Obesity, a global epidemic, has been strongly associated with impairment of brain function. Lycopene has several therapeutic properties and can cross the blood-brain barrier. However, its effects on obesity-provoked brain dysfunction remain unexplored. This study evaluated the potential remediating effects of lycopene on obesity-induced neurological derangements. Thirty-six female Wistar rats (150-200g) were distributed in six groups (n = 6); normal control, obese control, obese + lycopene (20 mg/kg), obese + lycopene (40 mg/kg), normal + lycopene (20 mg/kg), and normal + lycopene (40 mg/kg). Obesity was induced by feeding rats with the Western diet for eight weeks, while normal rats received the control diet. Afterwards, the brain was excised and processed for biochemical, gene expression analyses, and histological evaluations. Obesity-induced brain dysfunction was hallmarked by reduced brain organosomatic index, accumulation of lipids in the cerebrum, and hyperactivity of neurotransmitters-metabolizing enzymes (AChE, ADA, MAO-A, 5'-nucleotidase, and NTPdase). Also, obese rats had decreased antioxidant capacity, with increased oxidative damage, while the expressions of NF-κβ p65 and pro-inflammatory cytokines (IL-1β and IL-6) were elevated in the hypothalamus. These observations were validated by histomorphological evaluations, which showed vacuolation in the brain of obese rats. Treatment with lycopene significantly (p < 0.05) reduced the elevated lipid contents and activities of neuronal enzymes, alleviated oxidative stress and inflammation, while improving the histology of the brain, in a dose-dependent manner. Thus, lycopene abrogates obesity-provoked brain dysfunction and may present a safe and viable therapeutic option for the management of neurological perturbations associated with obesity.
Keywords: Inflammation; Lycopene; Neuro-signalling; Obesity; Oxidative stress.
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