We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Increased Calbindin D28k Expression via Long-Term Alternate-Day Fasting Does Not Protect against Ischemia-Reperfusion Injury: A Focus on Delayed Neuronal Death, Gliosis and Immunoglobulin G Leakage.
- Authors
Sim, Hyejin; Lee, Tae-Kyeong; Yoo, Yeon Ho; Ahn, Ji Hyeon; Kim, Dae Won; Kim, Bora; Lee, Jae-Chul; Park, Joon Ha; Lim, Soon-Sung; Park, Jung-Seok; Kang, Il Jun; Kim, Young-Myeong; Shin, Myoung Cheol; Cho, Jun Hwi; Park, Yoonsoo; Won, Moo-Ho
- Abstract
Calbindin-D28k (CB), a calcium-binding protein, mediates diverse neuronal functions. In this study, adult gerbils were fed a normal diet (ND) or exposed to intermittent fasting (IF) for three months, and were randomly assigned to sham or ischemia operated groups. Ischemic injury was induced by transient forebrain ischemia for 5 min. Short-term memory was examined via passive avoidance test. CB expression was investigated in the Cornu Ammonis 1 (CA1) region of the hippocampus via western blot analysis and immunohistochemistry. Finally, histological analysis was used to assess neuroprotection and gliosis (microgliosis and astrogliosis) in the CA1 region. Short-term memory did not vary significantly between ischemic gerbils with IF and those exposed to ND. CB expression was increased significantly in the CA1 pyramidal neurons of ischemic gerbils with IF compared with that of gerbils fed ND. However, the CB expression was significantly decreased in ischemic gerbils with IF, similarly to that of ischemic gerbils exposed to ND. The CA1 pyramidal neurons were not protected from ischemic injury in both groups, and gliosis (astrogliosis and microgliosis) was gradually increased with time after ischemia. In addition, immunoglobulin G was leaked into the CA1 parenchyma from blood vessels and gradually increased with time after ischemic insult in both groups. Taken together, our study suggests that IF for three months increases CB expression in hippocampal CA1 pyramidal neurons; however, the CA1 pyramidal neurons are not protected from transient forebrain ischemia. This failure in neuroprotection may be attributed to disruption of the blood–brain barrier, which triggers gliosis after ischemic insults.
- Subjects
CALBINDIN; IMMUNOGLOBULIN G; GLIOSIS; FASTING; INTERMITTENT fasting; CALCIUM-binding proteins; BLOOD-brain barrier; PYRAMIDAL neurons
- Publication
International Journal of Molecular Sciences, 2021, Vol 22, Issue 2, p644
- ISSN
1661-6596
- Publication type
Article
- DOI
10.3390/ijms22020644