Acute carbon monoxide (CO) poisoning may cause liver damage and liver dysfunction. Therefore, in this study, we aimed to compare the efficiency of normobaric (NBO) and high flow nasal cannula oxygen (HFNCO) treatments on liver injury. For that purpose, twenty-eight male Wistar albino rats were divided into four groups (Control, CO, CO + NBO, CO + HFNCO). The control group was allowed to breath room air for 30 min. Acute CO poisoning in CO, CO + NBO, CO + HFNCO was induced by CO exposure for 30 min. Thereafter, NBO group received 100% normobaric oxygen with reservoir mask for 30 min. HFNCO group received high-flow oxygen through nasal cannula for 30 min. At the end of the experiment, all animals were sacrificed by cardiac puncture under anesthasia. Serum liver function tests were measured. Liver tissue TAS, TOS and OSI levels, tissue histomorphology and immunoexpression levels of Bax, Caspase 3, TNF-α, IL-1β, and NF-κB were also examined. Our observations indicated that acute CO poisoning caused significant increases in blood COHb, serum AST, ALT, ALP, total protein, albumin, globulin levels but a decrease in albumin to globulin ratio (all, p < 0.05). Furthermore, acute CO poisoning significantly increased the OSI value, and the immunoexpresssion of Bax, Caspase 3, TNF-α, IL-1β, and NF-κB in liver tissue (all, p < 0.05). These pathological changes in serum and liver tissue were alleviated through both of the treatment methods. In conclussion, both the NBO and HFNCO treatments were beneficial to alleviate the acute CO poisoning associated with liver injury and dysfunction.

Background: Chemotherapy drugs may lead to hepatic injury, which is considered one of the limitations of these drugs.Objectives: The aim of this study was to evaluate the effect of quercetin (QUE) on M1/M2 macrophage polarization and hepatoprotective effect in cyclophosphamide (CTX)‐induced liver toxicity.Methods: Twenty‐four mice were divided into four groups (Control, QUE, CTX, CTX + QUE). The CTX and CTX + QUE groups received 200 mg/kg CTX. The animals in the QUE and CTX + QUE groups received 50 mg/kg QUE. All animals were sacrificed, and serum and liver samples were used for laboratory analyses.Results: Examinations indicated that CTX exposure led to disruption of liver functions and morphological degenerations. Tissue pro‐apoptotic Bax and caspase 3, pro‐inflammatory TNF‐α and IL‐1β, transcription factor NF‐κB, and M1 macrophage polarization marker CD86 were upregulated significant (p < 0.05) in this group. In addition, CTX exposure led to significantly (p < 0.05) upregulation of the Bax/Bcl‐2 mRNA ratio and DNA fragmentations. The PCNA‐positive hepatic cell ratio and anti‐apoptotic Bcl‐2 expression are remarkably suppressed (p < 0.05). Immunohistochemical analyses are also indicated that M2 macrophage polarization marker CD163 is slightly but remarkably (p < 0.05) downregulated in the CTX group compared to the Control and QUE groups. The morphological and biochemical disruptions were alleviated in QUE‐treated animals in the CTX + QUE group. Liver function test results, apoptosis, inflammatory, transcription factor NF‐κB, regeneration/proliferation, and apoptotic index results in this group were similar (p > 0.05) to the control and QUE groups. The M1 cell surface marker expression of CD86 is significantly (p < 0.05) downregulated, and M2 macrophage polarization marker expression of CD163 is upregulated significantly (p < 0.05) compared to the CTX group.Conclusions: This study indicates that QUE has the potential to downregulate CTX‐induced hepatic injury and regulate M1/M2 macrophage polarization to the M2 side, which indirectly demonstrates activation of anti‐inflammatory signalling and tissue repair.

Rationale: Adolescent depression is often linked to biological changes associated with stress. However, new approaches and treatment strategies for early intervention and prevention of depression in children and adolescents are still limited. Ashwagandha is an Ayurvedic herb widely used in the management of anxiety and stress. However, there is no information in the current literature on its potential effect on adolescent depression. Objectives: This study aimed to investigate the effects of depression on proapoptotic proteins and neuroinflammation and the antidepressant effect of Ashwagandha on depression-like symptoms in adolescent rats exposed to the Chronic Unpredictable Mild Stress (CUMS) model. Methods: In the study, CUMS model was used to induce depression in adolescent rats. Rats were treated with Ashwagandha or Sertraline. To evaluate the antidepressant effects, behavioral tests as well as biochemical and histological analyses were performed. Forced Swim Test (FST), Sucrose Test and Elevated Plus Maze Test were performed as behavioral tests. Brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) were measured by the ELISA method in the fronto-parietal cortex. Proapoptotic proteins (Bax and Caspase-3) and inflammatory markers (TNF-α and IL-1β), as well as glial fibrillary acidic protein (GFAP), were evaluated immunohistochemically in the fronto-parietal cortex. Results: Proapoptotic proteins (Bax and Caspase-3) and inflammatory markers (TNF-α and IL-1β) were increased in the CUMS group. BDNF and GFAP levels were decreased. Ashwagandha treatment was more effective than Sertraline in reducing the levels of these proteins and markers. Additionally, Ashwagandha prevented weight loss. Conclusions: Ashwagandha showed antidepressant-like effects in adolescent rats, reducing apoptosis, inflammation, and neuroinflammation, suggesting potential for treating adolescent depression. Graphical

Background/Objectives: Cerebral palsy (CP) is a motor disorder resulting from brain damage that is common in childhood. Iron is vital for the body’s basic functions. Iron metabolism disorders and inflammation contribute to the neurological complications seen in CP. The purpose of this research was to ascertain the association and correlation between markers of inflammation and iron metabolism in children with CP. Methods: A total of 181 children diagnosed with CP and 111 typically developing children were retrospectively included in the study. Demographic data, blood parameters, C-reactive protein, iron, total iron binding capacity, and inflammation markers were evaluated. Results: C-reactive protein (CRP), neutrophil-to-lymphocyte ratio (NLR) and systemic immuno-inflammatory index (SII) levels of CP children were found to be statistically significantly higher than those of control group children (p < 0.05). Iron (Fe) and ferritin levels were lower in the CP group, while total iron binding capacity (TIBC) was higher. Spearman correlation analysis showed significant correlations between iron, ferritin and TIBC and SII. Conclusions: Iron deficiency and chronic inflammation are associated with the pathophysiology of CP in patients with CP, and therefore it is important to monitor markers of iron metabolism and inflammation in these patients.

In order to investigate the effects of acute CO poisoning and subsequent oxygen therapy on cardiac necrosis in rats, with a specific focus on adiponectin levels, twenty–one male Wistar albino rats were divided into three groups (Control, CO, CO+O2). The Control group was placed in a container and exposed to room air for 30 min. Acute CO poisoning was induced in the CO group and CO+O2 group by exposing the rats to CO gas for 30 min. Following CO exposure, the CO+O2 group received oxygen therapy for 30 min, while the CO group did not receive any additional intervention. The animals were euthanized by cardiac puncture under anesthesia, following the approved ethical procedures. Carboxyhemoglobin (COHb), serum levels of creatine kinase (CK), creatine kinase myocardial band (CK–MB), C–reactive protein (CRP) and lactate dehydrogenase (LDH), as well as cardiac and serum adiponectin levels were measured. CO poisoning caused necrosis in cardiac tissue however, oxygen therapy alleviated the negative effect of CO on cardiac injury. COHb and LDH levels in CO group were increased, whereas both cardiac and serum adiponectin levels were decreased (all, P0.05). Oxygen therapy decreased COHb, but increased both cardiac and serum adiponectin levels (all, P<0.05). Adiponectin and LDH may serve as potential biomarkers for early diagnosis of cardiac necrosis caused by acute CO poisoning. The assessment or quantification of adiponectin can also be useful for the early prognosis of cardiac necrosis after oxygen therapy.