Purple sweet potato anthocyanin attenuates high fat-induced neuroinflammation. - GreenMedInfo Summary
Purple sweet potato color attenuates high fat-induced neuroinflammation in mouse brain by inhibiting MAPK and NF-κB activation.
Mol Med Rep. 2018 Jan 17. Epub 2018 Jan 17. PMID: 29344660
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 brainand 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 theeffects 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, andthe 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.