
Effect of Tongfu Xingshen capsule on the endogenous neural stem cells of experimental rats with intracerebral hemorrhage
Author(s) -
Zhizhong Cui,
Shanshan Liu,
Lingbo Hou,
Yifan Sun,
Haoxuan Chen,
Hui Mao,
Yuanqi Zhao,
Liang Qiao
Publication year - 2021
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2021.12263
Subject(s) - subventricular zone , neural stem cell , nestin , neun , endogeny , biology , neurotrophic factors , glial fibrillary acidic protein , intracerebral hemorrhage , stem cell , neuroscience , pathology , microbiology and biotechnology , medicine , immunology , endocrinology , receptor , immunohistochemistry , subarachnoid hemorrhage , biochemistry
Intracerebral hemorrhage (ICH) can stimulate neural regeneration, promoting tissue repair and recovery of nerve function. Tongfu Xingshen capsule (TXC) is a Chinese medicinal formula used to treat ICH and has been shown to protect brain tissue and improve nerve function in clinical studies. However, the effect of TXC on endogenous neural stem cells (NSCs) remains elusive. To explore the mechanisms underlying TXC action, a rat model of ICH was established. The effects of TXC on the proliferation and differentiation of NSCs were assessed in the subventricular zone (SVZ). TXC significantly improved nerve function defects, decreased brain water content and restored blood‑brain barrier integrity. Additionally, BrdU labeling showed that both high and low doses of TXC significantly increased the proportion of actively cycling NSCs positive for Nestin and glial fibrillary acidic protein, but did not affect the proliferation rates of NeuN‑positive neurons. Finally, TXC also upregulated the mRNA levels of brain‑derived neurotrophic factor and its receptor, TrκB, in affected brain tissues. Taken together, TXC accelerated neural repair and functional recovery after brain injury by potentially enhancing the proliferation and differentiation of endogenous NSCs into astroglial cells in the SVZ area.