Neuroprotective effects of visnagin on cerebral ischemia-reperfusion injury rats and the underlying mechanisms.

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.