Department of Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan.
Department of Applied Biological Science, Tokyo Noko University, Fuchu, Japan.
J Neurosci Res. 2018 Dec;96(12):1887-1899. doi: 10.1002/jnr.24326. Epub 2018 Sep 22.
Stachybotrys microspora triprenyl phenol (SMTP)-44D has both anti-oxidative and anti-inflammatory activities, but its efficacy has not been proved in relation to the pathological changes of neurovascular unit (NVU) and neurovascular trophic coupling (NVTC) in ischemic stroke. Here, the present study was designed to assess the efficacies of SMTP-44D, moreover, compared with the standard neuroprotective reagent edaravone in ischemic brains. ICR mice were subjected to transient middle cerebral artery occlusion (tMCAO) for 60 min, SMTP-44D (10 mg/kg) or edaravone (3 mg/kg) was intravenously administrated through subclavian vein just after the reperfusion, and these mice were examined at 1, 3, and 7 d after reperfusion. Compared with the vehicle group, SMTP-44D treatment revealed obvious ameliorations in clinical scores and infarct volume, meanwhile, markedly suppressed the accumulations of 4-HNE, 8-OHdG, nitrotyrosine, RAGE, TNF-α, Iba-1, and cleaved caspase-3 after tMCAO. In addition, SMTP-44D significantly prevented the dissociation of NVU and improved the intensity of NAGO/BDNF and the number of BDNF/TrkB and BDNF/NeuN double positive cells. These effects of SMTP-44D in reducing oxidative and inflammatory stresses were similar to or stronger than those of edaravone. The present study demonstrated that SMTP-44D showed strong anti-oxidative, anti-inflammatory, and anti-apoptotic effects, moreover, the drug also significantly improved the NVU damage and NVTC in the ischemic brain.
密粘褶菌三萜酚(SMTP)-44D 具有抗氧化和抗炎活性,但它在缺血性脑卒中神经血管单元(NVU)和神经血管营养偶联(NVTC)病理变化方面的疗效尚未得到证实。本研究旨在评估 SMTP-44D 的疗效,并与标准神经保护试剂依达拉奉进行比较。ICR 小鼠进行短暂性大脑中动脉闭塞(tMCAO)60min,再灌注后通过锁骨下静脉静脉内给予 SMTP-44D(10mg/kg)或依达拉奉(3mg/kg),在再灌注后 1、3 和 7 天进行检查。与载体组相比,SMTP-44D 治疗可明显改善临床评分和梗死体积,同时显著抑制 tMCAO 后 4-HNE、8-OHdG、硝基酪氨酸、RAGE、TNF-α、Iba-1 和 cleaved caspase-3 的积累。此外,SMTP-44D 还能明显阻止 NVU 的分离,并提高 NAGO/BDNF 的强度和 BDNF/TrkB 和 BDNF/NeuN 双阳性细胞的数量。SMTP-44D 减轻氧化应激和炎症反应的作用与依达拉奉相似或更强。本研究表明,SMTP-44D 具有较强的抗氧化、抗炎和抗凋亡作用,同时还能显著改善缺血性脑损伤中的 NVU 损伤和 NVTC。