Jung Sunyoon, Lee Mak-Soon, Chang Eugene, Kim Chong-Tai, Kim Yangha
Department of Nutritional Science and Food Management, Ewha Womans University, Seoul 03760, Korea.
Department of Food and Nutrition, Gangneung-Wonju National University, Gangneung 25457, Korea.
Antioxidants (Basel). 2021 Sep 13;10(9):1453. doi: 10.3390/antiox10091453.
The Mulberry ( L.) fruit is a rich source of polyphenolic compounds; most of these are anthocyanins. Obesity is intimately related to low-grade inflammation, with increased pro-inflammatory cytokine secretion and macrophage infiltration in white adipose tissue (WAT). This study investigated whether mulberry fruit extract (ME) has beneficial effects on obesity-induced inflammation and skeletal muscle mitochondrial dysfunction. Sprague-Dawley rats were divided into four groups and fed either a low-fat diet (LFD), high-fat diet (HFD), HFD + 5 g/kg of ME (ME-L), or HFD + 10 g/kg of ME (ME-H) for 14 weeks. ME alleviated dyslipidemia and lipid accumulation, as well as pro-inflammatory cytokine production such as tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and monocyte chemoattractant protein 1 (MCP1) in the WAT. ME mitigated nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) phosphorylation and macrophage infiltration in WAT. Notably, microRNA (miR)-21, miR-132, and miR-43 expressions were downregulated in the WAT of the ME groups compared to the HFD group. Moreover, ME increased the mitochondrial size and mitochondrial DNA (mtDNA) content, as well as key genes' expression related to mitochondrial function, including sirtuin (SIRT)1, peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), carnitine palmitoyltransferase 1β (CPT-1β), and uncoupling protein 3 (UCP3), and adenosine monophosphate-activated protein kinase (AMPK)/SIRT activities in skeletal muscle. These results suggested that ME might alleviate obesity-induced inflammation and mitochondrial dysfunction by regulating miR-21, miR-132, and miR-43 expression in WAT, and by activating the PGC-1α/SIRT1 pathway in muscle.
桑（L.）果是多酚类化合物的丰富来源；其中大部分是花青素。肥胖与低度炎症密切相关，白色脂肪组织（WAT）中促炎细胞因子分泌增加和巨噬细胞浸润。本研究调查了桑果提取物（ME）对肥胖诱导的炎症和骨骼肌线粒体功能障碍是否具有有益作用。将Sprague-Dawley大鼠分为四组，分别给予低脂饮食（LFD）、高脂饮食（HFD）、HFD + 5 g/kg ME（ME-L）或HFD + 10 g/kg ME（ME-H），持续14周。ME减轻了血脂异常和脂质积累，以及WAT中促炎细胞因子的产生，如肿瘤坏死因子-α（TNF-α）、白细胞介素6（IL-6）和单核细胞趋化蛋白1（MCP1）。ME减轻了WAT中活化B细胞核因子κB（NF-κB）的磷酸化和巨噬细胞浸润。值得注意的是，与HFD组相比，ME组WAT中微小RNA（miR）-21、miR-132和miR-43的表达下调。此外，ME增加了线粒体大小和线粒体DNA（mtDNA）含量，以及与线粒体功能相关的关键基因的表达，包括沉默调节蛋白（SIRT）1、过氧化物酶体增殖物激活受体γ共激活因子-1α（PGC-1α）、肉碱棕榈酰转移酶1β（CPT-1β）和解偶联蛋白3（UCP3），并增加了骨骼肌中腺苷单磷酸激活蛋白激酶（AMPK）/SIRT的活性。这些结果表明，ME可能通过调节WAT中miR-21、miR-132和miR-43的表达，以及激活肌肉中的PGC-1α/SIRT1途径，来减轻肥胖诱导的炎症和线粒体功能障碍。
