Purpose: This study aimed to investigate the hypothesis that cannabidiol (CBD), with known anti-inflammatory and anti-apoptotic effects, would reduce the severity of acute lung injury in pulmonary contusion following blunt chest trauma. Methods: Forty male Wistar Albino rats were randomly divided into four groups, each consisting of 10 rats: Sham, Trauma, Trauma + CBD, and CBD. The rats were treated with a single dose of 5 mg/kg CBD intraperitoneally 30 min before trauma. Then, the trauma were exposed to a weight of 200 g and a height of 1 m. After sacrifice, the lung tissues were removed for histopathological, immunohistochemical, biochemical, and genetic analyses. Results: Pulmonary injury of trauma group led to increases in tumor necrosis factor α, caspase-3, caspase-9, Bcl-2-associated X protein expressions, total oxidant status, oxidative stress index levels, and decreases in B-cell lymphoma expression and total antioxidant levels. Additionally, inflammatory cell infiltration, damage-related emphysema, pronounced hyperemia, and increased septal tissue thickness were observed histopathologically. CBD treatment ameliorated all these findings. Conclusion: CBD reduces lung damage in lung contusions caused by blunt chest trauma through its anti-inflammatory and antiapoptotic effects. More detailed studies investigating other important intracellular pathways are needed.

Radiotherapy (RAD) is a common cancer treatment method, but it can have unintended lung side effects. L-carnitine (LCAR) is an amino acid with antioxidant and anti-inflammatory properties. This study aims to demonstrate the effects of LCAR against radiation-induced acute lung injury and to elucidate its possible protective molecular mechanisms. A total of 32 Wistar albino rats were separated into four groups: control, RAD (10 Gy once on 1st day), RAD + LCAR (intraperitoneally, 200 mg/kg/d, for 10 days), and LCAR. At the end of the experiment, the rats were euthanized, and the lung tissues were collected for histopathological, immunohistochemical, biochemical, and genetic analysis. Emphysema, pronounced hyperemia, increased total oxidant status, and increased caspase-3 and TNF-α immunostainings were all seen in the lung tissues of the RAD group. LCAR treatment reduced these negative effects. In addition, AMPK and SIRT1 gene expressions increased in the RAD + LCAR group compared to the RAD group, while TGF-1ß gene expression decreased. While RAD caused major damage to the lungs of rats, LCAR application reduced this damage through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms. Specifically, LCAR reduced fibrosis while attenuating RAD-induced inflammation and oxidative stress via the AMPK/SIRT1/TGF-1ß pathway. Therefore, LCAR can be considered a supplement to reduce complications associated with RAD. Graphical abstract

Thoracic trauma (TRA) triggers inflammation, oxidative stress, apoptosis, and receptor-interacting protein kinase-1 (RIPK1)/receptor-interacting protein kinase-3 (RIPK3)/mixed lineage kinase domain-like protein (MLKL)-mediated necroptosis, all of which contribute to contusion-related lung injury. Dexpanthenol (DEX) has anti-inflammatory and cytoprotective properties, yet its antinecroptotic potential in trauma-induced lung injury has not been fully elucidated. Forty male rats were randomly assigned to SHAM, TRA, TRA + DEX, and DEX groups. A 200 g cylindrical weight was dropped from a height of 100 cm, inducing TRA. Lung injury was assessed by histopathology, immunohistochemical staining for tumor necrosis factor-alpha (TNF-α) and caspase-3 (Cas-3), biochemical measurements of total oxidant status (TOS)/total antioxidant status (TAS)/oxidative stress index (OSI), and as well as mRNA expression levels of RIPK1/RIPK3/MLKL. TRA markedly increased hyperemia, edema, inflammatory infiltration, TNF-α, Cas-3, OSI, and RIPK1/RIPK3/MLKL expression (p < 0.001 for all). DEX significantly attenuated lung injury by reducing inflammatory scores, decreasing TNF-α and Cas-3 immunoreactivity, lowering OSI (p < 0.01), and suppressing RIPK1/RIPK3/MLKL gene activation (p < 0.001 for all). Although DEX did not fully normalize isolated TOS and TAS values, the OSI reduction indicates a net shift toward antioxidant balance. DEX mitigates trauma-induced lung injury through anti-inflammatory, antiapoptotic, antioxidant, and antinecroptotic mechanisms. These findings are preliminary, and dose-dependent effects and long-term outcomes should be clarified in future studies before clinical translation.

Background: Malignant pleural effusion is defined as the presence of malignant cells in pleural effusion (PE) or biopsy specimens and occurs in 15% of all cancer patients. The most common cause is lung cancer in men and breast cancer in women. The reason for hospital admission is usually shortness of breath. The main goal of treatment is to relieve symptoms and prevent recurrence. PET/CT is an imaging system that combines the metabolic properties of PET with the morphologic properties of computed tomography. The patient can be managed more rapidly if malignant effusion can be detected on PET/CT. In this study, we aimed to predict the diagnostic impact of metabolic uptake of fluid in patients with malignant pleural effusion. Methods: In our study, we aimed to find the contribution of PET/CT to the diagnosis of malignant pleural effusion by examining patients between 18 and 90 years of age who had malignancy as a result of pleural cytology and who underwent PET/CT with a primary diagnosis of malignancy. 26 patients were evaluated. The values analyzed were; the presence of PE FDG uptake, the presence of single or double uptake in PE, the presence of multiple pulmonary nodules, the presence of pleural thickness (PT) increase, PK diameter, the presence of FDG uptake in PK, primary pathology being lung or other organ, PE Standardized Uptake Value (SUV) max, PE SUVmax/ Med SUVmax, PE SUVmax/ Liver SUVmax, PE SUVmax/ primary tumor SUVmax, primary tumor SUV values. Results: 6 of 26 patients had bilateral effusions and 12 patients had FDG uptake. 5 patients had pleural thickening and 4 of them had pleural uptake. In the ROC analysis, PE SUVmax, PE SUV / Med SUV, PE SUV / Liver SUV, and PE SUV / Primary tm SUV values were found to be significant in terms of predicting PE FDG uptake, while PT diameter was not significant. Conclusions: Patients with malignant pleural effusion have a short life expectancy. Diagnosis and treatment management of patients should be performed effectively and rapidly. PET/CT can be used as a noninvasive diagnostic method for this purpose. Therefore, if further studies are performed, PET/CT in the diagnosis of MPE will contribute to patient management.

This study aimed to investigate the vascular effects of a radiofrequency electromagnetic field (RF‐EMF) applied in the lung ischemia and reperfusion (IR) model on the hypoxia‐inducible factor 1 alpha (Hif‐1α)/endothelial nitric oxide synthase (eNOS) pathway and B cell lymphoma 2 (BCL2)/BCL‐2 associated X protein (BAX) signaling. Forty male Wistar rats were randomly divided into four groups, each consisting of 10 rats: Sham, IR, IR + RF‐EMF, and RF‐EMF. IR was applied to rats by 60 min of clamping hilus of left lungs and 60 min of reperfusion. Rats were kept in the RF‐EMF unit for 60 min with or without activation. After sacrification, lung tissues were excised for histopathological, immunohistochemical, biochemical, and genetic analyses. IR injury led to increased damage‐related emphysematous findings, significant hyperemia, and increased septal tissue thickness, as observed histopathologically, and immunoexpression levels of tumor necrosis factor‐alpha and caspase‐3. In addition, it was noted that the biochemical parameters total oxidant status, oxidative stress index, and genetic parameters Hif 1 α, eNOS, BAX increased, and BCL2 decreased due to IR damage. In the IR‐RF‐EMF group, improvement has been detected in all parameters. RF‐EMF applied in the IR model exerts antioxidant, antiapoptotic, and anti‐inflammatory effects on lung tissue damage through the Hif‐1α/eNOS pathway and BCL‐2/BAX signaling. The use of RF‐EMF in IR damage is promising, as models that examine the long‐term effects of RF‐EMF at different frequencies.

Aim: Radiotherapy (RT) is a cornerstone treatment for cancers of the esophagus, lung, head and neck, and mediastinum. However, its efficacy is often limited by serious side effects, such as radiation-induced esophagitis, which can compromise treatment continuity and patient quality of life. This study aimed to evaluate the potential protective role of Apigenin, a natural flavonoid with demonstrated anti-inflammatory and antioxidant properties, against RT-induced esophageal injury in an experimental rat model. Material and Methods: A total of 40 rats were divided into four groups: RT, RT+Apigenin+Dimethyl sulfoxide (DMSO), RT+DMSO, and Apigenin+DMSO. A single 16 Gy dose of RT was given to the cervical area in the appropriate groups. Histopathological examination and tumor necrosis factor-alfa (TNF-α) expression analysis were used to evaluate tissue damage and inflammation. Results: Histopathological examination revealed marked hyperemia, microhemorrhages, erosions, and mild inflammatory response in the esophageal tissue of the RT group (p<0.001). In contrast, the RT+Apigenin+DMSO group exhibited a significant reduction in these histopathological findings (p<0.001). Immunohistochemical analysis revealed a significant increase in TNF-α expression in the esophageal epithelial cells of the RT group (p<0.001). In the RT+Apigenin+DMSO group, a marked decrease in TNF-α levels was observed (p<0.001). Conclusion: This study suggests that Apigenin may serve as a potential radioprotective agent against RT-induced esophageal toxicity, with histopathological and immunohistochemical findings supporting its protective effects. Further preclinical and controlled clinical studies are needed to confirm its translational applicability.