• Int J Med Sci · Jan 2021

    Clemastine promotes recovery of neural function and suppresses neuronal apoptosis by restoring balance of pro-inflammatory mediators in an experimental model of intracerebral hemorrhage.

    • Cheng Zhi, Shulian Zeng, Yuan Chen, Degui Liao, Miaoling Lai, Zhaotao Wang, Yezhong Wang, and Shiyin Xiao.
    • Department of Pathology, the Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510260, China.
    • Int J Med Sci. 2021 Jan 1; 18 (3): 639-645.

    AbstractIntracerebral hemorrhage (ICH) represents a common acute cerebrovascular event that imparts high rates of disability. The microglia-mediated inflammatory response is a critical factor in determining cerebral damage post-ICH. Clemastine (CLM) is a histamine receptor H1 (HRH1) antagonist that has been shown to modulate the inflammatory response. However, the effects of CLM on ICH and the underlying mechanism remain to be determined. This investigation reveals that CLM resulted in reduction of cerebral hematoma volume, decreased cerebral edema and lower rates of neuronal apoptosis as well as improved behavioral scores in an acute ICH murine model. CLM treatment was noted to decrease pro-inflammatory effectors and increased anti-inflammatory effectors post-ICH. In addition, CLM reduced the deleterious effects of activated microglia on neurons in a transwell co-culture system. Our findings show that CLM likely mediates its therapeutic effect through inhibition of microglia-induced inflammatory response and apoptosis, thereby enhancing restoration of neuronal function.© The author(s).

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