科學(xué)家發(fā)現(xiàn),，把來自骨髓的人類干細(xì)胞直接注射到小鼠的大腦可以減少中風(fēng)導(dǎo)致的損傷,。此前的實(shí)驗(yàn)提示注射干細(xì)胞可以緩解動(dòng)物的中風(fēng)效應(yīng)，這可能是由于它誘導(dǎo)了新神經(jīng)元的生長,。
Darwin Prockop及其同事如今發(fā)現(xiàn)注射干細(xì)胞可以通過觸發(fā)現(xiàn)有細(xì)胞——小膠質(zhì)細(xì)胞（神經(jīng)細(xì)胞）和巨噬細(xì)胞（免疫細(xì)胞）——產(chǎn)生保護(hù)神經(jīng)元和減輕炎癥的生化物質(zhì)從而產(chǎn)生康復(fù)作用。這組科學(xué)家證明了注射干細(xì)胞可以減少小鼠死亡或損傷的神經(jīng)元數(shù)量。他們還調(diào)查了小鼠大腦血流暫時(shí)中斷的時(shí)候腦基因的表達(dá)如何改變,。這組作者發(fā)現(xiàn)在血流終止之后，586個(gè)基因的表達(dá)水平更高,。這組作者說,，但是當(dāng)干細(xì)胞注射進(jìn)大腦后，不到10%的基因表達(dá)上調(diào),，這提示這些基因很可能參與了炎癥和免疫應(yīng)答,。相關(guān)論文發(fā)表在美國《國家科學(xué)院院刊》（PNAS）上。（生物谷Bioon.com）
生物谷推薦原始出處：
PNAS,，doi: 10.1073/pnas.0803670105,，Hirokazu Ohtaki，Darwin J. Prockop
Stem/progenitor cells from bone marrow decrease neuronal death in global ischemia by modulation of inflammatory/immune responses
Hirokazu Ohtaki, Joni H. Ylostalo, Jessica E. Foraker, Andrew P. Robinson, Roxanne L. Reger, Seiji Shioda, and Darwin J. Prockop
Human mesenchymal stromal cells (hMSCs) were injected into the hippocampus of adult mice 1 day after transient global ischemia. The hMSCs both improved neurologic function and markedly decreased neuronal cell death of the hippocampus. Microarray assays indicated that ischemia up-regulated 586 mouse genes. The hMSCs persisted for <7 days, but they down-regulated >10% of the ischemia-induced genes, most of which were involved in inflammatory and immune responses. The hMSCs also up-regulated three mouse genes, including the neuroprotective gene Ym1 that is expressed by activated microglia/macrophages. In addition, the transcriptomes of the hMSC changed with up-regulation of 170 human genes and down-regulation of 54 human genes. Protein assays of the hippocampus demonstrated increased expression in microglia/macrophages of Ym1, the cell survival factor insulin-like growth factor 1, galectin-3, cytokines reflective of a type 2 T cell immune bias, and the major histocompatibility complex II. The observed beneficial effects of hMSCs were largely explained by their modulation of inflammatory and immune responses, apparently by alternative activation of microglia and/or macrophages.
