Introduction Necrotizing enterocolitis (NEC) is one of the major health problems of newborn period. To date, a large amount of chemicals have been tested for NEC and some showed limited beneficial effects. The research for better results still continues. This study aims to investigate the effects of quercetin (QE) on NEC treatment in rats. Methods Newborn rats were divided into control, NEC, and NEC + QE groups. In NEC and NEC + QE groups, experimental NEC was induced. NEC + QE group animals were also given QE. Weight changes of the animals were recorded, and serum total antioxidant status (TAS), total oxidant status (TOS), malondialdehyde (MDA), and glutathione (GSH) levels were measured. Histologic evaluation of the distal ileum and the terminal deoxynucleotidyl transferase dUTP nick end labeling staining were performed. Results A significant increase in the TAS levels was observed in NEC + QE group. Only NEC group exhibited significantly higher TOS and MDA levels and lower GSH levels. Rats in the NEC + QE group had better histopathology and less apoptosis than NEC group. Conclusion QE is effective in enhancing antioxidant defense mechanism, limiting oxidative stress, reducing intestinal damage, and preventing NEC development.

Background/aim: Acute lung injury (ALI) is a major cause of death in the intensive care unit. Lipopolysaccharide (LPS) induced lung injury is the most widely used experimental ALI model and provides opportunities for new targeting therapy. In this study, we investigated the effects of tocilizumab, adalimumab, and methylprednisolone in LPS-induced acute lung injury. Materials and methods: Lung injury was established by intratracheal instillation of LPS. The rats were randomly divided into six groups: LPS, control, and treatment groups (adalimumab, tocilizumab, methylprednisolone, adalimumab + tocilizumab). Bronchoalveolar lavage (BAL) and lung tissues were collected at 48 h and 96 h following LPS administration from each group. For histological analysis, hematoxylin-eosin (H&E) staining was performed. The sections were obtained for immunohistochemical analysis. IL-6 and TNF-alpha immunoreactivity were measured. Results: Intratracheal LPS application resulted in inflammatory cell infiltration of interstitial and alveolar spaces and thickening of the alveolar wall. All treatment groups showed significantly amelioration compared to LPS at 48 h. Interestingly, adalimumab and adalimumab + tocilizumab groups showed a significant amelioration of the lung histoarchitecture, compared to the prednisolone group at 96 h (p = 0.028, p = 0.025, respectively). Compared to the control group, LPS stimulation resulted in a significant increase in IL-6 and TNF-alpha immunoreactivity (p < 0.001). IL-6 and TNF-alpha expression were markedly reduced in all treatment groups at 48 h but the reduction was greater in the adalimumab and tocilizumab group than in the steroid. Administration with adalimumab and/or tocilizumab effectively decreased expression of TNF-alpha (p = 0.001) and IL-6 (p < 0.001) at 96 h, but prednisolone did not exert an effective decrease (p > 0.05). Conclusion: Adalimumab and/or tocilizumab significantly reduce the release of proinflammatory cytokines and improve the tissue inflammation in the experimental model of ALI. Our results suggest that adalimumab and/or tocilizumab have a more potent antiinflammatory effect on lung injury than the steroid.

Monensin is an ionophore antibiotic that inhibits the growth of cancer cells. The aim of this study was to investigate the apoptosis‐mediated anticarcinogenic effects of monensin in SH‐SY5Y neuroblastoma cells. The effects of monensin on cell viability, invasion, migration, and colony formation were determined by XTT, matrigel‐chamber, wound healing, and colony formation tests, respectively. The effects of monensin on apoptosis were determined by real‐time polymerase chain reaction, TUNEL, Western blot, and Annexin V assay. We have shown that monensin suppresses neuroblastoma cell viability, invasion, migration, and colony formation. Moreover, we reported that monensin inhibits cell viability by triggering apoptosis of neuroblastoma cells. Monensin caused apoptosis by increasing caspase‐3, 7, 8, and 9 expressions and decreasing Bax and Bcl‐2 expressions in neuroblastoma cells. In Annexin V results, the rates of apoptotic cells were found to be 9.66 ± 0.01% (p < 0.001), 29.28 ± 0.88% (p < 0.01), and 62.55 ± 2.36% (p < 0.01) in the 8, 16, and 32 μM monensin groups, respectively. In TUNEL results, these values were, respectively; 35 ± 2% (p < 0.001), 34 ± 0.57% (p < 0.001), and 75 ± 2.51% (p < 0.001). Our results suggest that monensin may be a safe and effective therapeutic candidate for treating pediatric neuroblastoma.

Neuroblastoma is the most common pediatric solid tumor originating from the neural crest. New treatment options are needed to improve treatment outcomes and the survival of patients with neuroblastoma. Monensin is an ionophore antibiotic with antiparasitic, antibacterial, and anticancer properties isolated from Streptomyces cinnamonensis. The aim of this study was to investigate the therapeutic effects of single and combined monensin and rapamycin treatments on mTOR (mammalian target of rapamycin) signaling pathway-mediated apoptosis and tumor growth in an SH-SY5Y neuroblastoma cell xenograft model. Control, monensin, rapamycin, and monensin + rapamycin groups were formed in the xenograft neuroblastoma model obtained from CD1 nude mice, and tumor volumes and animal weights were recorded throughout the treatment. In xenograft neuroblastoma tumor tissues, apoptosis was determined by TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling) and cleaved-caspase 3 immunohistochemistry, and PI3K (phosphoinositide-3-kinase)/AKT/mTOR expression was determined by the immunohistochemistry and immunofluorescence methods. The combination of monensin and rapamycin was to reduce the growth of xenograft neuroblastoma tumor tissues, trigger apoptosis, and suppress the expression of PI3K/AKT/mTOR. A significant increase in apoptotic cell rate was demonstrated in the combination group, supported by cleaved-caspase 3 immunohistochemistry results. In addition, it was reported that the combination treatment regime triggered apoptosis by reducing the expression of phosphorylated PI3K/AKT/mTOR. Our preclinical results may be a precursor to develop new therapeutic approaches to treat neuroblastoma.