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Liposomal curcumin nanocarrier ameliorates synaptic dysfunction after intracerebral hemorrhage.

Created on 18 Sep 2026

Authors

Kianoush Saberi, Nikki Ghadiminia, Abdumalik Mamataliyev, Telmon Turaev, Gulbahor Umarkulova, Otabek Nadjmitdinov, Abdukakhkhor Artikov, Sadridin Eshkaraev, Yuldash Takhirov, Barno Amirullayeva, Nargiza Ayubova, Rano Kuchkorova, Zamira Erdanova

Published in

Inflammopharmacology. Sep 17, 2026. Epub Sep 17, 2026.

Abstract

Neuroinflammation and synaptic dysfunction in the medial prefrontal cortex (mPFC) contribute to cognitive impairment after intracerebral hemorrhage (ICH). Curcumin, a natural polyphenol from Curcuma longa, has anti-inflammatory properties but limited bioavailability.
Liposomal curcumin (Lipo-Cur, 103.2 nm, 74% encapsulation) was prepared by thin-film hydration. Adult male rats were assigned to Sham, ICH (collagenase + empty liposomes), and ICH-Cur (collagenase + Lipo-Cur, 30 mg/kg, i.p. at 2, 24, 48 h post-surgery). On day 7, we assessed NLRP3/caspase-1 inflammasome activation, BDNF/TrkB/CREB/Erk signaling, PSD-95 expression, neuronal survival (Nissl staining), and working memory (Y-maze).
Lipo-Cur significantly suppressed NLRP3/caspase-1, restored p-CREB/CREB and p-TrkB/TrkB, normalized p-Erk/Erk, and upregulated PSD-95 (all p < 0.01). It also reduced neuronal loss, restored BDNF (p < 0.05), attenuated NLRP3 (p < 0.01), and improved Y-maze alternation (p < 0.001) without affecting locomotion.
These findings suggest that liposomal curcumin exerts neuroprotective effects in the mPFC after ICH, likely through mechanisms involving suppression of NLRP3/caspase-1 and enhancement of BDNF/TrkB/CREB signaling. This supports its potential as a natural product-based therapeutic for stroke-induced cognitive impairment, though further mechanistic studies are warranted.

PMID:
42753069
Bibliographic data and abstract were imported from PubMed on 18 Sep 2026.

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