スダ　サトシ   SUDA Satoshi   須田　智    所属   埼玉医科大学  医学部 国際医療センター　神経内科・脳卒中内科    職種   教授
論文種別	学術雑誌(原著)
言語種別	英語
査読の有無	査読あり
表題	Transplantation of human dental pulp stem cells ameliorates brain damage following acute cerebral ischemia.
掲載誌名	正式名：Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie ISSNコード：0753-3322
掲載区分	国外
巻・号・頁	108,1005-1014頁
著者・共著者	Chikako Nito,Kota Sowa,Masataka Nakajima,Yuki Sakamoto,Satoshi Suda,Yasuhiro Nishiyama,Aki Nakamura-Takahashi,Yuko Nitahara-Kasahara,Masayuki Ueda,Takashi Okada,Kazumi Kimura
発行年月	2018/12
概要	AIMS: Numerous experimental studies have shown that cellular therapy, including human dental pulp stem cells (DPSCs), is an attractive strategy for ischemic brain injury. Herein, we examined the effects of intravenous DPSC administration after transient middle cerebral artery occlusion in rats. METHODS: Male Sprague-Dawley rats received a transient 90 min middle cerebral artery occlusion. DPSCs (1 × 106 cells) or vehicle were administered via the femoral vein at 0 h or 3 h after ischemia-reperfusion. PKH26, a red fluorescent cell linker, was used to track the transplanted cells in the brain. Infarct volume, neurological deficits, and immunological analyses were performed at 24 h and 72 h after reperfusion. RESULTS: PKH26-positive cells were observed more frequently in the ipsilateral than the contralateral hemisphere. DPSCs transplanted at 0 h after reperfusion significantly reduced infarct volume and reversed motor deficits at 24 h and 72 h recovery. DPSCs transplanted at 3 h after reperfusion also significantly reduced infarct volume and improved motor function compared with vehicle groups at 24 h and 72 h recovery. Further, DPSC transplantation significantly inhibited microglial activation and pro-inflammatory cytokine expression compared with controls at 72 h after reperfusion. Moreover, DPSCs attenuated neuronal degeneration in the cortical ischemic boundary area. CONCLUSIONS: Systemic delivery of human DPSCs after reperfusion reduced ischemic damage and improved functional recovery in a rodent ischemia model, with a clinically relevant therapeutic window. The neuroprotective action of DPSCs may relate to the modulation of neuroinflammation during the acute phase of stroke.
DOI	10.1016/j.biopha.2018.09.084
PMID	30372800