These findings revealed that, curcumin reverse myocardial infarction and heart attack via its antioxidant, antiinflammatory and antiapoptotic properties.In animal study, curcumin administration reported to possess antiatherosclerotic activity by downregulating the expression of lipocalin in apolipoprotein E knockout mice. It oxidized LDL and lowered lipid levels in the serum of hypercholesterolemic rabbits. A clinical study demonstrated that turmeric attenuated hematuria, proteinuria and systolic blood pressure associated with refractory or relapsing nephritis in patients without any adverse events. In animal study, curcumin administration downregulated the expression angiotensin I receptor in vascular smooth muscle cells.In addition, it decreased the level of circulating angiotensin converting enzyme and induced vascular relaxation in hypertensive rats.Further, curcumin administration upregulated eNOS expression, decreased superoxide enzyme level and downregulated pphox NADPH oxidase expression in vascular tissues, which is known to be responsible for kidneyclip induced hypertension in rats. In another study, curcumin treatment increased the expression of eNOS, decreased oxidative stress, restored glutathione redox ratio in aortic tissues along with decrease in plasma protein carbonyls, MDA and urinary nitrate nitrite levels in cadmium intoxicated mice resulting in antihypertensive effect. In conclusion, curcumin supplementation effectively reduce hypertension via blocking angiotensin I receptor, reducing circulating angiotensinconverting enzyme, inducing vasodilation and mediating nephroprotection.In experimental study, clinicopathological evidence indicates that, curcumin treatment reduces cardiac dysrhythmias, ventricular fibrillation and tachycardia by attenuating oxidative stress in mesenteric vessels of rats during ischemiareperfusion injury. In in vitro study, curcumin administration inhibited human etheragogorelated gene potassium channels, resulting in cardiac repolarization prolongation, which might associated with the observed antiarrhythmic effects. Paradoxically, clinical report represented that curcumin treatment for one month causes complete atrioventricular block and after withdrawal of curcumin no further cardiac disturbances was observed. Further, curcumin administration reduced oxidative stress, inflammation and apoptosis in spinal cord as well as reversed locomotor deficit in rats. Curcumin administration increased the SOD activity in cerebral cortex and corpus striatum, inhibited brain LPO and reversed motor dysfunction in rats. Curcumin treatment diminished mortality, reduced infarct volume and cerebral damage, reduced the brain water content, downregulated iNOS expression and ameliorated neurological deficit as well as prevented bloodbrain barrier damage in focal cerebral ischemic rats. Mechanistically, curcumin administration reduced oxidative stress, inflammation, apoptosis, mitochondrial dysfunction, cerebral infract size and volume thereby ameliorates neurogenesis and behavioral performance in experimental stroke models.Therefore, curcumin may be a promising supplementary phytoconstituent for stroke in the future.A recent metaanalysis revealed that, curcumin or combined curcuminoids supplementation effectively lowered the level of fasting blood glucose in individuals with some degree of dysglycemia.In animal study, curcumin administration is reported to reduce glucose intolerance through induction of glucagonlike peptide secretion in CRITICAL REVIEWS IN FOOD SCIENCE AND NUTRITION rats. In addition, curcumin administration is known to reduce insulin resistance by downregulating phosphorylation of IRS serine residue and upregulating phosphorylation of IRS tyrosine in the skeletal muscle of rats fed with high fructose.Curcumin treatment also reduced glucose intolerance, hyperinsulinemia and homeostasis model assessmentinsulin resistance level.Additionally, curcumin significantly downregulated extracellular kinase and p protein expressions in skeletal muscle.A recent study demonstrated that, curcumin administration attenuated splenic damage and improved immunity in streptozotocininduced diabetic rats via antioxidant, antiinflammatory and antiapoptotic mechanisms.