ArticleExperimental and therapeutic medicine2020
Lithium chloride ameliorated spatial cognitive impairment through activating mTOR phosphorylation and inhibiting excessive autophagy in the repeated cerebral ischemia-reperfusion mouse model.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Exploring the Neuroprotective Effects of Lithium in Ischemic Stroke: A literature review.International journal of medical sciences · 2024Review
- Therapeutic approaches to activate the canonical Wnt pathway for bone regeneration.Journal of tissue engineering and regenerative medicine · 2022Review
- Lithium Biological Action Mechanisms after Ischemic Stroke.Life (Basel, Switzerland) · 2022Review
- Selenium attenuates ischemia/reperfusion injury‑induced damage to the blood‑brain barrier in hyperglycemia through PI3K/AKT/mTOR pathway‑mediated autophagy inhibition.International journal of molecular medicine · 2021Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
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Abstract
Lithium has been previously demonstrated to alleviate cognitive impairment caused by neurodegenerative diseases and acute brain injuries; however, the specific mechanism remains elusive. In the present study, the C57BL/6 mouse model of spatial cognitive impairment induced by repeated cerebral ischemia-reperfusion was established. Morris water maze test was performed to evaluate the levels of spatial cognitive impairment. Nissl staining was used to observe any morphological alterations, whilst western blotting was performed to measure the expression levels of microtubule-associated protein light chain 3 (LC3) and Beclin1 in addition to mTOR phosphorylation. LiCl was found to significantly improve spatial learning and memory impairments according to data from the Morris water maze test. Nissl staining indicated that LiCl inhibited neuronal damage in the CA1 region of the hippocampus. Additionally, LiCl increased mTOR phosphorylation, reduced beclin1 expression and reduced the LC3 II/I expression ratio. Taken together, these findings suggest that LiCl may alleviate the spatial cognitive impairment induced by repeated cerebral ischemia-reperfusion. This observation may be attributed to the inhibition of excessive autophagy by LiCl through mTOR signaling activation.
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