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[5] Kra lisch S, K le in J, L ossnerU, et Isoprotereno ,l TNFa lpha, and insulin down?? regulate ad ipose tr ig lycer ide lipase in 3T3?? L 1 adipocytes[ J]. M o l Cell Endoc ri?? no,l 2021, 240: 43?? 49 [6] K itan iT, O kuno S, FujisawaH. G rowth phase?? dependent changes in the subcel?? lula r loca liza tion o f pre?? B?? ce ll colony?? enhancing facto r [ J] . FEBS L et,t 2021, 544: 74?? 78. 簡介: 高遷移率蛋白 1( highmobility group box1, HMGB1) 為新近發(fā)現(xiàn)的介導(dǎo)脂多糖所致遲發(fā)死亡的細(xì)胞因子,其產(chǎn)生較TNF α和 IL 1 等細(xì)胞因子稍晚,但持續(xù)時間較長,故有“膿毒癥介質(zhì)”之稱。 [3] Ye S Q, Simon B A, Maloney J P, et al. Pre B cell colony enhancing factor as a potential novel biomarker in acute lung injury[J] . Am J Respir Crit Care M ed, 2021, 171( 4) : 361 370. 與糖類代謝: Fukuhara等 [4]研究證實 PBEF通過結(jié)合胰島素受體模擬胰島素作用而調(diào)節(jié)糖代謝。ALI、 ARDS生物標(biāo)志物 簡介: 前 B細(xì)胞克隆增強(qiáng)因子 (pre B cell colony enhancing factor, PBEF) PBEF最早在人類外周血淋巴細(xì)胞中被發(fā)現(xiàn),是 B細(xì)胞早期分化的一種生長因子,可以增強(qiáng)白介素 7促進(jìn)前 B細(xì)胞向 B細(xì)胞轉(zhuǎn)化的能力 [1] [1]Alessandrini F, Weichenmeier I, van M E, et al. Effects of ultrafine particles induced ox idative stress on Clara cells in allergiclung inflam mation[J] . Part Fibre Toxicol, 2021, 7: 11. 與 ALI/ARDS : Kitani等發(fā)現(xiàn)當(dāng)細(xì)胞處于增殖狀態(tài)時, PBEF主要分布在胞漿;處于非增殖狀態(tài)時,則主要出現(xiàn)在胞核內(nèi) [5],從而認(rèn)為 PBEF是與細(xì)胞周期有關(guān)的細(xì)胞內(nèi)蛋白。 [2] [2]Determann R M, Millo J L, Waddy S, et al. Plasma CC16 levels are as sociated with development of ALI/ ARDS in patients with ventilator associated pneumonia: a retrospective observational study[J] . BM C Pulm M ed, 2021, 9: 49. 與 ALI/ARDS : 在炎癥細(xì)胞因子促使中性粒細(xì)胞生存期延長的過程中,細(xì)胞內(nèi) PBEF表達(dá)增多,肺損傷時,炎癥介質(zhì)明顯增多,誘導(dǎo)細(xì)胞內(nèi)過度表達(dá) PBEF,同時血液中濃度明顯升高, Ye等 [3]對ALI時 PBEF進(jìn)行了研究,發(fā)現(xiàn) PBEF表達(dá)明顯增加;進(jìn)一步研究發(fā)現(xiàn) PBEF過度表達(dá)破壞血管內(nèi)皮細(xì)胞的屏障作用,引起肺毛細(xì)血管通透性增加,同時也調(diào)節(jié)炎性因子的分泌,導(dǎo)致ALI的發(fā)生。 [4]Fukuhara A,M a tsudaM, N ishizawaM, e t V isfa tin: a rotein secreted by v is cera l fat thatm im ics the effec