Targeting Neuroinflammation and Monoamine Dysregulation: Galangins Multifacedted Neuroprotective Role against LPS-Induced Brain Injury

Abstract

Background: Natural compounds with antioxidant and anti-inflammatory properties, such as galangin, have gained attention for their potential neuroprotective effects. This study aimed to evaluate the neuroprotective potential of galangin, a natural flavonoid derived from Alpinia galanga and propolis, against lipopolysaccharide (LPS)-induced neurotoxicity and neuroinflammation in a rat model. Methods: Forty adult male rats were randomly allocated into four groups (n=10/group): control, galangin (100 mg/kg/day, i.p.), LPS (2.5 mg/kg, i.p.) and galangin+LPS. Galangin was administered for 21 consecutive days prior to a single LPS injection. Result: Neurochemical analyses revealed that LPS significantly disrupted dopaminergic and noradrenergic neurotransmission, evidenced by reduced dopamine (DA) and norepinephrine (NE) levels, elevated monoamine oxidase (MAO) activity and decreased brain-derived neurotrophic factor (BDNF). LPS induced pronounced oxidative stress, marked by increased malondialdehyde (MDA and NO) and diminished antioxidant defenses (SOD, CAT, GSH). Proinflammatory cytokines (IL-1β, TNF-α, IL-6, NF-κB) were significantly increased, alongside enhanced apoptotic signaling (increased Bax and caspase-3, reduced Bcl-2). Galangin pretreatment effectively counteracted these LPS-induced alterations, restoring neurotransmitter balance, MAO and BDNF levels, reducing oxidative and inflammatory damage and regulating apoptotic pathways. These results suggest that galangin had neuroprotection against LPS-induced brain injury by modulating neurochemical, inflammatory and apoptotic mechanisms.