Department of Anatomy, Chengdu Medical College, Chengdu, Sichuan 610500, P.R. China.
Mol Med Rep. 2018 Mar;17(3):4823-4831. doi: 10.3892/mmr.2018.8440. Epub 2018 Jan 17.
Purple sweet potato color (PSPC) is a natural anthocyanin pigment that is derived from purple sweet potato storage roots. PSPC possesses a variety of biological activities, including antioxidant, anti‑inflammatory and neuroprotective effects; however, the detailed effects of PSPC on high‑fat diet (HFD)‑induced neuroinflammation remain to be determined. The aim of the present study was to investigate whether PSPC has a protective role in HFD‑associated neuroinflammation in the mouse brain and to provide novel insight into the mechanisms of the action. C57BL 6J mice were maintained on a normal diet (10 kcal% fat), a HFD (60 kcal% fat), a HFD with PSPC (700 mg/kg/day) or PSPC alone, which was administrated over 20 weeks. Open field and step‑through tests were used to evaluate the effects of HFD and PSPC on mouse behavior and memory function. Western blotting and ELISA analyses were used to assess the expression of inflammatory cytokines and the activation of mitogen‑activated protein kinase and nuclear factor‑κB (NF‑κB). The results demonstrated that PSPC treatment was able to significantly improve the HFD‑induced impairment of mouse behavior and memory function, and suppressed the increase in body weight, fat content, hyperlipemia and the level of endotoxin. PSPC treatment also markedly decreased the expression of cyclooxygenase‑2, inducible nitric oxide synthase, tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6, and increased the level of IL‑10 in the HFD‑treated mouse brain. In addition, PSPC inhibited the HFD‑induced phosphorylation of extracellular signal‑regulated kinase (ERK), c‑Jun N‑terminal kinase (JNK) and p38, and the activation of NF‑κB. These findings indicated that PSPC treatment may alleviate HFD‑induced neuroinflammation in the mouse brain by inhibiting ERK, JNK, p38 and NF-κB activation.
紫薯花色苷（PSPC）是一种天然的花色苷类色素，来源于紫薯的块根。PSPC 具有多种生物活性，包括抗氧化、抗炎和神经保护作用；然而，PSPC 对高脂肪饮食（HFD）诱导的神经炎症的确切作用仍有待确定。本研究旨在探讨 PSPC 是否对 HFD 相关的小鼠脑内神经炎症具有保护作用，并为其作用机制提供新的见解。将 C57BL/6J 小鼠分别维持在正常饮食（10%脂肪）、HFD（60%脂肪）、HFD 加 PSPC（700mg/kg/天）或 PSPC 单独喂养的条件下 20 周。旷场和避暗实验用于评估 HFD 和 PSPC 对小鼠行为和记忆功能的影响。Western blot 和 ELISA 分析用于评估炎症细胞因子的表达以及丝裂原活化蛋白激酶和核因子-κB（NF-κB）的激活情况。结果表明，PSPC 处理能够显著改善 HFD 诱导的小鼠行为和记忆功能障碍，并抑制体重、脂肪含量、高脂血症和内毒素水平的增加。PSPC 处理还显著降低了 COX-2、诱导型一氧化氮合酶、肿瘤坏死因子-α、白细胞介素（IL）-1β和 IL-6 的表达，并增加了 HFD 处理小鼠大脑中 IL-10 的水平。此外，PSPC 抑制了 HFD 诱导的细胞外信号调节激酶（ERK）、c-Jun N-末端激酶（JNK）和 p38 的磷酸化以及 NF-κB 的激活。这些发现表明，PSPC 处理可能通过抑制 ERK、JNK、p38 和 NF-κB 的激活来减轻 HFD 诱导的小鼠脑内神经炎症。
