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Acta Cir Bras. 2019 Feb 28;34(2):e201900208. doi: 10.1590/s0102-8650201900208.

Effects of icariside II on brain tissue oxidative stress and Nrf2/HO-1 expression in rats with cerebral ischemia-reperfusion injury1.

Author information

1
MD, Department of Anesthesiology, Jinan City Central Hospital Affiliated to Shandong University, P.R. China. Technical procedures, acquisition of data, statistics analysis, critical revision, final approval.
2
MD, Department of Anesthesiology, Jinan City Central Hospital Affiliated to Shandong University, P.R. China. Design of the study, manuscript preparation, critical revision, final approval.

Abstract

PURPOSE:

To investigate the effects of icariside II on brain tissue oxidative stress and Nrf2/HO-1 expression in rats with cerebral ischemia-reperfusion injury (CIRI).

METHODS:

One hundred SD rats were randomly divided into sham-operated, model, and 5, 10 and 20 mg/kg icariside II groups, 20 rats in each group. The middle cerebral artery occlusion model (ischemia for 2 h followed by reperfusion for 24 h) was established in the later 4 groups. In later 3 groups, at reperfusion beginning, the rats were intragastrically administrated with 5, 10 and 20 mg/kg icariside II, respectively. After 24 h of reperfusion, the neurological severity score, cerebral water content and cerebral infarction volume, brain tissue oxidative stress indexes and Nrf2 and HO-1 protein expressions were determined.

RESULTS:

Compared with model group, in 20 mg/kg icariside II group the neurological severity score, cerebral water content and cerebral infarction volume, brain tissue ROS content and MDA level were significantly decreased (P<0.05), and the brain tissue SOD, GSH-Px and catalase levels and Nrf2 and HO-1 protein levels were significantly increased (P<0.05).

CONCLUSION:

Icariside II can alleviate the CIRI in rats through reducing brain tissue oxidative stress and improving Nrf2/HO-1 expression.

PMID:
30843941
DOI:
10.1590/s0102-8650201900208
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