ArticleMolecular biology reports2026
Cistanoside A decreases Tau hyperphosphorylation and neuronal apoptosis through the AKT/GSK3β pathway in okadaic acid-induced in vivo and in vitro models of Alzheimer's disease.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThe multifactorial nature of Alzheimer's disease (AD) pathogenesis has driven the search for therapeutic agents with low toxicity that can act on multiple targets. Cistanoside A (Cis A), a bioactive compound derived from Cistanches Herba, exhibits anti-inflammatory, antioxidant, and antiapoptotic effects. Given that these processes are implicated in AD progression, we propose that Cis A may be a promising candidate for AD therapy.
methodsWe employed an okadaic acid (OA)-induced rat model in vivo and SH-SY5Y cells in vitro. Cognitive function was assessed using the Morris water maze and novel object recognition tests. Hematoxylin and eosin and Nissl staining were performed to evaluate histopathological changes. Neuronal damage was assessed using the Cell Counting Kit-8 assay for cell viability, TUNEL staining for apoptosis, and western blotting for protein expression. Mitochondrial damage was examined using JC-1 and MitoSOX Red staining.
resultsCis A significantly improved cognitive deficits. It attenuated OA-induced apoptosis, restored mitochondrial membrane potential, and reduced reactive oxygen species levels in rats and SH-SY5Y cells by inhibiting hyperphosphorylation of Tau protein via the AKT/GSK3β pathway. Furthermore, the protective effect of Cis A was attenuated by MK-2206 and AKT knockdown in vitro.
conclusionCis A significantly improves cognitive function and reduces AD-related pathology, highlighting its potential as a therapeutic candidate for AD.
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