A systematic review on anti-diabetic action of 7-O-galloyl-D-sedoheptulose, a polyphenol from Corni Fructus, in type 2 diabetic mice with hepatic and pancreatic damage.
Chan Hum Park, Jeong Sook Noh, Jin Pyeong Jeon, Takako Yokozawa
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引用次数: 0
Abstract
Traditional medicines are recently being focused on to treat diabetes and its complications because of their lack of toxic and/or side effects. This report describes the effects of 7-O-galloyl-D-sedoheptulose (GS), a polyphenolic compound isolated from Corni Fructus, on type 2 diabetic db/db mice with hepatic and pancreatic damage. We examined several biochemical factors and oxidative stress- and inflammation-related markers. In the serum, levels of glucose, leptin, insulin, C-peptide, resistin, tumor necrosis factor-α, and interleukin-6 were down-regulated, while adiponectin was augmented by GS treatment. In addition, GS suppressed the reactive oxygen species and lipid peroxidation in the serum, liver, and pancreas, but increased the pancreatic insulin and pancreatic C-peptide contents. These results were derived from attenuating the expression of nicotinamide adenine dinucleotide phosphate oxidase subunit proteins, Nox-4 and p22phox. Augmented nuclear factor (NF)-E2-related factor 2 and heme oxygenase-1 were reduced with a decrease in oxidative stress during GS treatment. NF-κB-related pro-inflammatory factors were also alleviated in hepatic tissue. Moreover, GS modulated the protein expressions of pro-inflammatory NF-κB, cyclooxygenase-2, inducible nitric oxide synthase, c-Jun N-terminal kinase (JNK), phosphor-JNK, activator protein-1, transforming growth factor-β1, and fibronectin. Based on these results, we demonstrated that the anti-diabetic action of GS may be due to its anti-oxidative stress property and anti-inflammatory action.
山茱萸多酚7- o -没食子酰-d -sedoheptulose对肝脏和胰腺损伤的2型糖尿病小鼠的抗糖尿病作用的系统综述。
传统药物由于没有毒性和/或副作用,最近正重点用于治疗糖尿病及其并发症。7- o -没食子酰- d -sedoheptulose (GS)是一种从山茱萸中分离出来的多酚类化合物,它对2型糖尿病db/db小鼠肝脏和胰腺损伤的影响。我们检查了几种生化因素以及氧化应激和炎症相关的标志物。血清中葡萄糖、瘦素、胰岛素、c肽、抵抗素、肿瘤坏死因子-α、白细胞介素-6水平下调,脂联素水平升高。此外,GS抑制了血清、肝脏和胰腺中的活性氧和脂质过氧化,但增加了胰腺胰岛素和胰腺c肽的含量。这些结果来源于减弱烟酰胺腺嘌呤二核苷酸磷酸氧化酶亚基蛋白Nox-4和p22phox的表达。增强核因子(NF)- e2相关因子2和血红素加氧酶-1随着GS处理期间氧化应激的降低而降低。肝组织中NF-κ b相关的促炎因子也有所减轻。此外,GS还可调节促炎因子NF-κB、环氧合酶-2、诱导型一氧化氮合酶、c-Jun n-末端激酶(JNK)、磷酸化JNK、激活蛋白-1、转化生长因子-β1和纤维连接蛋白的表达。基于这些结果,我们证明了GS的抗糖尿病作用可能是由于其抗氧化应激和抗炎作用。