Osteoarthritis (OA) is a chronic and debilitating disease of the knee joint. OA of the knee is initiated by physical damage and accumulated oxidative stress, followed by an exaggerated inflammation leading to cartilage damage. Currently, no effective and safe therapeutic option capable of restoring articular cartilage tissue and joint architecture is available. We here report a novel and highly bioavailable formulation of curcumin, labeled as Next Generation Ultrasol Curcumin (NGUC), which was 64.7 times more bioavailable than natural 95% curcumin extract as demonstrated in rat bioavailability studies. We further investigated the protective effect of NGUC against monosodium iodoacetate (MIA)‐induced knee OA in rats. Analysis of X-ray and histopathological images revealed that NGUC supplementation restored joint architecture and reduced swelling of joints induced by MIA. NGUC treatment caused a significant reduction in the levels of inflammatory mediators such as TNF-α, IL-1β, IL-6, COMP, and CRP, and expressions of MMP-3, 5-LOX, COX-2, and NFκB in synovial tissue of rats with MIA-induced OA. NGUC also decreased serum MDA level and increased the levels of antioxidant enzymes SOD, CAT, and GPX. Thus, our results indicate that a novel formulation of curcumin with enhanced bioavailability effectively ameliorates the pathophysiology of OA.

[Purpose]The aim of the study was to determine the effects of dietary CoQ10 on serum biochemical parameters, lipid peroxidation, and HSP expression in the liver and slow-twitch muscles (soleus and gastronemius deep portion) of exercise-trained rats.[Methods]A total of 42 Wistar albino rats were divided into six groups: 1) Control, 2) Coenzyme Q10 (CoQ10), 3) Chronic Exercise (CE), 4) CE + CoQ10, 5) Acute Exercise (AE), and 6) AE + CoQ10. The rats were subjected to the running test 5 days a week for 6 weeks after which CoQ10 was administered via the diet. AE (running on the treadmill until the rats were exhausted) was done on the last day[Results]The results showed no significant difference in serum glucose and liver functions in any of the groups. However, CoQ10 and exercise treatment were found to lower cholesterol and triglyceride levels. Serum and muscle malondialdehyde (MDA) levels were found to be lower in the CE and CE + CoQ10 groups compared to the control group. The highest levels of HSP60, HSP70, and HSP90 in liver and muscle were found in the AE group, and the lowest levels were found in CE + CoQ10 group. CoQ10 supplementation reduced HSP expression in both CE-and AE-trained rats (P < 0.05).[Conclusion]The results showed that CoQ10 supplementation could reduce MDA levels, protect against oxidative damage, and regulate HSP expression in CE-and AE-trained rats. CE and CoQ10 were shown to reduce oxidative stress synergistically.

In this study, the effects of L-Carnitine supplementation on the lipid peroxidation and expression of PPAR-γ and glucose transporters in the liver and muscles of chronically and acutely exercised rats were investigated. A total of 42 male Wistar Albino rats (8-week-old) were divided into six groups as follows: Control, L-Carnitine, Chronic Exercise (CE), Chronic Exercise + L-Carnitine, Acute Exercise (AE) and L-Carnitine + Acute Exercise. Chronic exercise consists of 30 m/min, 30 min/day, and 5 days/week for 6 weeks. Rats in the acute exercise groups were run on the treadmill at 30 m/min until exhaustion. L-Carnitine was given at the level of 300 mg per kilogram of diet for 6 weeks. There was no significant difference in the levels of serum ALT, AST, urea, creatinine and glucose levels between the exercise and L-Carnitine groups (P > 0.05). Cholesterol and triglyceride levels decreased by L- carnitine supplementation and chronic exercise in control groups but increased in the AE groups compared to the control group without reinforcement (P < 0.05). Serum, muscle, heart, and liver malondialdehyde (MDA) concentrations were lower in CE and higher in the AE groups (P < 0.001). However, L-Carnitine supplementation reduced MDA levels (P < 0.05). Liver and muscle PPAR-γ, liver GLUT-2 and muscle GLUT-4 mRNA expressions were lower in AE group than in all other groups (P < 0.001). Both chronic exercise and supplemental L-Carnitine increased liver and muscle PPAR-γ, GLUT-2 and GLUT-4 mRNA expression (P <0.05). As a result, although acute exercise increased oxidative stress, chronic exercise reduced oxidative stress by lowering lipid peroxidation level. L-Carnitine supplementation decreased oxidative stress and improved glucose and lipid metabolism by regulation of PPAR-γ, GLUT-2 and GLUT-4 mRNA expression in rats.

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Nutritional complementary choices that could make significant health interventions in the eating habits of humans and companion animals are getting more attention in the prevention of chronic diseases (Thompson et al., 2014;Willett et al., 2006). Even though people following a balanced diet do not generally need to take additional nutrients, many people also use supplements to meet their right micronutrient needs to be protected from chronic diseases with the versatile effects of the developing world (Tontisirin et al., 2002).Obesity is an important relationship between chronic medical conditions such as cardiovascular diseases, diabetes mellitus, hypertension, and various cancers, making it a health and financial burden from the past to the present (Hurt et al., 2010;Tremmel et al., 2017).Westernized diets contain high saturated fats and cholesterol, low fiber, as well as high sugar and salt, which is known to increase the