Aim: The effect of Diosmin Hesperidin on intestinal ischaemia reperfusion injury was evaluated in an experimental model in rats. Material and methods: Forty Spraque-Dawley rats were divided into 4 groups of (n = 10) (sham, sham + Diosmin Hesperidin, Reperfusion, Reperfusion + Diosmin Hesperidin). Diosmin Hesperidin oral gavage was administrated at a dose of 50 mg/kg to rats 14 and 2 hours before the operation and 30 minutes of ischaemia and 30 minutes of reperfusion was performed in the groups when appropriate. Ileum samples were resected for histopathological evaluation and tissue malondialdehyde (MDA) and myeloperoxidase (MPA) level determination. Results: Mean mucosal injury score of IR group (4,50 ± 0,23) was significantly higher than the other groups (p < 0.05). Although mean mucosal injury score of IR + DH group was higher than sham and sham + DH groups, difference was not statistically significant (p > 0.05). Tissue MDA and MPO activities of IR group were 45,55 ± 2.61 nmol/g/wet tissue and 1.68 ± 0.25 U/g/wet tissue respectively and were significantly higher than the other groups (p < 0.008). Although tissue MDA and MPO activities of IR + DH group was higher than sham and sham + DH groups, differences were not statistically significant (p > 0.008). Conclusion: Diosmin Hesperidin seems to be effective in the prevention of intestinal reperfusion injury.

Cardiovascular diseases are significant health problems that cause high mortality rates worldwide. Myocardial infarction (MI), in particular, is one of the leading conditions among these diseases. The aim of this study is to evaluate the potential therapeutic approach of carvacrol in the treatment of cardiovascular diseases by investigating its protective effects against myocardial infarction through oxidative stress and biomarker levels. In this study, 28 male Wistar albino rats were used, and divided into 4 groups: Control, Carvacrol, Myocardial Infarction (MI), and MI + Carvacrol. Carvacrol was administered at a dose of 50 mg/kg for six weeks. The induction of MI was performed during the last 2 days of carvacrol administration by administering 100 mg/kg isoproterenol subcutaneously. At the end of the experiment, blood pressure, biomarkers such as troponin T, BNP, GDF-15, and IL-6 were measured, and cardiac tissue was histopathologically examined. The results show that in the MI group, troponin T, BNP, IL-6 and GDF-15 levels were increased, while diastolic blood pressure and heart rate were decreased. In the carvacrol-treated group, troponin T, BNP, IL-6 and GDF-15 levels were decreased. Carvacrol did not significantly affect systolic, diastolic, mean arterial pressure, or heart rate in experimental groups. Moreover, carvacrol decreased necrosis, edema, and mononuclear cell infiltration in the heart tissue, which were increased due to MI. In conclusion, carvacrol demonstrated protective effects against myocardial infarction. Carvacrol alleviated histopathological damage by reducing inflammatory biomarkers. In addition to carvacrol improved troponin T and BNP markers.These findings suggest that carvacrol may be a promising agent in the treatment of cardiovascular diseases. However, more comprehensive and long-term studies are needed to confirm this effect and transfer it to clinical applications.

Hypoxia can adversely affect multiple organ systems. This study investigated the impact of intermittent hypoxia on serotonin levels and depression-like behaviors across distinct neuroanatomical regions. Sixteen adult female Wistar albino rats were divided into two groups: control (n = 8) and hypoxia (n = 8). The hypoxia group was exposed to a simulated altitude of 3000 for 5 h daily over 14 days. Behavioral assessments included locomotor activity (open field test) and depression-like behaviors (forced swimming test). Serotonin levels were quantified via ELISA in the prefrontal cortex, striatum, thalamus, hypothalamus, hippocampus, and serum. Intermittent hypoxia did not alter locomotor activity (p > 0.05) but significantly increased depression-like behavior (p < 0.05), accompanied by a pronounced reduction in swimming behavior (p < 0.0001), a marker associated with serotonergic function. Serotonin levels were significantly reduced in the prefrontal cortex (p < 0.005) and striatum (p < 0.05), while no changes were observed in other regions or serum (p > 0.05). These findings demonstrate that intermittent hypoxia induces depression-like behaviors and region-specific serotonin depletion, particularly in the prefrontal cortex and striatum. This underscores the need to evaluate hypoxia-related brain health implications in conditions such as sleep apnea and acute mountain sickness.

Kisspeptin–1 (KISS–1) and Spexin (SPX) are neuropeptides that play crucial roles in metabolism and sexual function, with their expression levels in tissues potentially influenced by antioxidant treatments. This study aimed to investigate the effects of cortexin treatment against ischemia–reperfusion injury (I/R) resulting from testicular torsion on KISS–1 and SPX levels in testicular tissues. Twenty–eight male Sprague–Dawley, rats, aged 8–10 weeks, were divided into four equal groups: control, torsion, torsion/ detorsion, and torsion/detorsion+cortexin. At the conclusion of the experiment, histopathological and immunohistochemical analyses were performed to assess the expressions of KISS–1, SPX, tumor necrosis factor–alpha (TNF–α), and Caspase–3 in the testicular tissues. For biochemical analyses, total antioxidant status (TAS) and total oxidant status (TOS) levels were measured in serum samples using the ELISA method, while malondialdehyde (MDA) levels were assessed spectrophotometrically in testicular tissues. The results showed that compared to the control group, the torsion and torsion/detorsion groups exhibited significant histopathological damage, along with increased levels of MDA, TOS, Caspase–3, and TNF–α, and decreased levels of TAS, KISS–1, and SPX in the testicular tissues. Conversely, in the torsion+detorsion+cortexin group, which received treatment for reperfusion injury, there was a notable reduction in tissue damage, with decreased levels of MDA, TOS, caspase–3, and TNF–α, alongside increased levels of TAS, KISS, and SPX. Cortexin decreases testicular damage by reducing oxidative stress, increases spermatogenesis by improving seminiferous tubule and germinal epithelial thickness, and regulates KISS–1 and SPX expression, which have effects on the reproductive system.

Artemin is a neurotrophic factor that belongs to the four-member family of Glial-derived growth factors. This study aims to investigate changes in artemin correlated with anxiety and depression-like behaviors in a neuroinflammation rodent model. In adult male Wistar rats, neuroinflammation was established through administration of 2 mg/kg LPS. Anxiety-like behaviors and locomotor activity were evaluated by the open field test. The sucrose preference test and the splash test analyzed depression-like behaviors. Tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and artemin levels were measured in the prefrontal cortex, striatum, and serum. In the neuroinflammation group, rearing, total distance traveled, time spent in the central region, and sucrose solution consumption decreased in the open-field test (p < 0.0001). Grooming time and frequency were shortened, and grooming latency was prolonged in the neuroinflammation group (p < 0.0001). TNF-α was significantly increased in the prefrontal cortex (p < 0.05) and striatum (p < 0.01). lL-1β did not change between groups (p > 0.05). Artemin levels decreased in the prefrontal cortex and striatum (p < 0.05). No difference was observed in serum artemin levels; however, artemin levels of brain regions were higher than those in the serum. An increase in anxiety–depression-like behaviors has accompanied decreased levels of artemin in the brain. Artemin may be a target molecule in psychiatric disorders. Further studies are needed to examine the role of artemin in neuropsychiatric disorders.