[Trillium tschonoskii Maxim saponin protects neurological function in rats with post-stroke cognitive impairment by promoting ER-phagy].

Authors

Dan Yang, Fangyu Zhao, Yiduo He, Hong Zhu, Xin Liu, Xianbing Chen

Published in

Nan fang yi ke da xue xue bao = Journal of Southern Medical University. Volume 46. Issue 6. Pages 1365-1373. Jun 20, 2026.

Abstract

To investigate the mechanism that mediates the neuroprotective effects of Trillium tschonoskii Maxim (TTM) against post-stroke cognitive impairment (PSCI) in rats.
Adult SD rats were randomized into Sham operation, PSCI model, TTM, rapamycin (an autophagy inducer), 3-methyladenine (an autophagy inhibitor), and TTM+3-MA groups, and rat models of cognitive impairment were established using a modified thread occlusion method. Cognitive function of the rats was assessed using Morris water maze test. Histopathological changes, neuronal apoptosis, dendritic spines, and protein expressions of FAM134B, LC3, ATG5, P62, GRP78, Bax, Bcl-2, IL-10, IL-1β, and TNF-α were evaluated using HE, Nissl, TUNEL, Golgi staining, immunohistochemistry, immunofluorescence staining, and Western blotting.
Compared with the sham-operated rats, the rat models of PSCI showed significantly prolonged escape latency, reduced target quadrant time and platform crossings, severe hippocampal damage, increased ATG5 and GRP78 expression, elevated apoptosis, increased IL-1β, TNF-α, Bax, GRP78, and P62 expressions, and decreased IL-10, Bcl-2, and LC3 expressions, with slightly increased FAM134B-LC3 and calnexin-LC3 co-localization. Compared with those in the model group, the rats receiving TTM treatment showed significantly shortened escape latency, increased target quadrant time and platform crossings, increased ATG5 and dendritic spines, decreased GRP78 expression, enhanced FAM134B-LC3 and calnexin-LC3 co-localization, reduced IL-1β, TNF-α, Bax, GRP78, and P62 expressions, and increased FAM134B, ATG5, LC3, IL-10, and Bcl-2 expressions; the rats treated with 3-MA showed the opposite changes.
Excessive ER stress is activated early after stroke, shifting from adaptive to pro-apoptotic signaling, with insufficient ER-phagy flux. TTM modulates ER-phagy, alleviates ERS, reduces neuroinflammation and apoptosis, protects dendritic spines, and improves cognitive function in rats with PSCI.

PMID:
42343845
Bibliographic data and abstract were imported from PubMed on 25 Jun 2026.

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