In recent years, the medical field had significantly progressed to a greater extent which was evidenced with increased life expectancy and decreased mortality rate. Due to the growth of medical field, numerous
communicable diseases are prevented and eradicated, whereas the
non-communicable disease incidence has been increased globally. One such
non-communicable disease which threatens the global population is
stroke.
Stroke tends to be the second leading cause of death and disability in older population. In lower- and middle-income countries, increased incidence rate of
stroke was also evidenced in younger population which is alarming. Lifestyle changes, poor physical activity, stress, consumption of alcohol, oral
contraception, and smoking tend to be the causative agents of
stroke. Since
thrombus formation is the major pathology of
stroke, drugs were targeted to thrombolysis. Currently thrombolytic, antiplatelet, and
anticoagulant therapies were given for the
stroke patients. But the recovery rate of
stroke patients with available drugs is very slow. Hence, it is a need of today to discover a
drug with increased recovery rate and decreased or nil side effects.
Phytochemicals are the best options to treat such
non-communicable chronic diseases.
Visnagin is one such compound which is used to regulate blood pressure, treat
kidney stones,
tumors of bile duct,
renal colic, and
whooping cough. It possesses anti-inflammatory, neuroprotective, and cardioprotective properties; it was also proven to treat epileptic
seizures. In this study, the anti-ischemic effect of a furanochrome
visnagin was assessed in in vivo rat model. Middle cerebral ischemic/reperfusion was induced in healthy male Sprague Dawley rats and treated with different concentrations of
visnagin. The
neuroprotective effect of
visnagin against
cerebral ischemia-induced rats was assessed by analyzing the neurological score,
brain edema, infract volume, and
Evans blue leakage. The anti-inflammatory property of
visnagin was assessed by quantifying proinflammatory
cytokines in serum and brain tissues of
cerebral ischemia-induced rats.
Prostaglandin E-2, COX-2, and NFκ-β were estimated to assess the anti-ischemic effect of
visnagin. Histopathological analysis with H&E staining was performed to confirm the
neuroprotective effect of
visnagin against
cerebral ischemia. Our results authentically confirm that
visnagin has prevented the
inflammation in brain region of
cerebral ischemia-induced rats. The neurological scoring and the quantification of PGE-2, COX-2, and NFκ-β prove the anti-ischemic effect of
visnagin. Furthermore, the histopathological analysis of hippocampal region provides evidence to the
neuroprotective effect of
visnagin against
cerebral ischemia. Overall, our study confirms
visnagin as a potent alternative
drug to treat
stroke.