Urolithin A Enhances Tight Junction Protein Expression in Endothelial Cells Cultured In Vitro via Pink1-Parkin-Mediated Mitophagy in Irradiated Astrocytes.

Radiation brain injury (RBI) is a complication of cranial tumor radiotherapy that significantly impacts patients' quality of life. Astrocyte-secreted vascular endothelial growth factor (VEGF) disrupts the blood-brain barrier (BBB) in RBI. However, further studies are required to elucidate the complex molecular mechanisms involved.

The efficacy of early rehabilitation in enhancing vestibular compensation in mice with unilateral vestibular neurectomy by promoting cellular proliferation and glial reaction.

Acute peripheral vestibular dysfunction is associated with a variety of postural and balance disturbances. Vestibular rehabilitation training (VRT) is widely acknowledged as an effective intervention for promoting vestibular compensation. Nevertheless, the broader implementation of early VRT is hindered by an incomplete understanding of its neurobiological mechanisms.

Mitochondrial dysfunction of Astrocyte induces cell activation under high salt condition.

Excess dietary sodium can accumulate in brain and adversely affect human health. We have confirmed in previous studies that high salt can induce activation of astrocyte manifested by the secretion of various inflammatory factors. In order to further explore the effect of high salt on the internal cell metabolism of astrocytes, RNA sequencing was performed on astrocytes under high salt environment, which indicated the oxidative phosphorylation and glycolysis pathways of astrocytes were downregulated.

Enhanced VEGF secretion and blood-brain barrier disruption: Radiation-mediated inhibition of astrocyte autophagy via PI3K-AKT pathway activation.

Radiation-induced damage to the blood-brain barrier (BBB) is the recognized pathological basis of radiation-induced brain injury (RBI), a side effect of head and neck cancer treatments. There is currently a lack of therapeutic approaches for RBI due to the ambiguity of its underlying mechanisms. Therefore, it is essential to identify these mechanisms in order to prevent RBI or provide early interventions.

FGIN-1-27 Mitigates Radiation-induced Mitochondrial Hyperfunction and Cellular Hyperactivation in Cultured Astrocytes.

Radiation-induced brain injury (RBI) poses a significant challenge in the context of radiotherapy for intracranial tumors, necessitating a comprehensive understanding of the cellular and molecular mechanisms involved. While prior investigations have underscored the role of astrocyte activation and excessive vascular endothelial growth factor production in microvascular damage associated with RBI, there remains a scarcity of studies examining the impact of radiation on astrocytes, particularly regarding organelles such as mitochondria. Thus, our study aimed to elucidate alterations in astrocyte and mitochondrial functionality following radiation exposure, with a specific focus on evaluating the potential ameliorative effects of translocator protein 18 kDa(TSPO) ligands.