Aloperine protects against cerebral ischemia/reperfusion injury via activating the PI3K/AKT signaling pathway in rats
- Zhimin Li
- Xing Cao
- Ligen Xiao
- Ruijiao Zhou
Affiliations: Department of Neurology, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan 637000, P.R. China, Department of Cardiothoracic Surgery, Nanchong Central Hospital, Nanchong, Sichuan 637000, P.R. China
- Published online on: July 22, 2021 https://doi.org/10.3892/etm.2021.10478
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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.