ABSTRACT
Monocyte chemoattractant/chemotactic protein-1 (MCP-1), a member of the CC chemokine family, is one of the key chemokines that regulate migration and tissue infiltration of monocytes/macrophages. Its role in the pathophysiology of several inflammatory diseases has been widely recognized, thus making MCP-1 a possible target for anti-inflammatory treatments. Curcumin (diferuloylmethane) is a natural polyphenol derived from the rhizomes of Curcuma Longa L. (turmeric). Anti-inflammatory action underlies numerous pharmacological effects of curcumin in the control and prevention of several diseases. The purpose of this review is to evaluate the effects of curcumin on the regulation of MCP-1 as a key mediator of chemotaxis and inflammation, and the biological consequences thereof. In vitro studies have shown that curcumin can decrease MCP-1 production in various cell lines. Animal studies have also revealed that curcumin can attenuate MCP-1 expression and improve a range of inflammatory diseases through multiple molecular targets and mechanisms of action. There is limited data from human clinical trials showing the decreasing effect of curcumin on MCP-1 concentrations and improvement of the course of inflammatory diseases. Most of the in vitro and animal studies confirm that curcumin exert its MCP-1-lowering and anti-inflammatory effects by down-regulating the mitogen-activated protein kinase (MAPK) and NF-κB signaling pathway. As yet, there is limited data from human clinical trials showing the effect of curcumin on MCP-1 levels and improvement of the course of inflammatory diseases. More evidence, especially from human studies, is needed to better assess the effects of curcumin on circulating MCP-1 in different human diseases and the role of this modulatory effect in the putative anti-inflammatory properties of curcumin.
Subject(s)
Anti-Inflammatory Agents, Non-Steroidal/pharmacology , Chemokine CCL2/metabolism , Curcumin/pharmacology , Curcumin/therapeutic use , Gene Expression Regulation/drug effects , Animals , Atherosclerosis/drug therapy , Cell Line , Chemokine CCL2/genetics , Clinical Trials as Topic , Curcumin/administration & dosage , Epilepsy/drug therapy , Humans , Inflammation/drug therapy , MAP Kinase Signaling System/drug effects , Mice , NF-kappa B/metabolism , Osteoarthritis/drug therapy , Signal Transduction/drug effectsABSTRACT
BACKGROUND: Oxidative stress has a key role in the pathogenesis of type II diabetes mellitus (T2DM) and its vascular complications. Antioxidant therapy has been suggested as a potential approach to blunt T2DM development and progression. The aim of this study was to assess the effects of supplementation with curcuminoids, which are natural polyphenolics from turmeric, on oxidative indices in diabetic individuals. METHODS: In this randomized double-blind placebo-controlled trial, 118 subjects with T2DM were randomized to curcuminoids (1000 mg/day co-administered with piperine 10 mg/day) or matching placebo for a period of 8 weeks. Serum total antioxidant capacity, superoxide dismutase (SOD) activities and malondialdehyde (MDA) concentrations were measured at baseline and after the supplementation period. RESULTS: Curcuminoids supplementation caused a significant elevation in serum total antioxidant capacity (TAC) (p < 0.001) and SOD activities (p < 0.001), while serum MDA levels were significantly reduced compared with the placebo group (p < 0.001). These results remained statistically significant after adjustment for potential confounders (baseline differences in body mass index and fasting serum insulin). CONCLUSION: The present results support an antioxidant effect of curcuminoids supplementation in patients with T2DM, and call for future studies to assess the impact of these antioxidant effects on the occurrence of diabetic complications and cardiovascular endpoints.
Subject(s)
Antioxidants/therapeutic use , Curcuma , Curcumin/therapeutic use , Diabetes Mellitus, Type 2/blood , Diabetes Mellitus, Type 2/drug therapy , Dietary Supplements , Adult , Antioxidants/pharmacology , Blood Glucose/drug effects , Blood Glucose/metabolism , Curcumin/pharmacology , Diabetes Mellitus, Type 2/diagnosis , Double-Blind Method , Female , Follow-Up Studies , Humans , Male , Middle Aged , Oxidative Stress/drug effects , Oxidative Stress/physiology , Treatment OutcomeABSTRACT
PURPOSE: There is now good evidence that 25-hydroxyvitamin D (25OHD) status may have an important impact on the development and progression of cardiovascular disease. Because of the potential involvement of vitamin D deficiency in blood pressure control and immune responses, we aimed to investigate whether there was a relationship between 25OHD status and the prevalence of metabolic syndrome in an Iranian population. MATERIAL/METHODS: The study was carried out on a sample of 846 subjects [357(42.19%) males and 489(57.80%) females], derived from MASHAD STUDY. Serum 25OHD levels were measured using a competitive electroluminescence protein binding assay. Anthropometric indices were measured using standard protocols. RESULTS: Serum 25OHD was 12.7 (6.8-18.4) ng/ml in the metabolic syndrome (MetS) group and 14.1 (8.8-19.0) ng/ml in the group without metabolic syndrome (P=0.43). The frequency of vitamin D deficiency was 80.7% and 79.0% in subjects with or without metabolic syndrome in Iranian population. CONCLUSIONS: We found no significant difference in serum 25OHD concentrations between individuals with or without MetS and no significant linear relationship between serum 25OHD and several CVD risk factors.
