Abstract
Ischemic stroke is a common type of cerebrovascular event and also the leading cause of disability. Post-stroke cognitive impairment occurs frequently in stroke survivors. Shexiang Baoxin Pill (SBP) is a proprietary Chinese medicine, initially used to treat cardiovascular diseases. Herein, we aim to explore the effects of SBP on oxygen glucose deprivation and reoxygenation (OGD/R) in neuronal cells (CATH.a) and cerebral ischemia/reperfusion injury induced post-stroke cognitive impairment in middle cerebral artery occlusion (MCAO) rat model. MCAO rats received two doses of oral SBP treatment (28 or 56 mg/kg) after 1 h of operation and once daily for 2 weeks continuously. Behavioral tests, immunoblotting, and immunofluorescence were examined after 14 days. Current data suggest that SBP enhanced cell viability and downregulated apoptosis via activating the PI3K/Akt signaling pathway in CATH. a cells. Furthermore, 14 days of SBP treatment promoted the recovery of learning and locomotor function in the MCAO rats. SBP up-regulated the expression of p-Akt, p-GSK3β, as well as the expression of NMDAR1, PSD-95, and AMPAR. Also, SBP down-regulated the expression of p-CaMKII. These results indicated that long-term SBP treatment might be a potential option for cognitive impairment induced by the ischemic stroke.
Highlights
Stroke is a leading cause of death and disability
The results showed that Shexiang Baoxin Pill (SBP) enhanced cell viability and downregulated apoptosis
We detected the protein expression of p-Akt and p-GSK3β by western blot in CATH. a, the results showed that compared to the oxygen glucose deprivation and reoxygenation (OGD/R) group, the expression of p-Akt and p-GSK3β was suppressed in CATH. a
Summary
Stroke is a leading cause of death and disability. 87% are ischemic stroke (G.B.D.N. Collaborators, 2019a; G.B.D.S. Collaborators, 2019b; Zhou et al, 2019a). With the development of critical medicine, the death rate of stroke has been significantly decreased. It has been confirmed that stroke could result in cognitive impairment known as poststroke cognitive impairment (Pasi et al, 2012; Shih et al, 2013). Covered by severe physical disability, post-stroke cognitive impairment is likely to be ignored in most cases (Pasi et al, 2012; Sun et al, 2014; Kwon et al, 2020). Delayed cellular loss within the hippocampus correlated with cognitive deficits and long-term prognosis following experimental or clinical ischemic stroke
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
