AMP-activated protein kinase as a mediator of mitochondrial dysfunction of multiple sclerosis in animal models: A systematic review.

Multiple sclerosis (MS) is a chronic central nervous system (CNS) disorder characterized by demyelination, neuronal damage, and oligodendrocyte depletion. Reliable biomarkers are essential for early diagnosis and disease management. Emerging research highlights the role of mitochondrial dysfunction and oxidative stress in CNS disorders, including MS, in which mitochondria are central to the degenerative process. Adenosine monophosphate-activated protein kinase (AMPK) regulates the mitochondrial energy balance and initiates responses in neurodegenerative conditions. This systematic review, following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, aimed to comprehensively assess the literature on AMPK pathways, mitochondrial dysfunction, and in vivo studies using MS animal models. The search strategy involved the use of AMPK syntaxes, MS syntaxes, and animal model syntaxes. The PubMed, Scopus, Web of Science, and Google Scholar databases were systematically searched on August 26, 2023 without publication year restrictions. The review identified and analyzed relevant papers to provide a comprehensive overview of the current state of related research. Eight studies utilizing various interventions and methodological approaches were included. Risk of bias assessment revealed some areas of low risk but lacked explicit reporting in others. These studies collectively revealed a complex relationship between AMPK, mitochondrial dysfunction, and MS pathogenesis, with both cuprizone and experimental autoimmune encephalomyelitis models demonstrating associations between AMPK and mitochondrial disorders, including oxidative stress and impaired expression of mitochondrial genes. These studies illuminate the multifaceted role of AMPK in MS animal models, involving energy metabolism, inflammatory processes, oxidative stress, and gene regulation leading to mitochondrial dysfunction. However, unanswered questions about its mechanisms and clinical applications underscore the need for further research to fully harness its potential in addressing MS-related mitochondrial dysfunction.

Morphological, cytotoxicity, and coagulation assessments of perlite as a new hemostatic biomaterial.

Hemorrhage control is vital for clinical outcomes after surgical treatment and pre-hospital trauma injuries. Numerous biomaterials have been investigated to control surgical and traumatic bleeding. In this study, for the first time, perlite was introduced as an aluminosilicate biomaterial and compared with other ceramics such as kaolin and bentonite in terms of morphology, cytotoxicity, mutagenicity, and hemostatic evaluations. Cellular studies showed that perlite has excellent viability, good cell adhesion, and high anti-mutagenicity. Coagulation results demonstrated that the shortest clotting time (140 seconds with a concentration of 50 mg mL-1) was obtained for perlite samples compared to other samples. Therefore, perlite seems most efficient as a biocompatible ceramic for hemorrhage control and other biomaterial designs.