European review for medical and pharmacological sciences · 2022
Neuroprotective effects of visnagin on cerebral ischemia-reperfusion injury rats and the underlying mechanisms.
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Rao X-L, Liu L-L, Huang J, Chen J
Аннотация
OBJECTIVE: Cerebral ischemia-reperfusion (I/R), caused by the treatments of ischemic stroke, usually leads to brain injury. Inflammation, oxidative stress, and autophagy play pivotal roles in the pathology. Visnagin presents a protective effect on I/R injured animal models of the heart, liver, kidney, and other organs. In our research, we identified the neuroprotective effects and the underlying mechanisms of visnagin in cerebral I/R injured models.
MATERIALS AND METHODS: We constructed rat models of cerebral I/R injury and categorized them into 5 groups: sham operation group, I/R model group, and visnagin treatment I/R group (10, 30, 60 mg/kg). The neurological deficits of the rats were analyzed after 24 hours of reperfusion, then, the contents of glutathione peroxidase, malondialdehyde, superoxide dismutase catalase, caspase-3, nuclear factor kappa-B p65 unit, tumor necrosis factor-α, interleukin-1β, and interleukin6 were measured in rat models. The expressions of Bcl-2 and Bax were detected by Western blot analysis.
RESULTS: Our results suggested that the administration of visnagin alleviated the cognitive dysfunction, reduced the activities of inflammatory factors, promoted the protein expression of Bcl-2, and downregulated the expression of Bax in the I/R injured rat model.
CONCLUSIONS: Visnagin exerts a neuroprotective effect during I/R injury in rats, the underlying mechanisms may be the effect of attenuating neuroinflammation, anti-oxidative and inhibition of apoptosis.
MATERIALS AND METHODS: We constructed rat models of cerebral I/R injury and categorized them into 5 groups: sham operation group, I/R model group, and visnagin treatment I/R group (10, 30, 60 mg/kg). The neurological deficits of the rats were analyzed after 24 hours of reperfusion, then, the contents of glutathione peroxidase, malondialdehyde, superoxide dismutase catalase, caspase-3, nuclear factor kappa-B p65 unit, tumor necrosis factor-α, interleukin-1β, and interleukin6 were measured in rat models. The expressions of Bcl-2 and Bax were detected by Western blot analysis.
RESULTS: Our results suggested that the administration of visnagin alleviated the cognitive dysfunction, reduced the activities of inflammatory factors, promoted the protein expression of Bcl-2, and downregulated the expression of Bax in the I/R injured rat model.
CONCLUSIONS: Visnagin exerts a neuroprotective effect during I/R injury in rats, the underlying mechanisms may be the effect of attenuating neuroinflammation, anti-oxidative and inhibition of apoptosis.