Background and Purpose— The role of interleukin (IL)-1β remains unknown in early brain injury (EBI) after subarachnoid hemorrhage (SAH), although IL-1β has been repeatedly reported to increase in the brain and cerebrospinal fluid. The aim of this study is to examine the effects of IL-1β inactivation on EBI after SAH in mice. Methods— The endovascular perforation model of SAH was produced and 112 mice were assigned to sham, SAH+ vehicle, and SAH+ N-Ac-Tyr-Val-Ala-Asp-chloromethyl ketone (Ac-YVAD-CMK, 6 and 10 mg/kg) groups. Ac-YVAD-CMK, a selective inhibitor of IL-1β converting enzyme, or vehicle was administered intraperitoneally 1 hour post-SAH. EBI was assessed in terms of mortality within 24 hours, neurological scores, brain water content at 24 and 72 hours, Evans blue dye extravasation and Western blot for IL-1β, c-Jun N-Terminal kinase (JNK), matrix metalloproteinase (MMP)-9, and zonula occludens (ZO)-1 at 24 hours after SAH. Results— High-dose (10 mg/kg) but not low-dose (6 mg/kg) treatment group significantly improved neurological scores, mortality, brain water content, and Evans blue dye extravasation compared with the vehicle group. Although both dosages of Ac-YVAD-CMK attenuated the mature IL-1β induction, only high-dose treatment group significantly inhibited the phosphorylation of JNK, MMP-9 induction, and ZO-1 degradation. Conclusion— IL-1β activation may play an important role in the pathogenesis of EBI after SAH. The neurovascular protection of Ac-YVAD-CMK may be provided by the inhibition of JNK-mediated MMP-9 induction and the consequent preservation of tight junction protein ZO-1.

Calcium oxide nanoparticles (CaO NPs) have unique catalytic and biological properties; their activities are highly influenced by their morphology; as a result, these characteristics are most needed for various applications in several fields, including material science, environmental science, and medicinal science. The primary motivation for synthesizing CaO NPs using a biological method is to suppress the usage of hazardous chemicals used in making its process, which will be more cost‐effective and ecologically profitable. However, due to the complexity of the biological extracts employed in chemical processes, large‐scale manufacturing of nanoparticles via the green synthesis approach remains a significant problem. As a result, the production of CaO NPs utilizing Moringa oleifera plant leaves aqueous extract as an alternative biological agent for capping, stabilizing, and reducing agents due to rich phytochemical parameters in synthesis was investigated in this study. The structural characterization of the CaO NPs obtained by using UV‐Vis, FTIR, XRD, and SEM‐EDS indicates the presence of purity and primarily aggregated spherical nanosized material with an average size of 32.08 nm observed. The XRD study revealed that heat annealing increased the size of the crystallites, favoring monocrystalline. Finally, these findings, together with the cheap cost of synthesizing the plant‐mediated CaO NPs produced, show good antimicrobial (gram‐positive) activities.

Background and Purpose— Recent studies have shown the antiapoptotic neuroprotective effects of lecithinized superoxide dismutase (PC-SOD) in different forms of brain injury. We tested the effects of PC-SOD in focal cerebral ischemia in the rat middle cerebral artery occlusion model (MCAO). Methods— Adult male Sprague-Dawley rats were treated with PC-SOD (0.3, 1.0, and 3.0 mg/kg) administered intravenously after 90 minutes of occlusion (beginning of reperfusion). Physiological parameters, neurological score, and infarct volume were assessed at 24 and 72 hours in 3 groups of animals: sham-operated (n=18), MCAO treated with vehicle (n=26), and MCAO treated with PC-SOD (n=37). Oxidative stress was evaluated by malondialdehyde assay, and the apoptotic mechanisms were studied by Western blotting. Results— PC-SOD treatment significantly reduced infarct volume and improved neurological scores at different time points compared with the vehicle-treated group. PC-SOD treatment decreased malondialdehyde levels, cytochrome c , and cleaved caspase 3 expression and increased mitochondrial Bcl-2 expression. Conclusions— Inhibition of oxidative stress with PC-SOD treatment improves outcomes after focal cerebral ischemia. This neuroprotective effect is likely exerted by antiapoptotic mechanisms.