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<p>Acute kidney injury (AKI) is a severe clinical challenge driven by oxidative stress and inflammation. Current therapeutic options for AKI remain limited. Herein, we developed a novel metal–phenolic nanoplatform named LBP@Ga-Bai NPs. We synthesized these nanoparticles by self-assembling baicalein (Bai) with gallium (Ga3⁺), followed by surface coating with <i>Lycium barbarum</i> polysaccharide (LBP). These nanoparticles showed excellent colloidal stability. Our in vitro studies showed that LBP@Ga-Bai NPs protected H₂O₂-injured HK-2 cells. They effectively scavenged ROS, colocalized with mitochondria, restored membrane potential, and prevented apoptosis. In a glycerol-induced AKI mouse model, oral delivery of LBP@Ga-Bai NPs significantly reduced kidney damage. They lowered serum creatinine by 43.48% and blood urea nitrogen by 41.09%. They also reduced tubular necrosis and tissue inflammation. Transcriptomic analysis further showed that the nanoparticles reversed metabolic dysfunction. They achieved this by reactivating organic acid catabolism and restoring the TCA cycle. In conclusion, LBP@Ga-Bai NPs offer a promising multifunctional treatment for AKI. They work effectively by clearing ROS, protecting mitochondria, and restoring metabolic balance.</p>

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A green metal-phenolic coordination nanoplatform based on baicalein and gallium for the treatment of acute kidney injury

  • 期刊论文

  • 发表日期：

    2026年7月18日

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  • Xiuxiu Li,
  • Shaoquan Wu,
  • Ying Shu,
  • Yuna Tong

摘要

Acute kidney injury (AKI) is a severe clinical challenge driven by oxidative stress and inflammation. Current therapeutic options for AKI remain limited. Herein, we developed a novel metal–phenolic nanoplatform named LBP@Ga-Bai NPs. We synthesized these nanoparticles by self-assembling baicalein (Bai) with gallium (Ga3⁺), followed by surface coating with Lycium barbarum polysaccharide (LBP). These nanoparticles showed excellent colloidal stability. Our in vitro studies showed that LBP@Ga-Bai NPs protected H₂O₂-injured HK-2 cells. They effectively scavenged ROS, colocalized with mitochondria, restored membrane potential, and prevented apoptosis. In a glycerol-induced AKI mouse model, oral delivery of LBP@Ga-Bai NPs significantly reduced kidney damage. They lowered serum creatinine by 43.48% and blood urea nitrogen by 41.09%. They also reduced tubular necrosis and tissue inflammation. Transcriptomic analysis further showed that the nanoparticles reversed metabolic dysfunction. They achieved this by reactivating organic acid catabolism and restoring the TCA cycle. In conclusion, LBP@Ga-Bai NPs offer a promising multifunctional treatment for AKI. They work effectively by clearing ROS, protecting mitochondria, and restoring metabolic balance.