Tat-NR2B9c attenuates oxidative stress via inhibition of PSD95-NR2B-nNOS complex after subarachnoid hemorrhage in rats.

Oxidative stress plays important roles in the pathogenesis of early brain injury (EBI) after subarachnoid hemorrhage (SAH). Tat-NR2B9c has shown efficacy as a neuroprotective agent in several studies. Here, we identified the neuroprotective role of Tat-NR2B9c after SAH and its related mechanisms. The results showed that Tat-NR2B9c treatment attenuated oxidative stress, therefore alleviated neuronal apoptosis and neurological deficits after SAH. Tat-NR2B9c treatment could alleviate mitochondrial vacuolization induced by SAH. Compared to SAH + vehicle group, Tat-NR2B9c resulted in the decrease of Acetylated superoxide dismutase2 (Ac-SOD2), Bcl-2-associated X protein (Bax) and cleaved-caspase3 (CC3) protein expression, and the up-regulation of Sirtunin 3 (Sirt3) and Bcl-2 protein level. Moreover, Tat-NR2B9c attenuated excitotoxicity by inhibiting the interaction of PSD95-NR2B-nNOS. Our results demonstrated that Tat-NR2B9c inhibited oxidative stress via inhibition of PSD95-NR2B-nNOS complex formation after SAH. Tat-NR2B9c may serve as a potential treatment for SAH induced brain injury.

The Drainage Dysfunction of Meningeal Lymphatic Vessels Is Correlated with the Recurrence of Chronic Subdural Hematoma: a Prospective Study.

Meningeal lymphatic vessels (mLVs) were recently discovered to be involved in the waste drainage process in the brain, which has also been associated with a variety of neurological diseases. This research paper hypothesizes that the drainage function of mLVs may be affected after chronic subdural hematoma (CSDH) and the alterations of mLVs' drainage may predict CSDH recurrence. In this prospective observational study, unenhanced 3D T2-fluid-attenuated inversion recovery (3D T2-FLAIR) MRI data were collected from CSDH patients and healthy participants for analysis. Patients with CSDH who underwent surgery received MRI scans before and after surgery, whereas healthy controls and patients with CSDH who received pharmaceutical treatment received only one MRI scan at enrollment. The signal unit ratio (SUR) of mLVs were then measured according to the MRI data and calculated to define mLVs' drainage function. Finally, the relationship between mLVs' drainage function and CSDH recurrence was analyzed accordingly. Thirty-four participants were enrolled in this study, including 27 CSDH patients and 7 controls. The SUR of mLVs in all CSDH patients changed significantly before and after surgery. Moreover, the drainage function of the mLVs ipsilateral to hematoma (mLVs-IH) in CSDH patients was significantly lower than that in the controls (p < 0.05). Last, a higher improvement rate of the drainage function of the mLVs-IH is correlated to a lower risk of recurrence (p < 0.05). This study revealed the mLVs' drainage dysfunction after CSDH through non-invasive MRI. Furthermore, the drainage function of mLVs is an independent predictive factor of CSDH recurrence.

White Matter Injury: An Emerging Potential Target for Treatment after Subarachnoid Hemorrhage.

Subarachnoid hemorrhage (SAH) refers to vascular brain injury mainly from a ruptured aneurysm, which has a high lifetime risk and imposes a substantial burden on patients, families, and society. Previous studies on SAH mainly focused on neurons in gray matter (GM). However, according to literature reports in recent years, in-depth research on the mechanism of white matter (WM) is of great significance to injury and recovery after SAH. In terms of functional recovery after SAH, all kinds of cells in the central nervous system (CNS) should be protected. In other words, it is necessary to protect not only GM but also WM, not only neurons but also glial cells and axons, and not only for the lesion itself but also for the prevention and treatment of remote damage. Clarifying the mechanism of white matter injury (WMI) and repair after SAH is of great importance. Therefore, this present review systematically summarizes the current research on WMI after SAH, which might provide therapeutic targets for treatment after SAH.