Background:&nbsp;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-1&beta;, TNF-&alpha;, IL-6, NF-&kappa;B) 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.

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

Background: This study investigated the protective capabilities of galangin, a naturally occurring flavonoid found in galangal and propolis, against glycerol-induced acute kidney injury (AKI), a serious complication associated with rhabdomyolysis. 
 
Methods: Rats were pre-treated with galangin (100 mg/kg) for 21 days before receiving a glycerol single injection (50%, 10 mg/kg, intramuscular) to induce AKI. According to the findings, the kidneys in the AKI group showed notable molecular, and functional alterations. 
 
Result: Treatment with galangin notably reduced kidney relative weight and decreased serum levels of urea and creatinine, indicating preservation of renal function. Furthermore, the intervention lowered concentrations of lactate dehydrogenase (LDH) and creatine kinase (CK), key indicators of muscle breakdown associated with rhabdomyolysis. A remarkable finding was galangin&rsquo;s ability to enhance the endogenous antioxidant defence system. Treatment led to increased activity of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR), along with elevated levels of reduced glutathione (GSH). Concurrently, galangin treatment resulted in reduced malondialdehyde (MDA) and nitric oxide (NO) concentrations, demonstrating effective suppression of oxidative stress markers. Similarly, animals receiving galangin exhibited significantly reduced levels of pro-inflammatory mediators, including interleukin-1&beta; (IL-1&beta;), tumor necrosis factor-&alpha; (TNF-&alpha;), myeloperoxidase (MPO), and nuclear factor kappa B (NF-&kappa;B). Simultaneously, there was an elevation in anti-inflammatory interleukin-10 (IL-10) compared to the untreated model group, in addition to a significant modulation of apoptotic pathways by decreased expression of pro-apoptotic proteins Bax and caspase-3, and increased in Bcl-2. The comprehensive findings from this study provide compelling evidence for galangin as a promising therapeutic agent against glycerol-induced acute kidney injury. Overall, galangin shows promise as a potential therapeutic agent for preventing or treating rhabdomyolysis-associated acute kidney injury.

Galngin Mitigates Glycerol-induced Rhabdomyolysis-associated Acute Kidney Injury by Modulating Nf-&kappa;b-mediated Cytokine Pathways and Apoptotic Responses