Curcuminoids modulates oxidative damage and mitochondrial dysfunction in diabetic rat brain

Abstract

Diabetes exacerbates neuronal injury induced by hyperglycemia mediated oxidative damage and mitochondrial dysfunction. The aim of the present study is to investigate the effects of curcuminoids, polyphenols of Curcuma longa (L.) on oxidative stress and mitochondrial impairment in the brain of streptozotocin (STZ)-induced diabetic rats. A marked increase in lipid peroxidation and nitrite levels with simultaneous decrease in endogenous antioxidant marker enzymes was observed in the diabetic rat brain, which was restored to normal levels on curcuminoids treatment. Down-regulation of mitochondrial complex I and IV activity caused by STZ induction was also up-regulated on oral administration of curcuminoids. Moreover, curcuminoids administration profoundly elevated the ATP level, which was earlier reduced in the diabetic brain. These results suggest that curcuminoids exhibit a protective effect by accelerating antioxidant defense mechanisms and attenuating mitochondrial dysfunction in the brain of diabetic rats. Curcuminoids thus may be used as a promising therapeutic agent in preventing and/or delaying the progression of diabetic complications in the brain.

Curcumin Protects from Cardiac Reperfusion Damage by Attenuation of Oxidant Stress and Mitochondrial Dysfunction

“…It has been shown that curcumin exerts a protective effect in several models of oxidant damage [14][15][16] including isoproterenol-induced cardiac injury [17] and I/R injury in rabbits [40]. Our data are consistent with these previous findings pointing to the attenuation of oxidant stress, which is a key finding in the protective effect of curcumin.…”

“…Phase II enzymes including glutathione peroxidase, glutathione reductase (GR), glutathione S-transferase (GST), c-glutamate cysteine ligase, and NADPH quinone oxidoreductase 1 protect cells from stress by diminishing oxidant stress or detoxifying carcinogens [11], and curcumin has shown to increase the expression of these enzymes by inducing nuclear translocation of the transcription factor Nrf2 (NF-E2-related factor-2) [12,13]. Several studies have shown that curcumin is able to ameliorate mitochondria-induced ROS production and lipid peroxidation in different models of oxidant damage [14][15][16], including that occurring in cardiac tissue [17,18]. In this respect, several reports have shown that mitochondria are both targets and sources of myocardial damage during ischemia and reperfusion [19,20].…”

Neuroprotective role of curcumin in the cerebellum of streptozotocin-induced diabetic rats

“…Curcuminoids exhibit a protective effect by accelerating anti-oxidant defence mechanisms and attenuating mitochondrial dysfunction in the brain of diabetic rats (Rastogi et al 2008). According to Meghana et al (2007) and Kanitkar et al (2009), curcumin protects pancreatic islets cells against streptozotocininduced death and dysfunction.…”

Curcumin micelles improve mitochondrial function in neuronal PC12 cells and brains of NMRI mice – Impact on bioavailability

“…425and complex I and IV activities(Rastogi et al, 2008). Similarly, curcumin administration (15 and 426 30mg/kg body weight/day for 6 weeks) improved oxidative defence, activities of respiratory 427 complexes I, II and III as well as cognitive tasks in a D-galactose induced mouse model of has been reported to have positive effects on mitochondrial function in 434 various animal studies (see above).…”