Curcumin Supplementation Lowers TNF-alpha, IL-6, IL-8, and MCP-1 Secretion in High Glucose-Treated Cultured Monocytes and Blood Levels of TNF-alpha, IL-6, MCP-1, Glucose, and Glycosylated Hemoglobin in Diabetic Rats. Antioxidants & redox signaling [Antioxid Redox Signal] Journal article | | Title | Curcumin Supplementation Lowers TNF-alpha, IL-6, IL-8, and MCP-1 Secretion in High Glucose-Treated Cultured Monocytes and Blood Levels of TNF-alpha, IL-6, MCP-1, Glucose, and Glycosylated Hemoglobin in Diabetic Rats. | | Author(s) | Jain SK, Rains J, Croad J, Larson B, Jones K | | Institution | Department of Pediatrics, Louisiana State University Health Sciences Center, Shreveport, Louisiana. | | Source | Antioxid Redox Signal 2008 Oct 31. | | Abstract | This study examined the hypothesis that curcumin supplementation decreases blood levels of IL-6, MCP-1, TNF-alpha, hyperglycemia, and oxidative stress by using a cell-culture model and a diabetic rat model. U937 monocytes were cultured with control (7 mM) and high glucose (35 mM) in the absence or presence of curcumin (0.01-1 muM) at 37 degrees C for 24 h. Diabetes was induced in Sprague-Dawley rats by injection of streptozotocin (STZ) (i.p., 65 mg/kg BW). Control buffer, olive oil, or curcumin (100 mg/kg BW) supplementation was administered by gavage daily for 7 weeks. Blood was collected by heart puncture with light anesthesia. Results show that the effect of high glucose on lipid peroxidation, IL-6, IL-8, MCP-1, and TNF-alpha secretion was inhibited by curcumin in cultured monocytes. In the rat model, diabetes caused a significant increase in blood levels of IL-6, MCP-1, TNF-alpha, glucose, HbA(1), and oxidative stress, which was significantly decreased in curcumin-supplemented rats. Thus, curcumin can decrease markers of vascular inflammation and oxidative stress levels in both a cell-culture model and in the blood of diabetic rats. This suggests that curcumin supplementation can reduce glycemia and the risk of vascular inflammation in diabetes. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 18976114 |
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