Effects of Luffa cylindrica (L.) Roem Extract on Microglial Activation-Mediated Mild Cognitive Impairment via Regulation of CREB Signaling Pathway
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Neuroinflammation is increasingly recognized as a pivotal contributor to mild cognitive impairment (MCI), with microglial activation playing a central role in this process. While Luffa cylindrica (L.) Roem is known for its anti-inflammatory properties, its effects on MCI and its active components have not been fully elucidated. In this study, we evaluated the anti-inflammatory and neuroprotective effects of Luffa cylindrica extract (LCE) on microglial activation and MCI-like behaviors induced by lipopolysaccharide (LPS). BV2 microglial cells were stimulated with LPS (1 μg/ml) and treated with LCE (25, 50, or 100 μg/ml). Microglial activation was assessed via Griess assay, western blotting, RTPCR, and ELISA. In vivo, male ICR mice were received LCE (50 or 300 mg/kg) orally for 7 days in combination with intraperitoneal LPS (0.5 mg/kg). Cognitive function was evaluated using passive avoidance and Y-maze tests. The hippocampus was harvested for biochemical analysis. Highperformance liquid chromatography (HPLC) was used to identify major bioactive components of LCE. LCE treatment significantly reduced the production of nitric oxide (NO), pro-inflammatory cytokine expression, and inflammation-associated protein levels in BV2 cells. These effects were associated with inhibition of the AKT-GSK3β-CREB signaling pathway. In vivo, oral LCE administration ameliorated LPS-induced cognitive impairment and decreased inflammatory markers in the hippocampus. HPLC analysis identified myricetin as a major component of LCE, which independently exhibited anti-inflammatory effects in microglia. These findings highlight the potential of LCE as a natural therapeutic agent for neuroinflammation-related cognitive impairment, with myricetin contributing to its pharmacological activity.
Abstract
Neuroinflammation is increasingly recognized as a pivotal contributor to mild cognitive impairment (MCI), with microglial activation playing a central role in this process. While Luffa cylindrica (L.) Roem is known for its anti-inflammatory properties, its effects on MCI and its active components have not been fully elucidated. In this study, we evaluated the anti-inflammatory and neuroprotective effects of Luffa cylindrica extract (LCE) on microglial activation and MCI-like behaviors induced by lipopolysaccharide (LPS). BV2 microglial cells were stimulated with LPS (1 μg/ml) and treated with LCE (25, 50, or 100 μg/ml). Microglial activation was assessed via Griess assay, western blotting, RTPCR, and ELISA. In vivo, male ICR mice were received LCE (50 or 300 mg/kg) orally for 7 days in combination with intraperitoneal LPS (0.5 mg/kg). Cognitive function was evaluated using passive avoidance and Y-maze tests. The hippocampus was harvested for biochemical analysis. Highperformance liquid chromatography (HPLC) was used to identify major bioactive components of LCE. LCE treatment significantly reduced the production of nitric oxide (NO), pro-inflammatory cytokine expression, and inflammation-associated protein levels in BV2 cells. These effects were associated with inhibition of the AKT-GSK3β-CREB signaling pathway. In vivo, oral LCE administration ameliorated LPS-induced cognitive impairment and decreased inflammatory markers in the hippocampus. HPLC analysis identified myricetin as a major component of LCE, which independently exhibited anti-inflammatory effects in microglia. These findings highlight the potential of LCE as a natural therapeutic agent for neuroinflammation-related cognitive impairment, with myricetin contributing to its pharmacological activity.