Publications by authors named "Hong-hai Hu"

Article Synopsis
  • - Major depressive disorder (MDD) affects around 16% of the global population, but its biological mechanisms remain largely unknown, with recent research highlighting the role of glial cells in its pathophysiology.
  • - A study identified ATP as a crucial factor in how astrocytes influence depression, finding lower ATP levels in mice prone to depression and demonstrating that ATP administration can rapidly alleviate depressive-like symptoms.
  • - Enhanced ATP release from astrocytes, particularly through P2X2 receptors in the medial prefrontal cortex, showed potential therapeutic effects, suggesting that targeting astrocytic ATP could provide new treatment options for MDD.
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Astrocytes are key components of the niche for neural stem cells (NSCs) in the adult hippocampus and play a vital role in regulating NSC proliferation and differentiation. However, the exact molecular mechanisms by which astrocytes modulate NSC proliferation have not been identified. Here, we identified adenosine 5'-triphosphate (ATP) as a proliferative factor required for astrocyte-mediated proliferation of NSCs in the adult hippocampus.

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Our previous data indicate that the inhibition of L-type calcium channels (LTCCs) might be the cause of post-ischemic neuronal injury and that the activation of LTCCs can give rise to neuroprotection. In the present study, we aimed to profile the intervention window of Bay K8644, an LTCC agonist, and determine the involved mechanisms. The four vessel occlusion and oxygen-glucose deprivation models were employed to mimic ischemia/reperfusion damage in vivo and in vitro.

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Ethnopharmacological Relevance: Xiao-Xu-Ming decoction (XXMD) has long been employed clinically to treat stroke in traditional Chinese Medicine.

Aim Of The Study: To investigate the neuroprotective effects of XXMD in vivo and in vitro stroke models and determine involved mechanisms.

Materials And Methods: Two models (four-vessel occlusion in adult Wistar rats and oxygen-glucose deprivation primary cultured neurons) were employed to mimic ischemia-reperfusion damage, in vivo and in vitro, respectively.

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