ArticleNeuropsychiatric disease and treatment2020
K-3-Rh Protects Against Cerebral Ischemia/Reperfusion Injury by Anti-Apoptotic Effect Through PI3K-Akt Signaling Pathway in Rat.
Article in Neuropsychiatric disease and treatment, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Advances in Ferroptosis-Inducing Agents by Targeted Delivery System in Cancer Therapy.International journal of nanomedicine · 2024Review
- Luteolin alleviates cerebral ischemia/reperfusion injury by regulating cell pyroptosis.Open medicine (Warsaw, Poland) · 2024Article
- Polyherbal and Multimodal Treatments: Kaempferol- and Quercetin-Rich Herbs Alleviate Symptoms of Alzheimer's Disease.Biology · 2023Review
- Novel mechanisms underlying inhibition of inflammation-induced angiogenesis by dexamethasone and gentamicin via PI3K/AKT/NF-κB/VEGF pathways in acute radiation proctitis.Scientific reports · 2022Article
- The PI3K/AKT Pathway-The Potential Key Mechanisms of Traditional Chinese Medicine for Stroke.Frontiers in medicine · 2022Review
- Total Flavonoids of Chuju Decrease Oxidative Stress and Cell Apoptosis in Ischemic Stroke Rats: Network and Experimental Analyses.Frontiers in neuroscience · 2021Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
aimsIschemic stroke is the main cause of nerve damage and brain dysfunction, accompanied by strong brain cell apoptosis. This study aimed to investigate the effect of kaempferol-3-O-rhamnoside (K-3-rh) on cerebral ischemia-reperfusion (I/R) injury. METHODS AND MATERIALS: A rat model of cerebral I/R injury was established. The effects of K-3-rh on cerebral infarction size, brain water content and neurological deficits in rats were evaluated. Apoptosis of ischemic brain cells after mouse I/R was observed by TUNEL staining and flow cytometry. Western blot and qRT-PCR were used to detect the effect of K-3-rh on the expression of apoptosis-related proteins.
resultsK-3-rh can improve the neurological deficit score, reduce the infarct volume and brain water content, and inhibit cell apoptosis. In addition, K-3-rh significantly downregulated the expression of Bax and p53 and upregulated the expression of Bcl-2, and the phosphorylation level of Akt. Blockade of PI3K activity by the PI3K inhibitor wortmannin not only reversed the effects of K-3-rh on infarct volume and brain water content but also reversed the expression level of p-Akt.
conclusionK-3-rh had obvious neuroprotective effects on brain I/R injury and neuronal apoptosis, and its mechanism may be related to activation of PI3K/Akt signaling pathway.
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