alamandine and Brain-Ischemia

Cerebrovascular diseases (CVDs) remain an important public health issue due to the increasing number of deaths worldwide. Changes in the synthesis and release of peptides in CVDs may play an important role in elucidating the physiopathology of the disease. Therefore, this study was to investigate the fate of maresin-1 (MaR-1), subfatin (SUB), asprosin (ASP), and alamandine (ALA) levels in patients with cerebral infarction (CI), intracranial hemorrhage (ICH), subarachnoid hemorrhage (SAH) evaluated within the scope of CVDs, and voluntary healthy controls.. The study participants were divided into 4 groups: CI patients, ICH patients, SAH patients, and healthy volunteers. The diagnosis of CVDs was made based on the National Institutes of Health Stroke Scale (NIHSS), Intracerebral Hemorrhage Score (ICHS), Botterel-Hunt-Hess Scale (BHHS), and cranial computed tomography (CT). The levels of MaR-1 (ng/mL), SUB (ng/mL), ASP (ng/mL), and ALA (pg/mL) in the blood samples collected from the participants were studied using the ELISA method. Other parameters included in the study were obtained from the patient records of our hospital.. The comparison of MaR-1 [(control 1.38 ± 0.14), SAH (0.98 ± 0.087), CI (0.67 ± 0.04), ICH (0.51 ± 0.03)], SUB [(control (13.2 ± 1.4), SAH (10.1 ± 1.2), CI (7.9 ± 0.8), ICH (5.8 ± 0.5)], and ALA [(control (67.2 ± 7.9), SAH (58.2 ± 4.3), CI (42.1 ± 3.7), and ICH (34.2 ±3.9)] values revealed a significant decrease compared to the control values. The comparison of the ASP values of SAH, CI, and ICH patients and control values (11.6 ± 1.2) showed significantly higher asprosin values in SAH (13.8 ± 1.1), CI (15.4 ± 1.2) and ICH (28.9 ± 2.8) patients. Similarly, systolic blood pressure (SBP), diastolic blood pressure (DBP), and glucose levels of CKD patients were also high.. Decreased MaR-1, SUB, ALA and increased ASP compared to the control values may play a role in the physiopathology of these diseases. MaR-1, SUB, ALA, and ASP differences between SAH, CI and ICH patients may also guide clinicians along with SBP, DBP and glucose values.

Topics: Brain Ischemia; Cerebral Hemorrhage; Cerebral Infarction; Glucose; Humans; Intracranial Hemorrhages; Subarachnoid Hemorrhage

Stroke, a leading cause of mortality and disability, characterized by neuronal death, can be induced by a reduction or interruption of blood flow. In this study, the role of Alamandine, a new peptide of the renin-angiotensin system, was evaluated in in-vitro and in-vivo brain ischemia models.. In the in-vitro model, hippocampal slices from male C57/Bl6 mice were placed in a glucose-free aCSF solution and bubbled with 95% N2 and 5% CO2 to mimic brain ischemia. An Alamandine concentration-response curve was generated to evaluate cell damage, glutamatergic excitotoxicity, and cell death. In the in-vivo model, cerebral ischemia/ reperfusion was induced by bilateral occlusion of common carotid arteries (BCCAo-untreated) in SD rats. An intracerebroventricular injection of Alamandine was given 20-30 min before BCCAo. Animals were subjected to neurological tests 24 h and 72 h after BCCAo. Cytokine levels, oxidative stress markers, and immunofluorescence were assessed in the brain 72 h after BCCAo.. Alamandine was able to protect brain slices from cellular damage, excitotoxicity and cell death. When the Alamandine receptor was blocked, protective effects were lost. ICV injection of Alamandine attenuated neurological deficits of animals subjected to BCCAo and reduced the number of apoptotic neurons/cells. Furthermore, Alamandine induced anti-inflammatory effects in BCCAo animals as shown by reductions in TNFα, IL- 1β, IL-6, and antioxidant effects through attenuation of the decreased SOD, catalase, and GSH activities in the brain.. This study showed, for the first time, a neuroprotective role for Alamandine in different ischemic stroke models.

Topics: Animals; Brain Ischemia; Disease Models, Animal; Humans; Ischemic Stroke; Male; Mice; Neuroprotection; Neuroprotective Agents; Oligopeptides; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Stroke