Abstract
BackgroundIschemia-reperfusion brain injury (IRBI) is an important cause for mortality and morbidity. Studies on humans and animals showed that oxidative stress (OS) plays a crucial role in ischemic stroke with or without reperfusion. Allicin is reported to be able to attenuate OS and has neuroprotective effects on rabbits’ ischemia–reperfusion spinal cord injury.AimTo explore whether Allicin pretreatment has neuroprotective effects on IRBI in mice.Methods and resultsTransient middle cerebral artery occlusion (MCAO) was conducted to induce IRBI in mice. The mice were pretreated with either Allicin (MCAOA) or normal saline in the same volume (MCAONS). Sham-operated groups [Allicin group (SOA) and normal saline group (SONS)] were also set. Blood pressure and cerebral blood flow measurements revealed comparable hemodynamics. Via brain MRI and neuronal nuclear antigen (NeuN) immune-histochemical staining, MCAOA mice had a significantly reduced stroke size than MCAONS mice (P < 0.05, n = 15). Allicin pretreatment could attenuate the OS, the activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, inflammation, dysfunction of mitochondrial respiratory chain, and apoptosis (all P < 0.05, n = 15). Furthermore, Allicin also increased the activities of endogenous antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX), and glutathione S-transferase (GST), and promoted the angiogenesis in the peri-infarct zone (all P < 0.05, n = 15).ConclusionWe showed that Allicin could protect mice from IRBI through a series of mechanisms. Allicin represents a new therapeutic direction of IRBI.
Highlights
Stroke is one of the most leading global causes of mortality across the world [1]
Morphometrical analysis revealed a significantly reduced stroke size in MCAOA mice compared with MCAO normal saline (MCAONS) mice (MCAOA: 27.33 ± 8.33 mm2 vs. MCAONS: 40.65 ± 10.35 mm2; *p < 0.05; n = 15; Figure 1)
The Neurological severity score (NSS) decreased to a median score of 13 in MCAONS group and 11 in MCAOA group after 24 hours of reperfusion (MCAONS 13.40 ± 1.31 vs. MCAOA 11.60 ± 1.54; *p = 0.002 < 0.05; n = 15), and gradually decreased to 9 and 7 respectively at 7 days eventually (3 days: MCAONS 12.00 ± 1.93 vs. MCAOA 9.93 ± 1.91; *p = 0.008 < 0.05; 7 days: MCAONS 9.13 ± 1.63 vs. MCAOA 7.40 ± 2.36; *p = 0.032 < 0.05; n = 15), suggesting that Allicin pretreatment had neurotrophic effects on Ischemia-reperfusion brain injury (IRBI)
Summary
Stroke is one of the most leading global causes of mortality across the world [1]. Despite ongoing advances in stroke imaging and treatment, ischemia-reperfusion brain injury (IRBI) stroke continues to debilitate patients with devastating outcomes at both personal and societal levels. Oxidative stress (OS) plays important roles in cardia-cerebrovascular diseases [2]. Targeting OS in both primary ischemic-injury and the following reperfusion-injury, lots of medicine, especially natural products extracted from medicinal plants, have been proved to have neuroprotective effects on IRBI [4]. Ischemia-reperfusion brain injury (IRBI) is an important cause for mortality and morbidity. Studies on humans and animals showed that oxidative stress (OS) plays a crucial role in ischemic stroke with or without reperfusion. Allicin is reported to be able to attenuate OS and has neuroprotective effects on rabbits’ ischemia–reperfusion spinal cord injury
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