Cell Treatment for Stroke in Type Two Diabetic Rats Improves Vascular Permeability Measured by MRI.
Cell Treatment for Stroke in Type Two Diabetic Rats Improves Vascular Permeability Measured by MRI.
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DOI：
10.1371/journal.pone.0149147
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Jiang Q
中科院分区：
文献类型：
--
作者：
Ding G;Chen J;Chopp M;Li L;Yan T;Li Q;Cui C;Davarani SP;Jiang Q
骨髓基质细胞（BMSC）治疗中风显着增强脑重塑，改善非糖尿病中风大鼠的神经功能。糖尿病是中风的主要危险因素，并引起可能影响中风治疗的神经血管变化。因此，有必要验证我们的假设，即用BMSC治疗中风对最常见的糖尿病形式2型糖尿病（T2 DM）具有治疗效果。在成年雄性Wistar大鼠中，通过给予高脂饮食联合单次腹腔注射（35 mg/kg）链脲佐菌素诱导T2 DM。然后对这些大鼠进行2 h的大脑中动脉闭塞（MCAo）。T2 DM大鼠在MCAo后3天通过尾静脉注射接受BMSC（5x 106，n = 8）或等体积的磷酸盐缓冲盐水（PBS）（n = 8）。对所有大鼠在MCAo后一天进行MRI，然后每周进行一次，持续5周。与溶剂处理的对照T2 DM大鼠相比，BMSC处理的T2 DM大鼠脑卒中显著（p<0.05）使用钆喷替酸盐的对比增强T1加权成像测量的中风后1周开始的血脑屏障破坏减少，并且使用磁敏感加权成像测量的中风后3周开始的脑出血点减少，尽管BMSC治疗没有减少由T2图划分的缺血性损伤体积。这些MRI测量结果与组织学数据一致。因此，在中风后3天开始的T2 DM大鼠中风的BMSC治疗显著减少缺血性血管损伤，尽管通过MRI测量，BMSC治疗没有改变T2 DM大鼠的梗死体积。
Treatment of stroke with bone marrow stromal cells (BMSC) significantly enhances brain remodeling and improves neurological function in non-diabetic stroke rats. Diabetes is a major risk factor for stroke and induces neurovascular changes which may impact stroke therapy. Thus, it is necessary to test our hypothesis that the treatment of stroke with BMSC has therapeutic efficacy in the most common form of diabetes, type 2 diabetes mellitus (T2DM). T2DM was induced in adult male Wistar rats by administration of a high fat diet in combination with a single intraperitoneal injection (35mg/kg) of streptozotocin. These rats were then subjected to 2h of middle cerebral artery occlusion (MCAo). T2DM rats received BMSC (5x106, n = 8) or an equal volume of phosphate-buffered saline (PBS) (n = 8) via tail-vein injection at 3 days after MCAo. MRI was performed one day and then weekly for 5 weeks post MCAo for all rats. Compared with vehicle treated control T2DM rats, BMSC treatment of stroke in T2DM rats significantly (p<0.05) decreased blood-brain barrier disruption starting at 1 week post stroke measured using contrast enhanced T1-weighted imaging with gadopentetate, and reduced cerebral hemorrhagic spots starting at 3 weeks post stroke measured using susceptibility weighted imaging, although BMSC treatment did not reduce the ischemic lesion volumes as demarcated by T2 maps. These MRI measurements were consistent with histological data. Thus, BMSC treatment of stroke in T2DM rats initiated at 3 days after stroke significantly reduced ischemic vascular damage, although BMSC treatment did not change infarction volume in T2DM rats, measured by MRI.