Ryu Ji Hyeon, Kim Yeonye, Kim Min Jae, Park Jisu, Kim Ji Won, Park Hye Sook, Kim Young Sil, Shin Hwa Kyoung, Shin Yong-Il
Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Yangsan 50612, Gyeongnam, Korea.
Department of Korean Medical Science, School of Korean Medicine, Pusan National University, Yangsan 50612, Gyeongnam, Korea.
Life (Basel). 2022 Mar 29;12(4):503. doi: 10.3390/life12040503.
Membrane-free stem cell extract (MFSCE) of human adipose tissues possesses various biological activities. However, the effects of MFSCE on blood-brain barrier dysfunction and brain damage are unknown. In this study, we determined the role of MFSCE in an ischemic stroke mouse model. Mice were treated with MFSCE once daily for 4 days and 1 h before ischemic damage. Experimental ischemia was induced by photothrombosis. Pretreatment with MFSCE reduced infarct volume and edema and improved neurological, as well as motor functions. Evans blue leakage and water content in the brain tissue were reduced by MFSCE pretreatment relative to those in the vehicle group. MFSCE increased the expression of the tight junction proteins zonula occludens 1 and claudin-5, as well as vascular endothelial-cadherin, but decreased that of matrix metalloproteinase 9. Notably, MFSCE treatment decreased cell death and the level of NOD-like receptor protein 3 inflammasome, consistent with the downregulated expression of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18 in the ischemic brain. These effects might have occurred via the suppression of the expression of Toll-like receptor 4 and activation of nuclear factor-κB. The results highlighted the potential of MFSCE treatment as a novel and preventive strategy for patients at a high risk of ischemic stroke.
人脂肪组织的无膜干细胞提取物(MFSCE)具有多种生物学活性。然而,MFSCE对血脑屏障功能障碍和脑损伤的影响尚不清楚。在本研究中,我们确定了MFSCE在缺血性中风小鼠模型中的作用。在缺血损伤前4天和1小时,每天对小鼠进行一次MFSCE治疗。通过光血栓形成诱导实验性缺血。MFSCE预处理可减少梗死体积和水肿,并改善神经功能以及运动功能。与载体组相比,MFSCE预处理可减少脑组织中的伊文思蓝渗漏和含水量。MFSCE增加了紧密连接蛋白闭合蛋白1和claudin-5以及血管内皮钙黏蛋白的表达,但降低了基质金属蛋白酶9的表达。值得注意的是,MFSCE治疗可减少细胞死亡和NOD样受体蛋白3炎性小体的水平,这与缺血脑中促炎细胞因子白细胞介素(IL)-1β和IL-18表达下调一致。这些作用可能是通过抑制Toll样受体4的表达和激活核因子-κB而发生的。结果突出了MFSCE治疗作为缺血性中风高危患者的一种新型预防策略的潜力。