Abstract
Neuronal apoptosis induced by oxidative stress is a major pathological process that occurs after cerebral ischemia-reperfusion. Calycosin-7-O-β-D-glucoside (CG) is a representative component of isoflavones in Radix Astragali (RA). Previous studies have shown that CG has potential neuroprotective effects. However, whether CG alleviates neuronal apoptosis through antioxidant stress after ischemia-reperfusion remains unknown. To investigate the positive effects of CG on oxidative stress and apoptosis of neurons, we simulated the ischemia-reperfusion process in vitro using an immortalized hippocampal neuron cell line (HT22) and oxygen-glucose deprivation/reperfusion (OGD/R) model. CG significantly improved cell viability and reduced oxidative stress and neuronal apoptosis. In addition, CG treatment upregulated the expression of SIRT1, FOXO1, PGC-1α, and Bcl-2 and downregulated the expression of Bax. In summary, our findings indicate that CG alleviates OGD/R-induced damage via the SIRT1/FOXO1/PGC-1α signaling pathway. Thus, CG maybe a promising therapeutic candidate for brain injury associated with ischemic stroke.
Highlights
Ischemic stroke is a neurodegenerative disease characterized by hypoxemia of the brain tissue due to vascular obstruction
To investigate the mechanism of CG in hippocampal neuronal cells after oxygen-glucose deprivation/reperfusion (OGD/R), we evaluated the effects of CG on the Silent information regulator 1 (SIRT1)/FOXO1/PGC-1α signaling pathway related to apoptosis
We demonstrated that CG prevented OGD/R-induced hippocampal cell injury by alleviating oxidative stress and apoptosis through the SIRT1/FOXO1/PGC-1α signaling pathway
Summary
Ischemic stroke is a neurodegenerative disease characterized by hypoxemia of the brain tissue due to vascular obstruction. This condition is characterized by high morbidity, disability, mortality, and high recurrence rate, creating a heavy burden on society [1,2,3]. TPA is the only drug approved by the US FDA for treating ischemic stroke [7]. This drug is hampered by its narrow therapeutic window and can cause secondary damage to the ischemic area, known as ischemia-reperfusion injury [8,9,10]. It is imperative to find new and effective drugs for treating ischemic stroke
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