Safety and Efficacy of Tirofiban Combined with Statins in the Perioperative Period of Intracranial Aneurysms: Systematic Review and Meta-Analysis.

Objective: In order to verify the safety and effectiveness of tirofiban combined with statins in the perioperative period of intracranial aneurysms, this study adopts systematic review and meta-analysis, so as to comprehensively understand the situation of intracranial aneurysms in the perioperative period, and tirofiban combined with statins was finally determined as an effective treatment drug. Methods: This study used systematic retrospective analysis and selected 80 patients with intracranial aneurysms treated in our hospital from June 2021 to June 2022 as the research objects. Through conventional drugs and tirofiban combined with statins used in this study, the intracranial levels, the probability of aneurysm rupture, and postoperative complications of the two groups were observed and recorded. Results: The analysis of 80 patients with intracranial aneurysms showed that the influence of intracranial levels in the observation group was better than that in the reference group, the rupture of aneurysms in the observation group was lower than that in the reference group, and the incidence of postoperative complications in the observation group was lower than that in the reference group. Conclusion: Through simulation verification, it is concluded that tirofiban combined with statins is safe and effective in the perioperative application of intracranial aneurysms. This drug can improve vascular recanalization, reduce the incidence of cerebrovascular disease events, and reduce the incidence of rebleeding. Its therapeutic effect is worthy of wide clinical application and promotion.

ZEB2, interacting with MDM2, contributes to the dysfuntion of brain microvascular endothelial cells and brain injury after intracerebral hemorrhage.

ZEB2 has been shown to be upregulated in the brain tissues of rats with intracerebral hemorrhage (ICH), but its role in ICH-caused brain injury remains unclear. Here, an ICH rat model was established via intracerebral injection of autologous blood, and the lentivirus-mediated ZEB2 short hairpin RNA (sh-ZEB2) or negative control (scramble) were administered 0.5 hours after ICH. Silencing ZEB2 alleviated ICH-induced neurologic deficits and the increase of BBB permeability, brain water content and ZEB2 expression. Next, OGD (oxygen glucose deprivation) plus hemin was used to treat primary brain microvascular endothelial cells (BMECs) to simulate the ICH condition in vitro. OGD plus hemin upregulated ZEB2 expression and apoptosis, but reduced cell viability, migration, TEER (transendothelial electric resistance) and the expression of vascular-endothelial (VE-) cadherin, occludin and claudin-5, which was reversed by inhibiting ZEB2. Mechanism researches showed that ZEB2 interacted with MDM2 to up-regulate MDM2 protein expression, and then increased E2F1 protein level by suppressing its ubiquitination, which in turn promoted the transcription of ZEB2 to induce its protein expression, so as to enhance the interaction between ZEB2 and MDM2, thereby contributing to OGD plus hemin-induced endothelial dysfunction. Additionally, the joint interference of ZEB2 and MDM2 in vivo had better mitigative effects on ICH-induced brain injury compared with silencing ZEB2 alone. In summary, ZEB2 interacted with MDM2 to promote BMEC dysfunction and brain damage after ICH.

Inhibition of EMMPRIN by microRNA-124 suppresses the growth, invasion and tumorigenicity of gliomas.

MicroRNAs (miR) are a group of non-coding, small RNAs, 18-20 nucleotides in length, that are frequently involved in the development of a variety of different types of cancer, including glioma, which is a type of severe tumor in the brain. Previous studies reported that miR-124 levels were downregulated in glioma specimens; however, the potential role of miR-124 in glioma currently remains unclear. The present study performed experiments, including dual-luciferase reporter assay (DLRA), MTT assay, transwell assay and flow cytometry, with the aim of elucidating the molecular mechanism of miR-124 in glioma. The results indicated that miR-124 expression was decreased in glioma tissues, accompanied by the increased expression of extracellular matrix metalloproteinase inducer (EMMPRIN). The expression of EMMPRIN was inhibited by miR-124 transfection. The DLRA results revealed that EMMPRIN directly targets miR-124. Furthermore, upon overexpression of miR-124 in the U87 cells, cell proliferation was significantly inhibited, apoptosis was increased, and cell migration and invasion were decreased. Furthermore, tumor growth was blocked by miR-124 in mice. Based on these results, the present study concluded that miR-124 is critical for amelioration of glioma by targeting EMMPRIN, thereby acting as a tumor suppressor. Thus, miR-124/EMMPRIN constitutes a plausible basis for the treatment of glioma.