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Stroke and cerebral ischemia/reperfusion (IR) injury are neurodegenerative conditions characterized by impaired blood flow to specific brain regions, resulting in brain tissue infarction and loss of sensorimotor function. Ginsenoside-MC1 (GMC1) has exhibited diverse effects in reducing various cerebrovascular disorders. Thereby, this study aimed to ascertain the neuroprotective effect of GMC1 against cerebral IR injury in a rat model of middle cerebral artery occlusion (MCAO) and examine the involvement of the AMPK/SIRT1 pathway in mediating this effect. Male Wistar rats (n=60, 250–280g, 12 weeks old) were used to induce cerebral IR through MCAO. GMC1 (10 mg/kg) was administered intraperitoneally for 28 days prior to tissue sampling. The assessment included measurements of cerebral infarct volume, neurological scores using the corner test and adhesive removal test, mitochondrial function indices (mitochondrial ROS, membrane potential, and ATP levels), oxidative stress markers (8-isoprostane and GSH), inflammatory markers (IL-6, IL-10, TNF-α, and p65-NF-κB), and the expression of p-AMPK and SIRT1 proteins. Treatment with GMC1 significantly reduced infarct volume, improved neurological scores, and enhanced mitochondrial function. Additionally, GMC1 administration increased enzymatic antioxidant activity, reduced 8-isoprostane levels, suppressed the inflammatory response, and upregulated p-AMPK and SIRT1 proteins. Notably, inhibiting AMPK with compound C, as an AMPK inhibitor, reversed the positive effects of GMC1 in rats with cerebral IR injury. GMC1 exhibited mitoprotective, antioxidative, and anti-inflammatory actions, providing neuroprotection against stroke outcomes in rats. The underlying mechanism involved the modulation of the AMPK/SIRT1 signaling pathway. Thus, GMC1 demonstrates promise as a potential therapeutic approach for improving the quality of life in stroke patients.
Li et al. (Sat,) studied this question.