Abstract
Purpose: To investigate the effect of myricetin 3-glucoside (M3GLS) on middle cerebral artery occlusion (MCAO)-induced cerebral ischemia in a rat model, and the mechanism of action involved.Methods: A cerebral ischemia rat model was established using MCAO under 10 % chloral hydrate anesthesia. Neurological severity score was determined by analyzing reflex, motor and sensory functions, as well as balancing potential. Infarction volume was determined using triphenyl tetrazolium chloride dye, while counting of Nissl bodies was done after toluidine blue staining. The protein expression levels of Bax and Bcl-2 were assayed using western blotting, while cytokine levels were determined by enzyme-linked immunosorbent assay (ELISA).Results: Treatment of cerebral ischemia rats with M3GLS effectively reduced infarct volume, when compared to vehicle-treated group (p < 0.05). Moreover, M3GLS treatment significantly increased the population of Nissl bodies and effectively improved neurologic scores (p < 0.05). In M3GLS-pretreated rats, cerebral ischemia-induced elevation of protein expressions of TNF-α, IL-6 and IL-1β were significantly suppressed. M3GL treatment significantly reversed cerebral ischemia-mediated downregulation of Bcl-2 protein level, but markedly reduced cerebral ischemia-induced upregulation of Bax protein level (p < 0.05).Conclusion: M3GLS exerts protective effect against cerebral ischemia-induced brain injury in rats via downregulation of inflammatory cytokines. It reduces infarction volume in the brain of cerebral ischemia rats, and regulates Bcl-2/Bax protein ratio. Thus, M3GLS has a potential for use in the clinical management of cerebral ischemia.
 Keywords: Myricetin, Neuroprotection, Anti-inflammation, Cerebral ischemia, Cytokines, Infarction
Highlights
Cerebral ischemia is one of the leading causes of long-term disabilities, and it is globally associated with high mortality
Infarct volumes were significantly higher in vehicle-treated rats after 24 h of cerebral ischemia than in myricetin 3-glucoside (M3GLS)-treated rats (Figure 2)
Treatment of the cerebral ischemia rats with M3GLS significantly enhanced the count of Nissl bodies, when compared to vehicle group (p < 0.05)
Summary
Cerebral ischemia is one of the leading causes of long-term disabilities, and it is globally associated with high mortality. Decline in blood flow leads to depletion of oxygen supply, Ca2+ ion overload, free radical formation, and mitochondrial and DNA damage in neuronal cells [1,2] These cellular events result in necrosis and apoptosis of brain cells. Ischemia causes activation and accumulation of microglial cells and leukocytes in brain tissues, leading to inflammatory injury. The cytokines usually linked to ischemia-mediated cell damage are tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 These cytokines promote leukocyte accumulation, leading to elimination of nerve cells via apoptosis or necrosis, which results in cerebral infarction [6]. After 24 h of MCAO exposure, the rats were sacrificed via decapitation under pentobarbital anesthesia (35 mg/kg), and their brains were excised immediately and cut into 2-mm sections. Rat brain tissues were excised and subsequently homogenized in RIPA-lysis buffer (Beyotime Institute of Biotechnology, Haimen China). Differences were assumed statistically significant at p < 0.05
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