ArticleSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition2025
[Neuroprotective Effects of Anisodine Hydromide in a Rat Model of Vascular Dementia and the Antioxidative Stress Mechanisms Involved].
Article in Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Unraveling the Effects ofInternational journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Vascular dementia (VD) is a common cognitive dysfunction associated with cerebrovascular disease. This study is aimed at investigating the therapeutic effect of anisodine hydromide (AH) on VD and the potential antioxidative stress mechanisms involved. Methods: A VD model was established in Sprague-Dawley (SD) rats through permanent bilateral common carotid artery occlusion. The rats were divided into a sham group, a VD model group, and AH treatment groups receiving AH at low, medium, or high doses ( Results: Compared with the sham group, the nerve function and limb coordination of rats in the VD model group were significantly impaired ( Conclusion: AH modulates SOD and MDA levels and reduces oxidative stress injury, thereby improving neurological function and limb coordination and showing potential therapeutic effects in VD. The neuroprotective effects of AH may be related to its antioxidative stress and antiapoptotic mechanisms, and the M2 receptor may be a potential target of its actions. These findings provide an important theoretical basis for the development of new therapeutic strategies for VD.
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