Upregulation of heme oxygenase‑1 protected against brain damage induced by transient cerebral ischemia‑reperfusion injury in rats

Abstract

The aim of the present study was to identify the effect of heme oxygenase (HO)-1 gene on cerebral ischemia-reperfusion injury. Sprague-Dawley rats were divided randomly into four groups: Sham group, vehicle group, empty adenovirus vector (Ad) group and recombinant HO-1 adenovirus (Ad-HO-1) transfection group. Rats in the vehicle, Ad and Ad-HO-1 groups were respectively injected with saline, Ad or Ad-HO-1 for 3 days prior to cerebral ischemia-reperfusion injury. Subsequently, the middle cerebral artery occlusion method was used to establish the model of cerebral ischemia-reperfusion injury. Following the assessment of neurological function, rats were sacrificed, and the infarction volume and apoptotic index in rat brains were measured. Furthermore, the protein expression levels of HO-1 in brain tissues were detected using western blot analysis. Results indicated that the neurological score of the Ad-HO-1 group was significantly increased compared with the Ad or vehicle groups, respectively (P<0.001). The volume of cerebral infarction and the index score of neuronal apoptosis in the vehicle and Ad groups was significantly increased compared with the Ad-HO-1 group (P<0.01). The death of neuronal cells following cerebral ischemia-reperfusion injury reduced remarkably induced by over-expression of HO-1. These findings suggest a neuroprotective role of HO-1 against brain injury induced by transient cerebral ischemia-reperfusion injury.

Platycarya strobilacea leaf extract protects mice brain with focal cerebral ischemia by antioxidative property

“…For example, it has been previously reported that neuronal expression of HO-1 is usually detected in rodent brains challenged with anoxic stimuli, including hypoxia or oxidative stress [41]. Furthermore, genetically engineered HO-1-deficient mice exhibit exaggeration in ischemic damage when compared to wild type controls [42,43]. Together with the results of this study, these findings suggest that PSL possesses a powerful neuroprotective effect, which may be effective against cerebral ischemia via upregulation of HO-1.…”

Purmorphamine Attenuates Neuro-Inflammation and Synaptic Impairments After Hypoxic-Ischemic Injury in Neonatal Mice via Shh Signaling

“…However, DHE is also easily oxidized by heme peroxidases. In the ischemic brain, heme peroxidase is elevated and released, which leads to an increase in ROS formation when monitored by ROS-sensitive fluorescent probes (Kim et al, 2016;Lu et al, 2018). To complement this, there are ongoing attempts to develop a new generation of ROS probes to measure ROS activity in vivo.…”

Emodin relieves hypoxia-triggered injury via elevation of microRNA-25 in PC-12 cells

“…More importantly, a growing number of researches have corroborated that EMO might be a neuroprotective agent for remedy nervous system diseases [17,25]. Cerebral ischemia injury belongs to central nervous system (CNS) injury, which gives rise to irreversible brain damage and even neurological sequelae [26]. Hence, our research attempted to further disclose whether EMO emerges the protective action in cerebral ischemia injury.…”