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

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.

<p>Rutaecarpine may improve neuronal injury, inhibits apoptosis, inflammation and oxidative stress by regulating the expression of ERK1/2 and Nrf2/HO-1 pathway in rats with cerebral ischemia-reperfusion injury</p>

“…Jin et al found that IL-1ra inhibits oxidative stress and inflammation caused by I/R injury by promoting the expression of Nrf2 and HO-1 and the phosphorylation level of Nrf2 15. Similarly, Li et al found that icariside II can improve oxidative stress in brain tissue of rats with CIR injury by activating Nrf2/HO-1 pathway 16. In addition, upregulation of Nrf2 and HO-1 protein levels improved neurological deficits, cerebral infarction volume and body weight after CI/R.…”

“…The Nrf2/HO-1 pathway has been reported to play an important role in I/R injury 15. Activation of the Nrf2/HO-1 pathway attenuates oxidative stress and inflammation caused by I/R injury, restores neurological deficits and reduces cerebral infarction volume 16. Extracellular regulated protein kinases (ERK), as part of the MAPK signaling molecule, is also involved in the regulation of neural function.…”

Loganin exerts a protective effect on ischemia–reperfusion‐induced acute kidney injury by regulating JAK2/STAT3 and Nrf2/HO‐1 signaling pathways

“…As an important antioxidant regulator, nuclear factor erythroid 2‐related factor 2 (Nrf2) can combine with antioxidant response elements to regulate hemeoxygenase‐1 (HO‐1) expression (Jin et al, 2019). Recent study found that activation of Nrf2/HO‐1 pathway can reduce the oxidative stress and inflammation caused by ischemia/reperfusion (I/R) injury, and restore neurological dysfunction (Li & Meng, 2019). In the mouse I/R model, activating Nrf2/HO‐1 can reduce the oxidative stress factors in kidney tissues and cells, thereby reducing the symptoms of kidney injury (Diao et al, 2019).…”

Icariside II Attenuates Methamphetamine-Induced Neurotoxicity and Behavioral Impairments via Activating the Keap1-Nrf2 Pathway

“…These results proved that ICS could attenuate the METH-induced neurotoxicity via modulating the Keap1-Nrf2 pathway and the oxidative stress. Although previous studies have shown that ICS might achieve antioxidant effects by activating Nrf2-related protein expression and decreasing ROS levels in several diseases [ 50 – 52 ], we collected evidence for the first time that ICS could combat METH-induced neurotoxicity and PD-like symptoms through mediating the classic antioxidant Keap1-Nrf2 pathway and oxidative stress.…”