Increase in blood-brain barrier permeability does not directly induce neuronal death but may accelerate ischemic neuronal damage

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  • Ohmori Chiemi
    Department of Animal Physiology, Division of Bioscience, Nagahama Institute of Bio-Science and Technology, 1266 Tamura, Nagahama, Shiga 526-0829, Japan
  • Sakai Yusuke
    Department of Animal Physiology, Division of Bioscience, Nagahama Institute of Bio-Science and Technology, 1266 Tamura, Nagahama, Shiga 526-0829, Japan
  • Matano Yasuki
    Department of Animal Physiology, Division of Bioscience, Nagahama Institute of Bio-Science and Technology, 1266 Tamura, Nagahama, Shiga 526-0829, Japan
  • Suzuki Yasuhiro
    School of Pharmaceutical Sciences, Ohu University, 31-1 Tomita-cho Aza Sankaku-do, Koriyama, Fukushima 963-8611, Japan
  • Umemura Kazuo
    Department of Pharmacology, Hamamatsu University School of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Shizuoka 431-3192, Japan
  • Nagai Nobuo
    Department of Animal Physiology, Division of Bioscience, Nagahama Institute of Bio-Science and Technology, 1266 Tamura, Nagahama, Shiga 526-0829, Japan

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<p>It is observed that the increase in blood-brain barrier (BBB) permeability (BBBP) is associated with ischemic stroke and thought to trigger neuronal damage and deteriorate ischemic infarction, even though there is no experimental proof. Here, we investigated the effect of BBBP increase on brain damage, using a combination of photochemically-induced thrombotic brain damage (PIT-BD) model, a focal brain ischemic model, and transient bilateral carotid artery occlusion model (CAO, a whole brain ischemic model), in mice. In PIT-BD, BBBP increased in the region surrounding the ischemic damage from 4 h till 24 h with a peak at 8 h. On day 4, the damaged did not expand to the region with BBBP increase in mice with PIT-BD alone or with 30 min CAO at 1 h before PIT-BD, but expanded in mice with 30 min CAO at 3.5 h after PIT-BD. This expansion was paralleled with the increase in the number of apoptotic cells. These findings indicate that increase in BBBP does not cause direct neuronal death, but it facilitates ischemic neuronal loss, which was attributed, at least partially, to acceleration of apoptotic cell death.</p>

Journal

  • Experimental Animals

    Experimental Animals 67 (4), 479-486, 2018

    Japanese Association for Laboratory Animal Science

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