Abstract
The air-dried aerial parts of Lavandula angustifolia Mill, a traditional Uygur herbal drug, is used as resuscitation-inducing therapy to treat neurodisfunctions, such as stroke. This study was designed to assess the neuroprotective effects of lavender oil against ischemia/reperfusion (IR) injury in mice. Focal cerebral ischemia was induced by the intraluminal occlusion method with a nylon string. The neurodysfuntion was evaluated by neurological deficit and the infarct area was showed by 2,3,5-triphenyltetrazolium chloride (TTC) staining. The histopathological changes were observed by hematoxylin and eosin staining. The levels of mitochondria-generated reactive oxygen species (ROS), malondialdehyde (MDA) and carbonyl, the ratio of reduced glutathione (GSH)/glutathione disulfide (GSSG), the activities of superoxide dismutase (SOD), catalase (CAT) and glutathion peroxidase (GSH-Px) in brain tissue were measured to estimate the oxidative stress state. Neurological deficit, infarct size, histopathology changes and oxidative stress markers were evaluated after 22 h of reperfusion. In comparison with the model group, treatment with lavender oil significantly decreased neurological deficit scores, infarct size, the levels of MDA, carbonyl and ROS, and attenuated neuronal damage, upregulated SOD, CAT, GSH-Px activities and GSH/GSSG ratio. These results suggested that the neuroprotective effects of lavender oil against cerebral ischemia/reperfusion injury may be attributed to its antioxidant effects.
Highlights
Cerebral ischemia is one of the leading causes of human death and disability across the World and its incidence is speculated to rise with the increase in the number of the aging population
The model group had a significantly increased infarct size as compared to the sham group
The results clearly demonstrated that ischemia/reperfusion resulted in an increase of MDA formation compared with the sham group and MDA content reduced in a dose dependent manner in the lavender oil groups (Figure 4), p < 0.05 at dose of 50 or 100 mg/Kg, and p < 0.01 at dose of 200 mg/Kg
Summary
Cerebral ischemia is one of the leading causes of human death and disability across the World and its incidence is speculated to rise with the increase in the number of the aging population. A variety of mechanisms are involved in ischemic brain injury, including excitotoxicity, acidotoxicity, ionic imbalance, peri-infarct depolarization, oxidative and nitrative stress, inflammation and apoptosis [2,3]. Recent studies have demonstrated that the brain damages after ischemia/reperfusion may result from oxidative stress [4,5]. Ischemia/reperfusion leads to an imbalance between antioxidants and accumulations of toxic free radicals increasing the susceptibility of brain tissues to oxidative damage via lipid peroxidation, protein oxidation, DNA oxidation and so on [6]. For this reason, antioxidants have been the focus of studies for developing neuroprotective drugs to be used in cerebral ischemia therapy. Many antioxidants have been investigated in in vitro and in vivo experiments and some of them have been tested in clinical studies of cerebral ischemia [1,3,7,8,9]
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