a potential complementary strategy for obesity-associated liver diseases.