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<p>Alcoholic fatty liver disease (AFLD) is a global health burden driven by ethanol-induced steatosis, inflammation, and oxidative stress. Clam extracts have demonstrated hepatoprotective potential, attributed to abundant bioactive compounds. In this work, clam (<i>Geloina erosa</i>)-derived nanoparticles (CNPs) were isolated via tangential flow filtration and characterized as 62.2 ± 3.0 nm, negatively charged nanoscale particles enriched in phospholipids, diacylglycerols, and bioactive metabolites. Oral administration of CNPs for nine weeks in ethanol-fed mice significantly alleviated ethanol-induced liver injury. CNPs modulated hepatic inflammation by downregulating TLR4/MyD88 signaling and pro-inflammatory cytokines, rebalanced lipid metabolism through suppression of SREBP-1c and activation of PPARα, and restored antioxidant defenses by reactivating the Nrf2/HO-1 pathway. Moreover, CNPs enhanced ethanol detoxification by upregulating ADH and ALDH while inhibiting CYP2E1, and promoted a macrophage phenotype shift toward M2. Restoration of fecal short-chain fatty acids and intestinal retention supported their gut-liver axis activity. These findings suggest that CNPs act as multifunctional nanocarriers delivering endogenous bioactives for AFLD mitigation.</p><p></p>

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Bioactive nanoparticles from clam extracts mitigate alcoholic liver injury by modulating multiple pathways

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月12日

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  • Ya-Ru Kuo,
  • Kai-Jiun Lo,
  • Min-Hsiung Pan

摘要

Alcoholic fatty liver disease (AFLD) is a global health burden driven by ethanol-induced steatosis, inflammation, and oxidative stress. Clam extracts have demonstrated hepatoprotective potential, attributed to abundant bioactive compounds. In this work, clam (Geloina erosa)-derived nanoparticles (CNPs) were isolated via tangential flow filtration and characterized as 62.2 ± 3.0 nm, negatively charged nanoscale particles enriched in phospholipids, diacylglycerols, and bioactive metabolites. Oral administration of CNPs for nine weeks in ethanol-fed mice significantly alleviated ethanol-induced liver injury. CNPs modulated hepatic inflammation by downregulating TLR4/MyD88 signaling and pro-inflammatory cytokines, rebalanced lipid metabolism through suppression of SREBP-1c and activation of PPARα, and restored antioxidant defenses by reactivating the Nrf2/HO-1 pathway. Moreover, CNPs enhanced ethanol detoxification by upregulating ADH and ALDH while inhibiting CYP2E1, and promoted a macrophage phenotype shift toward M2. Restoration of fecal short-chain fatty acids and intestinal retention supported their gut-liver axis activity. These findings suggest that CNPs act as multifunctional nanocarriers delivering endogenous bioactives for AFLD mitigation.