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<p>Alzheimer’s disease (AD) lacks effective disease-modifying therapy. This study evaluated the neuroprotective efficacy of quercetin-loaded cellulose nanofibers (QNP) in a streptozotocin (STZ)-induced AD rat model, focusing on memory impairment and endoplasmic reticulum (ER) stress. Forty-eight male Wistar rats were randomly allocated to six groups (<i>n</i> = 8): Control, AD model (ICV STZ 3&#xa0;mg/kg on days 1 and 3), STZ + empty cellulose nanoparticles, STZ + free quercetin (10&#xa0;mg/kg IP), STZ + QNP (10&#xa0;mg/kg IP, equivalent quercetin dose), and STZ + donepezil (1&#xa0;mg/kg IP) for 14 days. Morris water maze testing revealed that QNP significantly reduced escape latency during acquisition (31%, <i>P</i> &lt; 0.001 vs. AD model) and increased time spent in the target quadrant during the probe trial (<i>P</i> &lt; 0.01). QNP treatment resulted in significantly greater improvement compared to an equivalent dose of free quercetin (<i>P</i> &lt; 0.05). RT-PCR demonstrated XBP-1 mRNA splicing exclusively in the AD model group, indicating activation of the unfolded protein response (UPR). Both free quercetin and QNP completely prevented this splicing, demonstrating potent suppression of ER stress. Cellulose nanofiber-mediated delivery significantly enhances quercetin’s bioavailability and therapeutic efficacy, ameliorating cognitive deficits in AD likely via mitigation of ER stress. QNP represents a promising, biocompatible nano-therapeutic strategy for Alzheimer’s disease.</p>

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Quercetin-loaded cellulose nanofibers improve memory, learning, and attenuate endoplasmic reticulum stress in a rat model of Alzheimer’s disease

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月26日

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  • Mahdi Jalili,
  • Parvin Babaei,
  • Mostafa Golshekan,
  • Mahmood Abedinzade,
  • Sina Andalib

摘要

Alzheimer’s disease (AD) lacks effective disease-modifying therapy. This study evaluated the neuroprotective efficacy of quercetin-loaded cellulose nanofibers (QNP) in a streptozotocin (STZ)-induced AD rat model, focusing on memory impairment and endoplasmic reticulum (ER) stress. Forty-eight male Wistar rats were randomly allocated to six groups (n = 8): Control, AD model (ICV STZ 3 mg/kg on days 1 and 3), STZ + empty cellulose nanoparticles, STZ + free quercetin (10 mg/kg IP), STZ + QNP (10 mg/kg IP, equivalent quercetin dose), and STZ + donepezil (1 mg/kg IP) for 14 days. Morris water maze testing revealed that QNP significantly reduced escape latency during acquisition (31%, P < 0.001 vs. AD model) and increased time spent in the target quadrant during the probe trial (P < 0.01). QNP treatment resulted in significantly greater improvement compared to an equivalent dose of free quercetin (P < 0.05). RT-PCR demonstrated XBP-1 mRNA splicing exclusively in the AD model group, indicating activation of the unfolded protein response (UPR). Both free quercetin and QNP completely prevented this splicing, demonstrating potent suppression of ER stress. Cellulose nanofiber-mediated delivery significantly enhances quercetin’s bioavailability and therapeutic efficacy, ameliorating cognitive deficits in AD likely via mitigation of ER stress. QNP represents a promising, biocompatible nano-therapeutic strategy for Alzheimer’s disease.