30]][“L Metabolism”

Diabetic neuropathy is a type of neuronal damage, associated with chronic diabetes, characterized by demyelination and deterioration of nerve fibers, alterations in the microvasculature and loss of sensory fibers that leads to pain, foot ulcers, amputations, depression, phobias, anorexia, loss of memory and reduction in complex reasoning skills upregulated BDNF in frontal cortex and hippocampus alongside reduced oxidative damage in the hippocampus of diabetic dbdb mice. Curcumin administration significantly increased reduced lactate dehydrogenase ATP activity in brain homogenate of alloxan induced diabetic mice.In addition, it reduced the expression level of insulin receptor and choline acetyltransferase in brainstem.Curcumin treatment upregulated the gene expression of choline acetyltransferase, SOD and insulin receptor in cortex.It is known to upregulate the expression level of muscarinic cholinergic receptor in brainstem and cerebral cortex as well as attenuate cognitive deficits in streptozotocin induced diabetic rats downregulated the expression level of dopaminergic D and D receptor in the cortex.In addition, curcumin administration significantly upregulated dopaminergic D receptor and downregulated D receptor in the cerebellum of diabetic rodents.In addition, curcumin administration attenuated NMDA and AMPA receptor mediated oxidative stress and excitotoxicity in the cerebral cortex of streptozotocin induced diabetic rats with animals diet decreased bdglucuronidase activity, nitric oxide level, total oxidant status, MDA level and oxidative stress index in streptozotocin induced diabetic rats. Curcumin treatment at the dose of mgkg for weeks downregulated the S.In addition, curcumin treatment reduced inflammation and oxidative stress in the hippocampus and cerebral cortex of streptozotocin induced diabetic rats reduced thermal hyperalgesia as well as attenuated the nitrite levels in brain homogenate of streptozotocin induced diabetic mice. Chronic diabetes has been reported to induce complications such as central and peripheral neuronal dysfunction.Curcumin might prove to be a better therapy for diabetic neuropathy due to its antioxidant and antiinflammatory potential, which needs further investigation.In addition, mice treated with nanocurcumin reduced morphine mediated acute opioid dependence.Administration of nanocurcumin significantly attenuated the chronic morphine induced tolerance and physical dependence in mice.A recent report suggested that curcumin inhibits DNA methyl transferases and histone acetyltransferases activity, and attenuates morphine withdrawal signs in rats. Preclinical data have conclusively proved that, curcumin administration reduce drug addiction and withdrawal symptoms, possibly through modulation of histone acetyltransferases, DNA methyl transferases activity, CREB, BDNF expressions, therefore clinical studies are warranted to assess the therapeutic potential of curcumin in this field.In addition, curcumin administration decreased MDA and nitrite levels while increased the reduced GSH levels in striatum.Curcumin nanoparticles significantly prevented hypolocomotion via reversal of mitochondrial dysfunctions. Curcumin administration increased the survival rate of glioblastoma affected rodents. The suggested mechanisms of curcumin effects against glioblastoma are cell cycle arrest, suppression of proliferation, inhibition of glioma cell angiogenesis and invasion, and induction of apoptosis. It is characterized by shortness of breath, chest pain, discomfort in the upper part of the body, sweating, dizziness, lightheadedness, nausea and vomiting.In clinical study, curcumin administration significantly attenuated myocardial infarction associated with coronary artery bypass grafting via antioxidant and antiinflammatory effects significantly reduced oxidative stress, apoptosis and infract size via stimulating janus kinase signal transducer and activator of transcription CRITICAL REVIEWS IN FOOD SCIENCE AND NUTRITION.

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