1.Role of metabolic crosstalk between astrocytes and neurons in ischemic brain injury
Min SUN ; Zibu WANG ; Yun XU ; Yanting CHEN
International Journal of Cerebrovascular Diseases 2023;31(9):703-710
Ischemic stroke is a common cerebrovascular disease with high mortality and disability rates. Astrocytes, as the most abundant glial cells in the brain, have the function of maintaining the homeostasis of the central nervous system, which requires precise coupling between neurotransmission and energy metabolism. Therefore, the metabolic crosstalk between astrocytes and neurons plays an important role in the occurrence and development of ischemic stroke. On the one hand, ischemic stroke leads to neuronal excessive excitation, metabolic disorders, and even death, simultaneously promoting changes in astrocyte metabolism profile and increased heterogeneity. On the other hand, the metabolic crosstalk between astrocytes and neurons can also affect the outcome of ischemic stroke. This article reviews the role of the metabolic crosstalk between astrocytes and neurons in ischemic brain injury, and looks forward to potential research directions and treatment targets in the future, in order to provide theoretical reference for the treatment of ischemic stroke.
2.Compound from Magnolia officinalis Ameliorates White Matter Injury by Promoting Oligodendrocyte Maturation in Chronic Cerebral Ischemia Models.
Zhi ZHANG ; Xin SHU ; Qian CAO ; Lushan XU ; Zibu WANG ; Chenggang LI ; Shengnan XIA ; Pengfei SHAO ; Xinyu BAO ; Liang SUN ; Yuhao XU ; Yun XU
Neuroscience Bulletin 2023;39(10):1497-1511
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.
Magnolia
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White Matter
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Brain Ischemia/metabolism*
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Oligodendroglia/metabolism*