Background: Subarachnoid hemorrhage (SAH) is a severe neurological condition with high mortality and morbidity rates, often exacerbated by secondary complications such as inflammation, cerebral vasospasm, and apoptosis. Proinflammatory cytokines, including interleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6), play critical roles in these pathological processes. Anakinra, an IL-1 receptor antagonist, has demonstrated significant anti-inflammatory effects in various disease models. This study aimed to evaluate the efficacy of anakinra in mitigating inflammation, vasospasm, and apoptosis in an experimental rat model of SAH. Methods: Thirty-two male Sprague Dawley rats were divided into four groups: Control (healthy), SAH (no treatment), Saline (0.2 mL saline subcutaneously), and Anakinra (50 mg/kg subcutaneously, twice daily). Proinflammatory markers (CRP, TNF-α, IL-1, IL-6, and fibrinogen) were measured in serum and cerebrospinal fluid (CSF) at 3, 7, and 10 days post-SAH. Basilar artery diameter was evaluated histopathologically, and Caspase-3 expression was assessed immunohistochemically to determine apoptotic activity. Results: SAH significantly increased levels of CRP, TNF-α, IL-1, IL-6, and fibrinogen in both serum and CSF, reduced basilar artery diameter, and elevated Caspase-3 expression compared to the Control group. Saline treatment provided limited improvements, with inflammatory markers and histopathological parameters remaining elevated. Anakinra treatment significantly reduced inflammatory markers, restored basilar artery diameter, and lowered Caspase-3 expression, highlighting its efficacy in mitigating inflammation, vasospasm, and apoptosis. Conclusions: Anakinra effectively suppresses inflammation, alleviates cerebral vasospasm, and inhibits apoptosis in an experimental model of SAH. These findings suggest its potential as a therapeutic agent for managing SAH and its complications. Further research is needed to explore its clinical applicability and long-term effects.

Background: Exercise or exercise capacity is a vital physiological function. It is known that certain cytokines support muscle function during exercise and, as a result, increase exercise capacity. Aims: In this study, the effect of metformin administered in combination with exercise on osteocalcin (OCN), insulin, and interleukin-6 (IL-6) levels in rats was investigated. Methods: Forty-two male Wistar rats were used in this study. The animals were randomly divided into six groups: control (CONT), only exercise (EXE), metformin_100 mg/kg (Met100), metformin_200 mg/kg (Met200), metformin_100 mg/kg+exercise (Met100+EXE), and metformin_200 mg/kg+exercise (Met200+EXE). A 10-week intervention was conducted, excluding exercise training. During the experiment, the groups receiving metformin application (100 or 200 mg/kg) were administered with metformin. At the end of the study, serum samples were collected from the rats to determine the levels of osteocalcin, insulin, and IL-6 using the enzyme-linked immunosorbent assay method. In addition, glucose levels and body weights were evaluated. GraphPad Prism was used for the analyses. Results: The OCN and insulin levels of the Met100+EXE and Met200+EXE groups were found to be higher compared to the CONT, Met100, and Met200 groups ( P < 0.05). The IL-6 level of the EXE group was determined to be higher than that of the CONT, Met100, and Met200 groups ( P < 0.01). It was observed that both exercise and the individual or combined application of metformin resulted in lower blood glucose levels compared to the CONT group. The mean body weight of the EXE group was higher than that of the other groups. Conclusion: The combined application of metformin and exercise has increased osteocalcin and insulin levels compared to metformin application alone.

Objective: Subarachnoid hemorrhage (SAH) is a life-threatening cerebrovascular condition that triggers a robust inflammatory response and cerebral vasospasm. This study aimed to evaluate the effects of anakinra, an interleukin-1 receptor antagonist, and tocilizumab, an interleukin-6 receptor antagonist, on inflammation and vasospasm in an experimental rat SAH model. Methods: Forty male Sprague Dawley rats (200–250 g) were randomly assigned to five groups: control, SAH, SAH + anakinra (ANA), SAH + tocilizumab (TCZ), and SAH + anakinra + tocilizumab (ANA+TCZ). SAH was induced by injecting non-heparinized arterial blood into the cisterna magna. Treatment groups received anakinra (50 mg/kg twice daily), tocilizumab (8 mg/kg once daily), or their combination for three days. Blood and cerebrospinal fluid (CSF) samples were analyzed for inflammatory markers (IL-1, IL-6, TNF-α, CRP), and histopathological evaluations were conducted to assess vasospasm and apoptosis. Results: SAH significantly increased pro-inflammatory cytokines (IL-1, IL-6, TNF-α, CRP) and fibrinogen levels in serum and CSF while reducing the basilar artery lumen diameter (p < 0.001). Anakinra and tocilizumab treatments significantly reduced inflammatory markers and vasospasm severity compared to the SAH group (p < 0.05). Combination therapy was more effective in reducing inflammation and vasospasm than either treatment alone (p < 0.05). Anakinra showed a stronger effect on IL-1 reduction, while tocilizumab was more effective in lowering IL-6 levels. The ANA+TCZ group exhibited a significant decrease in caspase activity, indicating reduced apoptosis (p < 0.05). Conclusions: Anakinra and tocilizumab effectively mitigated inflammation and vasospasm in an experimental SAH model, with combination therapy showing superior efficacy. These findings suggest that targeting both IL-1 and IL-6 pathways may be a promising therapeutic strategy for managing SAH complications. Further studies are warranted to evaluate long-term outcomes and clinical implications.

The aim of this study is to determine the protective effects of lupeol on acute exhaustive exercise-induced oxidative stress in male rats. Rats were randomly selected and divided into four groups (n=6/group): Control, exercise, lupeol and exercise+lupeol groups. At the end of the exercise protocol, the rats were sacrificed by cervical dislocation, blood samples were taken. The levels of superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), glutathione (GSH), coenzyme Q10 (CoQ10) and α-lipoic acid (ALA) and oxidative stress levels in serum samples were measured. As a result, it has been determined that lupeol, a natural triterpenoid compound, contributes positively to the level of antioxidants produced by the body and helps suppress oxidants. It has been observed that free radicals caused by oxidative stress that occur as a result of high-intensity exercise are reduced by lupeol. Accordingly, it has been determined that the use of lupeol during exercise in experimental animals exposed to oxidative stress inhibits free radicals formed by stress. In the light of these results, it is thought that lupeol may be included in the composition of pharmaceutical products against exercise-induced oxidative damage.

Heart diseases constitute a significant global burden of mortality and morbidity. This encompassing word refers to a variety of illnesses, including coronary artery disease, heart failure, myocardial infarction, and valvular heart disease. Given the imperative need to comprehend and address these ailments, experimental studies are indispensable. Experimental animal models serve as indispensable tools in elucidating the mechanisms of heart disease. They are pivotal for developing novel treatments and assessing the efficacy of existing therapies. Among the commonly utilized animal models in heart disease research are mice, rats, rabbits, dogs, and pigs. Each model offers distinct advantages and limitations, allowing researchers to probe specific facets of cardiac pathology and unravel the intricate mechanisms involved in heart disease. In this comprehensive review, it was aimed to provide a succinct overview of the various animal models employed in heart disease research. The advantages and drawbacks of each model were delineated, the aspects of human heart disease they emulate were elucidated, and pivotal research findings facilitated by their utilization were highlighted. By synthesizing this information, it was the endeavor to provide researchers and clinicians with valuable insights into the diverse array of animal models available for investigating heart diseases, ultimately paving the way for enhanced understanding and treatment of these debilitating conditions.