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

Patients undergoing thoracic surgery or intensive care are frequently exposed to high-voltage electric fields generated by medical devices; however, the duration-dependent effects of such exposure on lung tissue remain unclear. This study aimed to investigate the histopathological and immunoinflammatory effects of exposure to a uniform 10 kV/m electric field for varying durations using a rat model. Thirty-five adult female Wistar rats were randomly assigned to five groups (n = 7): control, and 1, 5, 15, and 30 min exposure groups. Lung tissues were analyzed histologically with hematoxylin and eosin staining, and the immunohistochemical expression of IL-1β, RANKL, and TNF-α was semi-quantitatively assessed. Histopathological examination revealed a duration-dependent increase in lung injury, with the 30 min group showing marked epithelial loss, mononuclear infiltration, edema, and vascular congestion (p < 0.001). The expression of IL-1β, RANKL, and TNF-α remained minimal in the 1–15 min groups but was significantly elevated in the 30 min group (p < 0.001). These findings suggest that prolonged exposure to high-voltage electric fields induces substantial pulmonary inflammation and tissue damage, indicating the presence of a threshold beyond which inflammatory pathways are abruptly activated. These results highlight the importance of establishing safety guidelines for electric field exposure in clinical settings.

Surgical intervention is often an inevitable process in individuals’ lives and constitutes a significant source of stress not only physically but also psychologically. The fear and anxiety associated with surgery typically begin in the preoperative period, extend through the intraoperative phase, and may persist even after discharge. This situation directly affects patients’ adaptation to the surgical process and the speed of postoperative recovery, thereby significantly influencing both individuals’ quality of life and the overall effectiveness of healthcare services. This cross-sectional and analytical study was conducted with 100 patients aged 18 years and older who had no communication problems and underwent elective surgery in the department of thoracic surgery. Participants completed a questionnaire consisting of a sociodemographic data form, the Surgical Fear Questionnaire (SFQ), and the Post-Discharge Recovery Scale (PDRS). Descriptive statistics were presented using frequencies, means, standard deviations, and minimum and maximum values. For variables with normal distribution, the independent samples t-test and Pearson correlation test were used for analysis. A p-value of <0.05 was considered statistically significant. Among the participants, 73.0% were male, 50.0% were primary school graduates, and 76.0% were married. The mean post-discharge recovery score of the study group was 55.4±14.5. Participants who were married, had no chronic illness, had a spouse as a caregiver, had two or fewer previous hospitalizations, and had undergone one or fewer previous surgeries had significantly higher post-discharge recovery scores (p=0.033, p=0.047, p=0.033, p=0.045, and p=0.008, respectively). Post-discharge recovery was moderately and negatively correlated with surgical fear (r=-0.400, p=0.034). In this study, the relationship between preoperative surgical fear levels and post-discharge recovery was evaluated, and a significant negative correlation was identified. The findings are consistent with previously reported results in the literature, supporting the notion that surgical fear may adversely affect the recovery process through both physiological and psychological mechanisms. According to the study results, patients who were married and received postoperative care from their spouses had higher levels of recovery. This suggests that social support—particularly spousal support—serves as an important protective factor during the surgical process. Additionally, individuals with chronic illnesses were found to have significantly lower levels of post-discharge recovery. This may be explained by the physiological burden of chronic diseases, their impact on the immune system, and challenges in treatment adherence. In summary, the study highlights that reducing surgical fear, strengthening social support systems, and improving chronic disease management may contribute positively to the postoperative recovery process.

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.