Lipopolysaccharide (Lps) is an essential component responsible for the virulence of gram-negative bacteria. Lps can cause damage to many organs, including the heart, kidneys, and lungs. Dexpanthenol (Dex) is an agent that exhibits anti-oxidative and anti-inflammatory effects and stimulates epithelialization. In this study, we aimed to investigate the effects of Dex on Lps-induced cardiovascular toxicity. Rats were divided into four groups: control, Lps (5 mg/kg, intraperitoneal), Dex (500 mg/kg, intraperitoneal), and Lps + Dex. The control group received saline intraperitoneally (i.p.) once daily for three days. The Lps group received saline i.p. once daily for three days and a single dose of Lps i.p. was administered on the third day. The Dex group received Dex i.p. once daily for three days and saline on the third day. The Lps + Dex group received Dex i.p. once daily for three days and a single dose of Lps i.p. on the third day. Heart and aortic tissues were taken for biochemical, histopathological, immunohistochemical, and genetic analysis. Lps injection caused histopathological changes in both heart and aortic tissues and significantly increased total oxidant status and oxidative stress index levels. Interleukin-6, and Tumor necrosis factor-α mRNA expressions were significantly altered in heart and aorta, likely do to the anti-inflammatory and antioxidative effects of Dex. Furthermore, Dex affected Caspase-3 and Hypoxia-inducible factor 1-α staining patterns. Our results show that Dex treatment has a protective effect on Lps-induced cardiac and endothelial damage in rats by reducing inflammation, oxidative stress, and apoptosis.

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.

There has been scarce research on the potential neuroprotective effects of remifentanil (REM) in septic individuals. We aimed to investigate the role and underlying mechanism of REM in LPS‐induced neuroinflammation. Thirty‐two rats were randomly divided to control, lipopolysaccharide (LPS), LPS + REM, and REM groups. Depending on the group, 4 h after intraperitoneal administration of LPS or saline, REM or saline was infused intravenously for 40 min. Following the sacrification, blood samples and brain tissues were collected for analysis. Brain tissues (prefrontal cortex, cerebellum, and hippocampus) were stained with hematoxylin and eosin, caspase‐3 (Cas‐3), and tumor necrosis factor alpha (TNF‐α). Quantitative reverse transcription‐polymerase chain reaction analysis was used to detect claudin‐5 (CLDN5), zonula occludens‐1 (ZO‐1), phosphatidylinositol 3‐kinase (PI3K), serine–threonine protein kinase (AKT), and hypoxia‐inducible factor 1 alpha (HIF‐1α) gene expression levels. Histopathologic and immunohistochemical analyses showed that REM treatment improved LPS‐induced histological changes. REM does not reduce TOS and OSI levels or increase TAS levels, suggesting that it is ineffective through oxidative stress. LPS‐induced changes in gene expression levels (PI3K, AKT, HIF‐1α, and CLDN5) were also reversed by REM. REM was found to prevent neuroinflammation, and apoptosis by restoring blood–brain barrier, and regulating the PI3K/AKT/HIF‐1α pathway. These findings suggest that REM is protective against neuroinflammation.

Background: To reduce maternal-fetal morbidity and mortality, it is becoming increasingly important for anesthetists to understand and implement enhanced recovery after surgery (ERAS) cesarean delivery guidelines. Our aim was to reveal the knowledge of anesthesia assistants in Turkey about ERAS during cesarean delivery and to increase their awareness of ERAS. Methods: This descriptive study was conducted in the city of Isparta, Turkey in 2023. The survey, which was approved by the ethics committee, was distributed to participants across Turkey via e-mail and online messages. The survey comprises of a total of 42 questions evaluating perioperative ERAS recommendations. Results: Of the 404 participants in our survey, 59.9% were associated with university hospitals and 65.8% had completed three or more years of education. A total of 87.9% of the participants were familiar with ERAS; however, only 42.8% had received ERAS training. Although 93.8% of the participants’ institutions performed a cesarean delivery, ERAS recommendations were only implemented at a rate of 48%. This may be due to the absence of an ERAS team, which was identified in our survey at a high rate of 66.6%. Conclusion: Awareness about ERAS was high among the participants, but the implementation rates of some recommendations were low. The reason for this may be the inability to form a multidisciplinary team and inadequate training of participants. For this purpose, we recommend the formation of a multidisciplinary team for ERAS protocol implementation and increased participant training opportunities.

Acute lung injury secondary to sepsis remains a major problem in critical patients. Lipopolysaccharide (LPS)-induced lung injury is characterized by inflammatory infiltration, oxidative stress, and extensive apoptosis, particularly via the mitochondrial pathway. Omega-3 (OM3) polyunsaturated fatty acids have been proposed as promising modulators of inflammation and oxidative damage. However, their role in regulating mitochondria-mediated apoptosis in sepsis remains underexplored. Thirty-two female Wistar albino rats were randomized into four groups: Control, LPS (5 mg/kg, i.p. 3th), LPS-OM3 (400 mg/kg/day, i.p., 3 day), and OM3 only. After 72 h, lung tissues were collected for histopathological scoring, immunohistochemistry as tumor necrosis factor-alpha (TNF-α), heat shock protein (HSP70), caspase-3 (Cas-3); biochemical analyses as total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI) and qRT-PCR for mitochondrial apoptosis markers B cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), cytochrome-c (Cyt-c) and Cas-9. LPS induced ALI characterized by bronchiolar epithelial degeneration, alveolar hemorrhage, inflammation, and hyaline membrane formation. Biochemically, TOS and OSI levels were significantly elevated, while TAS remained unchanged. Immunohistochemical and genetic analysis showed marked upregulation of TNF-α, HSP70, and Cas-3 Bax, Cyt-c, and Casp-9 expression and decreased Bcl-2 expression in the LPS group. OM3 supplementation significantly attenuated histopathological damage, reduced oxidative stress markers, suppressed immunopositivity of proinflammatory and apoptotic proteins, and favorably modulated the apoptosis-related gene expressions. OM3 fatty acids exert a potent protective effect against LPS-induced ALI by suppressing mitochondrial apoptosis, reducing oxidative stress, and modulating the inflammatory response. These findings highlight the therapeutic potential of OM3 in mitigating sepsis-associated pulmonary damage through mitochondrial preservation.