首页> 美国卫生研究院文献>Antioxidants Redox Signaling >Curcumin Supplementation Lowers TNF-α IL-6 IL-8 and MCP-1 Secretion in High Glucose-Treated Cultured Monocytes and Blood Levels of TNF-α IL-6 MCP-1 Glucose and Glycosylated Hemoglobin in Diabetic Rats
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Curcumin Supplementation Lowers TNF-α IL-6 IL-8 and MCP-1 Secretion in High Glucose-Treated Cultured Monocytes and Blood Levels of TNF-α IL-6 MCP-1 Glucose and Glycosylated Hemoglobin in Diabetic Rats

机译:补充姜黄素可降低高糖处理的培养单核细胞中TNF-αIL-6IL-8和MCP-1的分泌并降低糖尿病患者的TNF-αIL-6MCP-1葡萄糖和糖基化血红蛋白的血液水平老鼠

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摘要

This study examined the hypothesis that curcumin supplementation decreases blood levels of IL-6, MCP-1, TNF-α, 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 μM) at 37°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-α 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-α, glucose, HbA1, 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. Antioxid. Redox Signal. 11, 241–249.
机译:这项研究通过使用细胞培养模型和糖尿病大鼠模型研究了补充姜黄素可降低血液中IL-6,MCP-1,TNF-α,高血糖症和氧化应激的假设。在不存在或存在姜黄素(0.01-1μM)的情况下,将U937单核细胞与对照(7μmM)和高葡萄糖(35μmM)培养在37°C下培养24μh。通过注射链脲佐菌素(STZ)(即65μmg/ kg体重)在Sprague-Dawley大鼠中诱发糖尿病。每天通过管饲法补充对照缓冲液,橄榄油或姜黄素(100μmg/ kg体重),持续7周。在轻度麻醉下通过心脏穿刺收集血液。结果表明,姜黄素可抑制培养的单核细胞中高葡萄糖对脂质过氧化,IL-6,IL-8,MCP-1和TNF-α分泌的影响。在大鼠模型中,糖尿病引起血液中IL-6,MCP-1,TNF-α,葡萄糖,HbA1和氧化应激的显着升高,而姜黄素补充的大鼠则明显降低了血液中的IL-6,MCP-1,TNF-α,葡萄糖,HbA1和氧化应激。因此,姜黄素可以减少糖尿病大鼠细胞培养模型和血液中血管炎症和氧化应激水平的标志物。这表明补充姜黄素可以降低糖尿病患者的血糖和血管发炎的风险。抗氧化。氧化还原信号。 11,241–249。

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