School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, 100029, China.
School of Chinese Medicine, Beijing University of Chinese Medicine, Beijing, 100029, China.
BMC Complement Altern Med. 2019 Nov 21;19(1):326. doi: 10.1186/s12906-019-2742-y.
It has been testified that Diabetes mellitus (DM) has a close association with chronic inflammation and Toll-like Receptors (TLRs), and DM could be prevented by mulberry leaf. Therefore, a hypothesis came into being that mulberry leaf could ameliorate proinflammation and insulin resistance (IR) through TLRs and insulin signalling pathways.
Water extracts of mulberry leaf (WEM) was given to diabetic mice by gavage for 10 weeks, and the diabetic mice was injected with low-dose streptozocin, fed with high-fat and high-sugar diet. Oral glucose tolerance tests (OGTTs) were conducted. At the same time, homeostasis model assessment of insulin (HOMA-IR) and the level of the inflammatory factor, tumour necrosis factor-α (TNF-α) was measured. The expressions of critical nodes of TLRs and insulin signalling pathway were also examined.
WEM contributed to a significant decrease in fasting blood glucose, AUC from the investigation of OGTTs and HOMA-IR. The levels of the inflammatory factor, tumour necrosis factor-α (TNF-α) also declined. Moreover, WEM suppressed the expression of TLR2, myeloid differentiation primary-response protein 88 (MyD88), tumour-necrosis-factor receptor-associated factor 6 (TRAF6), nuclear factor kappa B (NF-κB) in the skeletal muscle. WEM could up-regulate the expression of insulin receptor (InsR) and insulin receptor substrate 1 (IRS1), and down-regulate the phosphorylation of IRS1 in adipose tissue.
Through this study, a conclusion could be made that WEM mitigates hyperglycemia, IR, and inflammation through the interactions among TLR2 signalling pathway, insulin signalling pathway and TNF-α.
有研究表明糖尿病(DM)与慢性炎症和 Toll 样受体(TLRs)密切相关,桑叶可以预防糖尿病。因此,产生了一种假说,即桑叶可以通过 TLRs 和胰岛素信号通路改善前炎症和胰岛素抵抗(IR)。
通过灌胃给予糖尿病小鼠桑叶水提取物(WEM)10 周,用低剂量链脲佐菌素注射,用高脂肪高糖饮食喂养。进行口服葡萄糖耐量试验(OGTTs)。同时,测量胰岛素稳态模型评估(HOMA-IR)和炎症因子肿瘤坏死因子-α(TNF-α)的水平。还检查了 TLRs 和胰岛素信号通路的关键节点的表达。
WEM 显著降低空腹血糖、OGTT 调查的 AUC 和 HOMA-IR。炎症因子肿瘤坏死因子-α(TNF-α)的水平也下降。此外,WEM 抑制了骨骼肌中 TLR2、髓样分化初级反应蛋白 88(MyD88)、肿瘤坏死因子受体相关因子 6(TRAF6)、核因子 kappa B(NF-κB)的表达。WEM 可以上调胰岛素受体(InsR)和胰岛素受体底物 1(IRS1)的表达,并下调脂肪组织中 IRS1 的磷酸化。
通过这项研究,可以得出结论,WEM 通过 TLR2 信号通路、胰岛素信号通路和 TNF-α 之间的相互作用,减轻高血糖、IR 和炎症。