Chrysin attenuates global cerebral ischemic reperfusion injury via suppression of oxidative stress, inflammation and apoptosis
El Khashab I.H.; Abdelsalam R.M.; Elbrairy A.I.; Attia A.S.
Date issued:
2019
Publisher:
Elsevier Masson SAS
Series Info:
Biomedicine and Pharmacotherapy
112
Type:
Article
Keywords:
Antioxidant
,
Apoptosis
,
Chrysin
,
Inflammation
,
Ischemia-reperfusion
,
Neuroprotection
,
chrysin
,
interleukin 10
,
interleukin 6
,
neurotransmitter
,
protein bcl 2
,
tumor necrosis factor
,
chrysin
,
flavonoid
,
neuroprotective agent
,
animal experiment
,
animal model
,
apoptosis
,
Article
,
blood brain barrier
,
brain ischemia
,
common carotid artery
,
comparative study
,
controlled study
,
decapitation
,
enzyme activation
,
inflammation
,
male
,
nonhuman
,
oxidation reduction reaction
,
oxidative stress
,
priority journal
,
rat
,
reperfusion injury
,
animal
,
apoptosis
,
brain ischemia
,
drug effect
,
inflammation
,
metabolism
,
oxidative stress
,
pathology
,
physiology
,
Wistar rat
,
Animals
,
Apoptosis
,
Brain Ischemia
,
Flavonoids
,
Inflammation
,
Male
,
Neuroprotective Agents
,
Oxidative Stress
,
Rats
,
Rats, Wistar
Abstract:
Global cerebral ischemia is a leading cause of mortality worldwide. Several biomechanisms play a role in the pathology of cerebral ischemia reperfusion damage, such as oxidative stress, inflammation, apoptosis and excitotoxicity. Chrysin, a natural flavonoid with many important biological activities, was investigated in the present study for its possible neuroprotective properties in a rat model of global ischemia reperfusion. Male Wistar rats were allocated into three groups: sham-operated, ischemia/reperfusion, and chrysin (30 mg/kg) groups. All animals were subjected to ischemia for 15 min followed by reperfusion for 60 min, except for the sham-operated group. Rats were decapitated, then both hippocampi were rapidly excised to evaluate several biomarkers that reflect ischemic injury. The obtained results showed that pre-treatment with chrysin attenuated ischemia-induced oxidative stress by: (i) restoring the glutathione level; and (ii) depressing the levels/activities of thiobarbituric acid reactive substances, the hippocampal NADPH, as well as the xanthine oxidase. Exposure to chrysin also suppressed the inflammation accompanying the ischemia/reperfusion (I/R) damage, through increasing the interleukin-10 level, while decreasing the levels of both interleukin-6 and tumour necrosis factor-alpha. Moreover, an increase in Bcl2 and a decrease in both BAX and Hsp90 levels were recorded following chrysin exposure, which was also accompanied with elevated glutamate and aspartate levels. In conclusion, chrysin has demonstrated an anti-ischemic potential, through attenuation of the mechanisms underlying I/R injury. These data add to the knowledge on the significance of natural flavonoids as neuroprotective agents. � 2019 The Authors
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