ArticleExperimental and therapeutic medicine2021
Aloperine protects against cerebral ischemia/reperfusion injury via activating the PI3K/AKT signaling pathway in rats.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- HMG-CoA reductase inhibition preserves testicular function after torsion/detorsion by modulating oxidative stress and AKT signaling.Scientific reports · 2025Article
- Aloperine Alleviates Myocardial Injury Induced by Myocardial Ischemia and Reperfusion by Activating the ERK1/2/β-catenin Signaling Pathway.Cardiovascular drugs and therapy · 2025Article
- Targeting PI3K/Akt in Cerebral Ischemia Reperfusion Injury Alleviation: From Signaling Networks to Targeted Therapy.Molecular neurobiology · 2024Review
- Aloperine Suppresses Cancer Progression by Interacting with VPS4A to Inhibit Autophagosome-lysosome Fusion in NSCLC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Luteolin alleviates cerebral ischemia/reperfusion injury by regulating cell pyroptosis.Open medicine (Warsaw, Poland) · 2024Article
- A New Therapeutic Trend: Natural Medicine for Ameliorating Ischemic Stroke via PI3K/Akt Signaling Pathway.Molecules (Basel, Switzerland) · 2022Review
- Aloperine: A Potent Modulator of Crucial Biological Mechanisms in Multiple Diseases.Biomedicines · 2022Review
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4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Cerebral ischemia is among the leading causes of death and long-term disability worldwide. The aim of the present study was to investigate the effects of aloperine (ALO) on cerebral ischemia/reperfusion (I/R) injury in rats and elucidate the possible underlying mechanisms. Therefore, a rat model of reversible middle cerebral artery occlusion (MCAO) was established to induce cerebral I/R injury. Following pretreatment with different doses of ALO, the histopathological changes in the brain tissue were evaluated by hematoxylin and eosin staining. The degree of cerebral infarction was determined using by 2,3,5-triphenyltetrazolium chloride staining. Additionally, the levels of oxidative stress- and inflammation-related factors were measured using commercially available kits. Cell apoptosis was assessed by TUNEL staining, while the expression levels of apoptosis- and PI3K/AKT signaling pathway-related proteins were determined by western blot analysis. The results demonstrated that ALO alleviated histopathological injury in the brain tissue and the area of cerebral infarction in a dose-dependent manner. Furthermore, significantly reduced levels of reactive oxygen species and malondialdehyde were observed in the ALO-treated rats post-MCAO/reperfusion, accompanied by increased levels of superoxide dismutase, catalase and glutathione. Consistently, treatment with ALO notably decreased the concentration of inflammatory factors, including TNF-α, IL-1β and IL-6, in a dose-dependent manner. In addition, ALO attenuated neuronal cell apoptosis, downregulated the expression of Bax and upregulated that of Bcl-2. I/R markedly reduced the expression levels of phosphorylated (p-)PI3K and p-AKT, which were dose-dependently restored by ALO intervention. Collectively, the aforementioned findings indicated that ALO could improve cerebral I/R injury and alleviate oxidative stress, inflammation and cell apoptosis via activating the PI3K/AKT signaling pathway, thus supporting the therapeutic potential of ALO against cerebral I/R injury in ischemic stroke.
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