Curcumin Attenuates Oxidative Stress and Activation of Redox-Sensitive Kinases in High Fructose- and High-Fat-Fed Male Wistar Rats

Abstract

The present study was carried out to investigate the effects of curcumin on oxidative stress and redox-sensitive kinases in high fructose- and high-fat-fed rats. Sixty rats were randomly divided into six groups with ten animals each. Rats were fed with a standard rodent diet, high fructose diet (60%), and high-fat diet (30%). Curcumin was administered to control, high fructose and high fat diet groups for ten weeks. At the end of the study, body weight and blood glucose levels were measured. The antioxidant enzymes GSH (reduced glutathione), GPx (glutathione peroxidase), and catalase activities were estimated in the blood. MDA, TAS, and TOS were estimated in the plasma, liver, and kidney. Curcumin treatment decreased body weight and blood glucose levels in the rats fed with fructose and high-fat diet. Antioxidant enzymes and plasma TAS were significantly improved by curcumin treatment in high fructose-fed rats, whereas in high-fat-fed rats, there was an increase only in the GPx activity. Curcumin significantly attenuated the elevation of plasma MDA and TOS in both diet groups. Hepatic MDA and TOS were found to be decreased upon curcumin supplementation in both diet groups, whereas a decrease in the renal MDA levels was observed only in fructose-treated rats, not in fat-fed rats. Curcumin treatment elevated liver TAS in rats fed only with the fructose-rich diet. Curcumin showed a significant decrease in the oxidative stress index (OSI) in plasma, liver, and kidney tissues in both diet groups. ERK phosphorylation was significantly decreased in both diet groups by curcumin treatment. Similarly, curcumin reduced the phosphorylation of p38 MAPK only in the high fructose-fed rats, not in the high-fat-fed rats. No significant changes were found in JNK phosphorylation in both diet groups. Thus, curcumin may be effective in the management of diet-induced oxidative stress and could be explored as a therapeutic adjuvant against complications associated with obesity and diabetes.

Antioxidant and anti-inflammatory effects of DHK-medicated serum on high glucose-induced injury in endothelial cells

“…MDA, a secondary product of lipid peroxidation, is a common index used to evaluate excess oxidative stress (7,8,25). Excessive quantities of MDA in serum and tissues lead to the development of diabetic vascular complications (14,15,31). In the present study, DHK-medicated serum led to a reduction in the level of MDA (Fig.…”

Antidiabetic Properties of Curcumin II: Evidence from In Vivo Studies

“…Curcumin treatment increased antioxidant glutathione, GPx, catalase and total antioxidant serum levels, while MDA and total oxidant serum and liver levels were significantly reduced, indicating reduced oxidative stress. In addition, phosphorylated ERK and p38 protein levels were significantly decreased with curcumin treatment, suggesting that the effects may be mediated by ERK/p38 MAPK signaling [66].…”

“…Supplementation of high-fructose, high-fat (HFHF; 60% kcal fructose and 30% kcal fat)-fed Wistar rats with curcumin (200 mg/kg b.w./day) for 10 weeks resulted in significantly reduced serum glucose and body weight [66]. Curcumin treatment increased antioxidant glutathione, GPx, catalase and total antioxidant serum levels, while MDA and total oxidant serum and liver levels were significantly reduced, indicating reduced oxidative stress.…”

Gold-quercetin nanoparticles prevent metabolic endotoxemia-induced kidney injury by regulating TLR4/NF-kB signaling and Nrf2 pathway in high fat diet fed mice

“…11,[13][14][15] On the other hand, HFD significantly increases the production of reactive oxygen species (ROS), which further release superoxide anion and cause oxidative stress in the kidney by stimulating podocyte injury. [15][16][17] Hence, antioxidant therapy may be involved in the pathological process of kidney injury. Previous reports show that TLR4/ NF-kB and mitogen-activated protein kinase (MAPK) pathways are involved in cellular inflammation in response to oxidative stress.…”