Background/Objectives: Sepsis-associated acute kidney injury caused by lipopolysaccharide (LPS) is related to hypoxia, amplification of the inflammatory response, oxidative stress, mitochondrial dysfunction, and apoptosis. This study aims to explore the protective effects of a radiofrequency electromagnetic field (RF-EMF) and a pulsed magnetic field (PMF) on acute kidney injury in rats. Materials and methods: Forty female Wistar albino rats were randomly divided into five groups (each containing eight rats): control, LPS, RF-EMF, PMF, and RF-EMF + PMF groups. Six hours after LPS application, blood and tissues were removed for histopathological, immunohistochemical, biochemical, and genetic analysis. Results: Histopathological findings, caspase-3, inducible nitric oxide synthase and tumor necrosis factor-alpha immunoexpressions, total oxidant status and oxidative stress index levels, and interleukin-6, hypoxia-inducible factor alpha, Bcl-2-associated X protein, and caspase 9 gene expression in kidney tissue and blood urine nitrogen and creatinine levels in blood were increased, whereas endothelial nitric oxide synthase and B-cell lymphoma 2 gene expression were decreased in the LPS groups. Both RF-EMF and PMF reversed all these findings and recovered renal tissues. Conclusions: Noninvasive, nontoxic, low-cost PMF and RF-EMF, both single and combined, have been demonstrated to have renoprotective anti-inflammatory, antioxidant, and antiapoptotic effects.

Sepsis-induced acute kidney injury (AKI) is a major cause of mortality in critically ill patients. Inflammation, oxidative stress, and apoptosis are key contributors to sepsis-related renal damage. Dapagliflozin (DPG), an SGLT2 inhibitor, has demonstrated anti-inflammatory and nephroprotective effects. This study aimed to investigate the renoprotective effects of DPG in a lipopolysaccharide (LPS)-induced sepsis model, focusing on inflammation, oxidative stress, and apoptosis in the kidneys. Thirty-two male Wistar albino rats were divided into four equal groups: (1) Control group, which received saline for 5 days; (2) LPS group, which received oral saline for 5 days and a single intraperitoneal LPS injection (5 mg/kg on day 5); (3) LPS+DPG group, which received oral DPG (10 mg/kg/day) for 5 days and a single intraperitoneal LPS injection (5 mg/kg on day 5); (4) DPG group, which received oral DPG (10 mg/kg/day) for 5 days. At the end of the experiment, samples were collected for histopathological, immunohistochemical, biochemical, and genetic analyses. DPG significantly reduced serum urea and creatinine levels, indicating improved renal function. Histopathological analysis of the kidney tissues revealed reduced inflammation, hemorrhage, and necrosis in the LPS+DPG group compared to the LPS group. Also, DPG lowered the expression of pro-inflammatory markers (APAF-1, TNF-α, VCAM-1), reduced oxidative stress (decreased OSI), and downregulated NLRP3, caspase-1, IL-1β, and IL-18 gene expression. Prophylactic DPG administration exerts notable renoprotective effects in sepsis-induced AKI by mitigating inflammation, oxidative stress, and apoptosis. These findings highlight its potential as a preventive strategy, warranting further investigation in therapeutic contexts.

Sepsis and septic shock are clinical conditions with high mortality and an ever-increasing prevalence, and early diagnosis is of great importance in treating these diseases. Increase in serum Galectin-3 protein in septic patients is associated with increased inflammation, which in turn is associated with mortality. This study aimed to investigate the diagnostic importance of serum Galectin-3 levels and its relationship with in-hospital mortality in sepsis and septic shock patients.

Background and Objectives: Traumatic brain injury (TBI) triggers oxidative stress, mitochondrial dysfunction, and sterile inflammation. Amantadine (ATD), a weak NMDA receptor antagonist, has shown neuroprotective potential, but its mechanistic basis remains unclear. This study examined whether ATD treatment is associated with changes in molecular and histological markers related to the HIF-1α/BNIP3L/HMGB1-mediated hypoxia–mitophagy–inflammation response in a rat TBI model. Materials and Methods: Thirty-two Wistar rats were assigned to four groups: sham, trauma, trauma + ATD (1 day), and trauma + ATD (7 days). TBI was induced using the impact-acceleration model, and ATD (45 mg/kg, i.p.) was administered post-injury. Oxidative stress indices (TOS, TAS, OSI), histopathology, inflammatory/apoptotic markers (CRP, TNF-α, Caspase-3), and gene expression (HIF-1α, BNIP3L, HMGB1) were evaluated. Results: ATD improved oxidative balance and histopathological integrity while reducing TNF-α, CRP, and Caspase-3 immunoreactivity. qPCR analysis showed lower HIF-1α, BNIP3L, and HMGB1 expression in ATD-treated groups, which is consistent with attenuation of hypoxia-related, mitochondrial stress-associated, and damage-associated molecular pattern-associated signaling after injury. Conclusions: In this experimental model, amantadine ameliorated oxidative, inflammatory, and apoptotic markers and was associated with reduced expression of HIF-1α, BNIP3L, and HMGB1. These findings support a mechanistic correlation between ATD treatment and suppression of secondary injury signatures; however, causal pathway relationships and functional neurological outcomes were not assessed.

Early physiologic warning scores (EPWS) are used to detect clinical deterioration by monitoring vital signs and early warning signs. However, their role in the obstetric population, particularly during the preoperative period before cesarean delivery, remains underexplored. To evaluate the effectiveness of three maternal early physiologic warning systems—Modified Early Obstetric Warning Score (MEOWS), Maternal Early Warning Criteria (MEWC), and Maternal Early Warning Triggers (MEWT)—in predicting short-term maternal and neonatal outcomes in the parturient patients undergoing cesarean section. In this prospective observational study, 304 parturient patients scheduled for cesarean delivery at a tertiary care hospital were evaluated. Preoperative physiological data were used to calculate MEOWS, MEWC, and MEWT scores. Patients were classified into “high risk” (Group 1) or “no risk” (Group 2) categories based on predefined thresholds. Primary outcomes included intensive care unit (ICU) admission and neonatal APGAR scores. Secondary outcomes involved Aldrete scores, intraoperative hemodynamic parameters, and type of anesthesia. Patients identified as “high risk” by MEOWS had significantly lower neonatal APGAR and maternal Aldrete scores, along with higher systolic and diastolic blood pressures and heart rates (p < 0.05). MEOWS also more effectively predicted ICU admission compared to MEWC and MEWT (p < 0.05). No maternal deaths were recorded. Emergency procedures were more frequent in patients identified as “high risk” by MEWC and MEWT. MEOWS, MEWC, and MEWT scores can help identify preoperative high-risk patients who may require cesarean sections. MEOWS demonstrated superior sensitivity in predicting postoperative complications and ICU admission. Incorporating EPWS in the preoperative evaluation may improve maternal and neonatal outcomes.

Sepsis, a severe consequence of infection leading to organ failure, incites damage in frequently affected brain tissue through inflammation and oxidative stress. This study aimed to assess the effectiveness of amantadine, an N-methyl-D-aspartate (NMDA) receptor antagonist, in mitigating sepsis-induced brain damage. Thirty-two Wistar albino male rats were allocated into four groups: control, LPS (lipopolysaccharide 5 mg/kg, intraperitoneal, single-dose), LPS + amantadine, and amantadine alone. Six hours post-LPS administration, rats were euthanized under anesthesia. The neutrophilic infiltration and necrosis reaction were assessed in lung tissues through histopathological analysis, while expressions of interferon-alpha (IFN-α), caspase-3 (Cas-3), and Tumor necrosis factor-alpha (TNF-α) were examined using the immunohistochemical method. Levels of biochemical total anti-oxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) were evaluated via the ELISA method. IL-1β, Cas-1, NLRP3, and IL-18 were evaluated via real-time qPCR. The LPS group exhibited histopathologically significant hyperemia, increased septal tissue thickness, hemorrhage, and inflammatory cell infiltrates, and increased IFN-α, Cas-3, TNF-α immunohistochemical expressions, and IL-1 beta, IL-18, NLRP3, and Cas-1, gene expressions compared to the control group. All these findings were significantly reversed with amantadine treatment. The pathophysiology of brain damage due to systemic inflammation is complex. Our findings suggest that amantadine reduces neuronal injury in the brain by alleviating oxidative stress and inflammation. Notably, amantadine’s efficacy appears to extend beyond NMDA receptors, implicating involvement in alternative pathways, such as Cas-1 activation by the NLRP3 inflammasome.