Compound from Magnolia officinalis Ameliorates White Matter Injury by Promoting Oligodendrocyte Maturation in Chronic Cerebral Ischemia Models.
10.1007/s12264-023-01068-z
- Author:
Zhi ZHANG
1
;
Xin SHU
1
;
Qian CAO
1
;
Lushan XU
1
;
Zibu WANG
1
;
Chenggang LI
1
;
Shengnan XIA
2
;
Pengfei SHAO
2
;
Xinyu BAO
2
;
Liang SUN
1
;
Yuhao XU
2
;
Yun XU
3
Author Information
1. Department of Neurology, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, 210008, China.
2. Department of Neurology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School and State Key Laboratory of Pharmaceutical Biotechnology and Institute of Translational Medicine for Brain Critical Diseases, Nanjing University, Nanjing, 210008, China.
3. Department of Neurology, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, 210008, China. xuyun20042001@aliyun.com.
- Publication Type:Journal Article
- Keywords:
Honokiol;
Oligodendrocyte;
Vascular dementia;
White matter injury
- MeSH:
Magnolia;
White Matter;
Brain Ischemia/metabolism*;
Oligodendroglia/metabolism*
- From:
Neuroscience Bulletin
2023;39(10):1497-1511
- CountryChina
- Language:English
-
Abstract:
Chronic cerebral hypoperfusion leads to white matter injury (WMI), which subsequently causes neurodegeneration and even cognitive impairment. However, due to the lack of treatment specifically for WMI, novel recognized and effective therapeutic strategies are urgently needed. In this study, we found that honokiol and magnolol, two compounds derived from Magnolia officinalis, significantly facilitated the differentiation of primary oligodendrocyte precursor cells (OPCs) into mature oligodendrocytes, with a more prominent effect of the former compound. Moreover, our results demonstrated that honokiol treatment improved myelin injury, induced mature oligodendrocyte protein expression, attenuated cognitive decline, promoted oligodendrocyte regeneration, and inhibited astrocytic activation in the bilateral carotid artery stenosis model. Mechanistically, honokiol increased the phosphorylation of serine/threonine kinase (Akt) and mammalian target of rapamycin (mTOR) by activating cannabinoid receptor 1 during OPC differentiation. Collectively, our study indicates that honokiol might serve as a potential treatment for WMI in chronic cerebral ischemia.
