10.6084/M9.FIGSHARE.15031669
Lixian Huang
Lixian
Huang
Bo Zhao
Bo
Zhao
Qunxian Li
Qunxian
Li
Jing Wu
Jing
Wu
Hui Jiang
Hui
Jiang
Qingbin Li
Qingbin
Li
Ephedrine alleviates middle cerebral artery occlusion-induced neurological deficits and hippocampal neuronal damage in rats by activating PI3K/AKT signaling pathway
<p>Inflammation and oxidative stress are crucial in ischemic stroke. Ephedrine (EPH) has been proven to have anti-inflammatory and anti-oxidative stress effects. The present study analyzes whether EPH possessed neuroprotective effects and explored the underlying mechanisms of EPH based on an experimental model of middle cerebral artery occlusion (MCAO). We found that intraperitoneal injection with EPH attenuated the neurological deficit, cerebral infarction, and cerebral edema induced by MCAO in rats. Besides, EPH treatment alleviated MCAO-induced brain tissue damage and morphological abnormality, as well as neuronal loss. Moreover, EPH treatment upregulated GPx and CAT activity and downregulated MDA and NO content. EPH also evidently decreased the levels of IL-6 and TNF-α but increased IL-4 and IL-10 levels. Of note, EPH treatment promoted the phosphorylation of PI3K and AKT proteins in MCAO rats. Furthermore, administration of PI3K/AKT pathway inhibitor LY294002 abolished the beneficial effects of EPH. These results confirmed that EPH alleviated brain injury induced by MCAO via activating PI3K/AKT signaling pathway.</p>
Biochemistry
Cell Biology
Molecular Biology
Neuroscience
Physiology
Pharmacology
Evolutionary Biology
Immunology
Mental Health
Taylor & Francis
2021
2021-07-21
2023-06-11
Journal contribution
19532 Bytes
10.1080/21655979.2021.1953218
CC BY 4.0