Department of Food Science & Nutrition, The Catholic University of Korea, 43 Jibong-ro, Wonmi-gu, Bucheon 14662, Korea.
Department of Food and Nutrition, Seoul National University, 1Gwanak-ro, Gwanak-gu, Seoul 08826, Korea.
Molecules. 2021 Jun 2;26(11):3363. doi: 10.3390/molecules26113363.
Obesity is characterized by elevated infiltration of macrophages into adipose tissue, leading to the development of insulin resistance. The black soybean seed coat is a rich source of anthocyanins with antioxidative and anti-inflammatory activities. This study investigated the effects of black soybean anthocyanin extract (BSAn) on obesity-induced oxidative stress, the inflammatory response, and insulin resistance in a coculture system of hypertrophied 3T3-L1 adipocytes and RAW264 macrophages. Coculture of adipocytes with macrophages increased the production of reactive oxygen species and inflammatory mediators and cytokines (NO, MCP-1, PGE, TNFα, and IL-6) and the release of free fatty acids but reduced anti-inflammatory adiponectin secretion. BSAn treatment (12.5, 25, 50, and 100 μg/mL) alleviated the coculture-induced changes ( < 0.001) and inhibited coculture-induced activation of JNK and ERK signaling ( < 0.01). BSAn also blocked the migration of RAW264.7 macrophages toward 3T3-L1 adipocytes. In addition, treatment with BSAn increased PPARγ expression and glucose uptake in response to insulin in hypertrophied 3T3-L1 adipocyte and RAW264.7 macrophage coculture ( < 0.01). These results demonstrate that BSAn attenuates inflammatory responses and improves adipocyte metabolic function in the coculture of hypertrophied 3T3-L1 adipocytes and RAW264.7 macrophages, suggesting the effectiveness of BSAn for obesity-induced insulin resistance.
肥胖的特征是巨噬细胞浸润脂肪组织增加,导致胰岛素抵抗的发展。黑大豆种皮是一种富含具有抗氧化和抗炎活性的花青素的丰富来源。本研究调查了黑大豆花青素提取物(BSAn)对肥胖诱导的氧化应激、炎症反应和胰岛素抵抗的影响,该研究采用肥大的 3T3-L1 脂肪细胞和 RAW264 巨噬细胞共培养系统。脂肪细胞与巨噬细胞共培养会增加活性氧物质和炎症介质及细胞因子(NO、MCP-1、PGE、TNFα 和 IL-6)的产生,以及游离脂肪酸的释放,但会减少抗炎性脂联素的分泌。BSAn 处理(12.5、25、50 和 100μg/mL)缓解了共培养诱导的变化(<0.001),并抑制了共培养诱导的 JNK 和 ERK 信号通路的激活(<0.01)。BSAn 还阻止了 RAW264.7 巨噬细胞向 3T3-L1 脂肪细胞的迁移。此外,BSAn 处理增加了在肥大的 3T3-L1 脂肪细胞和 RAW264.7 巨噬细胞共培养中对胰岛素的 PPARγ 表达和葡萄糖摄取(<0.01)。这些结果表明,BSAn 减轻了炎症反应,并改善了共培养中肥大的 3T3-L1 脂肪细胞和 RAW264.7 巨噬细胞的脂肪细胞代谢功能,提示 BSAn 对肥胖诱导的胰岛素抵抗有效。