•980•
sights from investigation of neurons and microglia [ J ].
Mol Cell Endocrinol，2016, 438:18-26.
[7] Lemus MB，Bayliss JA，Lockie SH，et al. A stereological
analysis of NPY, POMC, Orexin, GFAP astrocyte, and
Ibal microglia cell number and volume in diet-induced
obese male mice [ J ]. Endocrinology, 2015 , 156 ( 5 )：1701-1713.
[8 ] Cawley NX, Li Z, Loh YP. 60 years of POMC ：biosynthe
sis, trafficking, and secretion of pro-opiomelanocortin-de-
rived peptides [J]. J Mol Endocrinol, 2016, 56(4) ：T77-
T97.
[9] Lowry P. 60 years of POMC ：purification and biological
characterisation of melanotrophins and corticotrophins [ J ].
J Mol Endocrinol, 2016, 56(4) ：T1-T12.
[10] Raffan E，Dennis RJ，0 ’ Donovan CJ，et al. A deletion in
the canine POMC gene is associated with weight and appe
tite in obesity-prone labrador retriever dogs [ J ]. Cell
Metab, 2016, 23(5) ：893-900.
[11] Low MJ. Neuroendocrinology ：New hormone treatment for
obesity caused by POMC-deficiency[ J]. Nat Rev Endocri
nol, 2016, 12(11) ：627-628.
[12] Chronwall BM. Anatomy and physiology of the neuroendo
crine arcuate nucleus [ J ]. Peptides, 1985 , 6 ( Suppl 2)：1-11.
[13] Schwartz MW, Woods SC, Porte D Jr, et al. Central nerv
ous system control of food intake [ J ]. Nature，2000，404
(6778) ：661-671.
[14] Barsh GS, Schwartz MW. Genetic approaches to studying
energy balance ：perception and integration [ J ]. Nat Rev
Genet, 2002, 3(8) ：589-600.
[15] Lam TK，Schwartz GJ，Rossetti L. Hypothalamic sensing
of fatty acids[ J]. Nat Neurosci, 2005, 8(5) ：579-584. [16] Waise TM, Toshinai K, Naznin F, et al. One-day high-fat
diet induces inflammation in the nodose ganglion and hypo
thalamus of mice [ J ]. Biochem Biophys Res Commun,
2015, 464(4) ：1157-1162.
(责任编辑：卢萍，罗森）
Protectin D X可以通过改善炎症和调节巨噬细胞表型
提局胺毒症小鼠的存活率
近期的一系列研究表明，源自Omega-3脂肪酸二十二碳六烯酸（docosahexaenoic acid, DHA)的脂质介质在多种炎症性疾 病中具有消炎或抗炎作用。因此，夏海发等试图评估Protectm DX(PDX;Pr〇tectm D1的异构体，一种新的脂质介质）是否可以 保护小鼠对抗脓毒症（sepsis),并探索其潜在机制。他们采用盲肠结扎穿孔（cecum ligation and puncture, CLP)建立脓毒症动 物模型，结果发现PDX可以提高脓毒症小鼠8d内的总体生存率，并减轻多器官损伤。除此之外，PDX可以在CLP术后24 h 减少促炎症因子和细菌载量。同时,PDX提高脓毒症小鼠腹腔巨噬细胞的吞噬能力，并增加M2型巨噬细胞的比例。在体外，PDX可以上调Raw264.7细胞中M2型巨噬细胞标志物（A rgl和Y m l)及其转录调节因子（过氧化物酶体增生物激活受体7,
peroxisome proliferator-activated receptor-7, PPAR-~y)的表达；反之，PPAR-~y 抑制剂 GW9662 和 PPAR-~y siRNA 可以消除 PDX 对 Raw264. 7细胞中A rgl和Y m l的诱导。综上所述，该研究结果表明PDX能够促进巨噬细胞的M2极化，增强其吞噬活性，加 快炎症消散，从而提高脓毒症小鼠的存活率。
Sci Rep, 2017, 7(1) :99(戴晓萌）
