Comparative Analysis of Fatty Acids Concentration in Liver and Muscle Tissues of Rats and Mice

This study conducted a comparative analysis of fatty acids (FAs) concentration derived from polar (PL) and non-polar (NPL) lipids in the liver and muscle tissues of rats and mice. The objective was to elucidate species-specific differences in tissue FA distribution. Employing targeted GC/MS-based methodology, the study aimed to provide insights into conserved and species-specific aspects of lipid metabolism, thereby enhancing future experimental design, linked with comprehension of the interactions between diet, metabolism, and health. Results revealed markedly higher levels of total fatty acids (TFAs) derived from PL in mice skeletal muscle compared to rats and elevated saturated fatty acids (SFAs) levels in mice. Unsaturated fatty acid levels, mainly monounsaturated fatty acids (MUFAs) and polyunsaturated fatty acids (PUFAs), were substantially higher in mice muscle across all lipid classes, resulting in a higher PUFA/TFA ratio in mice muscle. Detailed analysis of specific unsaturated fatty acids (C16:1, C18:1n9c, C18:2n6c, C22:6n3) indicated elevated levels in mice relative to rats. Conversely, rats exhibited higher SFA levels derived from the NPL fraction in the liver, particularly in myristic (C14:0), stearic (C18:0), and tricosanoic (C23:0) acids. Mice liver PL fractions displayed significantly elevated unsaturated FA levels, with notably higher MUFAs and lower PUFAs in NPL fractions compared to rats. Analysis of specific unsaturated FAs revealed higher levels of palmitoleic acid (C16:1) in mice, while rats exhibited increased linoleic (C18:2n6c) and linolenic (C18:3n3) acids. In conclusion, significant differences in FAs tissue distribution between rats and mice underscore the importance of considering species-specific FAs variations when utilizing these animal models and interpreting experimental results related to FA metabolism

Analysis of Serum Markers of Perioperative Brain Injury and Inflammation Associated with Endovascular Treatment of Intracranial Aneurysms: A Preliminary Study

Embolization is the preferred method for treating intracranial aneurysms due to its less invasive nature. However, recent findings suggest that even uncomplicated embolization may cause structural damage to the brain through ischemic or inflammatory mechanisms. This study aimed to find possible biomarkers of brain injury and inflammation in patients suffering from intracranial aneurysms who underwent endovascular treatment by measuring serological markers indicating brain damage. The study involved 26 patients who underwent uncomplicated intravascular stenting for unruptured intracranial aneurysms between January 2020 and December 2021. Blood samples were collected before the procedure, at 6–12 h, and at 24 h after the procedure. The following protein biomarkers levels were tested with ELISA: S100B, hNSE, TNF, hsCRP, FABP7, NFL, and GP39. Statistical analysis of the results revealed significant increases in serum levels for the four biomarkers: FABP7—before 0.25 (ng/mL) vs. 6–12 h 0.26 (p = 0.012) and vs. 24 h 0.27 (p p = 0.011) and vs. 24 h 0.57 (p = 0.001); hsCRP—before 1.65 (μg/mL) vs. 24 h 4.17 (p = 0.037); NFL—before 0.01 (pg/mL) vs. 6–12 h 3.99 (p = 0.004) and vs. 24 h 1.86 (p = 0.033). These biomarkers are recognized as potential indicators of neurovascular damage and should be monitored in clinical settings. Consequently, serum levels of NFL, GP39, hsCRP, and FABP7 measured before and 24 h after endovascular procedures can serve as important markers for assessing brain damage and indicate avenues for further research on biomarkers of neurovascular injury

The Relevance of Reperfusion Stroke Therapy for miR-9-3p and miR-9-5p Expression in Acute Stroke—A Preliminary Study

Reperfusion stroke therapy is a modern treatment that involves thrombolysis and the mechanical removal of thrombus from the extracranial and/or cerebral arteries, thereby increasing penumbra reperfusion. After reperfusion therapy, 46% of patients are able to live independently 3 months after stroke onset. MicroRNAs (miRNAs) are essential regulators in the development of cerebral ischemia/reperfusion injury and the efficacy of the applied treatment. The first aim of this study was to examine the change in serum miRNA levels via next-generation sequencing (NGS) 10 days after the onset of acute stroke and reperfusion treatment. Next, the predictive values of the bioinformatics analysis of miRNA gene targets for the assessment of brain ischemic response to reperfusion treatment were explored. Human serum samples were collected from patients on days 1 and 10 after stroke onset and reperfusion treatment. The samples were subjected to NGS and then validated using qRT-PCR. Differentially expressed miRNAs (DEmiRNAs) were used for enrichment analysis. Hsa-miR-9-3p and hsa-miR-9-5p expression were downregulated on day 10 compared to reperfusion treatment on day 1 after stroke. The functional analysis of miRNA target genes revealed a strong association between the identified miRNA and stroke-related biological processes related to neuroregeneration signaling pathways. Hsa-miR-9-3p and hsa-miR-9-5p are potential candidates for the further exploration of reperfusion treatment efficacy in stroke patients

After Ischemic Stroke, Minocycline Promotes a Protective Response in Neurons via the RNA-Binding Protein HuR, with a Positive Impact on Motor Performance

Ischemic stroke is the most common cause of adult disability and one of the leading causes of death worldwide, with a serious socio-economic impact. In the present work, we used a new thromboembolic model, recently developed in our lab, to induce focal cerebral ischemic (FCI) stroke in rats without reperfusion. We analyzed selected proteins implicated in the inflammatory response (such as the RNA-binding protein HuR, TNFa, and HSP70) via immunohistochemistry and western blotting techniques. The main goal of the study was to evaluate the beneficial effects of a single administration of minocycline at a low dose (1 mg/kg intravenously administered 10 min after FCI) on the neurons localized in the penumbra area after an ischemic stroke. Furthermore, given the importance of understanding the crosstalk between molecular parameters and motor functions following FCI, motor tests were also performed, such as the Horizontal Runway Elevated test, CatWalk (TM) XT, and Grip Strength test. Our results indicate that a single administration of a low dose of minocycline increased the viability of neurons and reduced the neurodegeneration caused by ischemia, resulting in a significant reduction in the infarct volume. At the molecular level, minocycline resulted in a reduction in TNFa content coupled with an increase in the levels of both HSP70 and HuR proteins in the penumbra area. Considering that both HSP70 and TNF-a transcripts are targeted by HuR, the obtained results suggest that, following FCI, this RNA-binding protein promotes a protective response by shifting its binding towards HSP70 instead of TNF-a. Most importantly, motor tests showed that reduced inflammation in the brain damaged area after minocycline treatment directly translated into a better motor performance, which is a fundamental outcome when searching for new therapeutic options for clinical practice

Use of ebselen as a neuroprotective agent in rat spinal cord subjected to traumatic injury

Spinal cord injury (SCI) causes disturbances of motor skills. Free radicals have been shown to be essential for the development of spinal cord trauma. Despite some progress, until now no effective pharmacological therapies against SCI have been verified. The purpose of our experiment was to investigate the neuroprotective effects of ebselen on experimental SCI. Twenty-two rats subjected to SCI were randomly subjected to SCI with no further treatment (n = 10) or intragastric administration of ebselen (10 mg/kg) immediately and 24 hours after SCI. Behavioral changes were assessed using the Basso, Beattie, and Bresnahan locomotor scale and footprint test during 12 weeks after SCI. Histopathological and immunohistochemical analyses of spinal cords and brains were performed at 12 weeks after SCI. Magnetic resonance imaging analysis of spinal cords was also performed at 12 weeks after SCI. Rats treated with ebselen presented only limited neurobehavioral progress as well as reduced spinal cord injuries compared with the control group, namely length of lesions (cysts/scars) visualized histopathologically in the spinal cord sections was less but cavity area was very similar. The same pattern was found in T2-weighted magnetic resonance images (cavities) and diffusion-weighted images (scars). The number of FluoroGold retrogradely labeled neurons in brain stem and motor cortex was several-fold higher in ebselen-treated rats than in the control group. The findings suggest that ebselen has only limited neuroprotective effects on injured spinal cord. All exprimental procedures were approved by the Local Animal Ethics Committee for Experiments on Animals in Katowice (Katowice, Poland) (approval No. 19/2009)