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Purpose: The G-protein coated receptor (GPCR) family, including the Insulin-Like Peptide 3 (INSL3) receptor, is involved in the Nuclear Factor kappa B (NF-κB)-mediated pathway in inflammation. In this regard, it can be thought that INSL3 plays a role in inflammation via the NF-κB pathway. In this study, we investigated the effect of INSL3 on inflammation and cell viability in the lipopolysaccharide (LPS)-induced N9 microglia cell line. Materials and Methods: N9 microglial cells were pretreated with INSL3 for 2 hours, and then treated with LPS for 6 hours. Cell viability was identified by WST-8 assay. Immunostaining was performed to evaluate the levels of Interleukin-1β (IL-1β), Tumor necrosis factor (TNF)-α, and NF-κB. Results: The cells in the LPS group showed degenerative changes in morphology and decreased cell viability. In the INSL3+LPS group (1.21±0.06), the general appearance and viability of the cells were more similar to the control group (1.92±0.04) compared to the LPS group (0.61±0.05). It was determined that INSL3 prevented the LPS-induced increase in IL-1β, TNF-α, and NF-κB levels and decreased cell death. Conclusion: INSL3 suppresses inflammation and thus promotes cellular healing and can be considered a therapeutic agent that reduces inflammation. [ABSTRACT FROM AUTHOR]

Purpose: The aim of this study is to investigate the antiinflammatory and anti-apoptotic effects of naringin (NRG), which has many biological properties, on bacterial endotoxin-induced small intestine damage in rats. Materials and Methods: For this purpose, 40 female Wistar albino rats were divided into 4 groups as Control (group given no treatment), LPS (group given 10 mg/kg/i.p lipopolysaccharide), NRG (group given 100 mg/kg/i.p naringin for 14 days) and LPS + NRG (group given 100 mg/kg/i.p naringin for 14 days before 10 mg/kg/i.p lipopolysaccharide injection). After experimental procedure, small intestine tissues of animals were extracted and prepared according to tissue processing protocol. Hematoxylin and Eosin staining were performed to evaluate the histopathological changes and histological damage scoring was applied to compare experimental groups in terms of histopathological changes. Moreover, TNF-α and Caspase-3 expression levels were detected by immunohistochemical staining and the density of immunoreactivity were scored to determine the difference in the expression levels of TNF-α and Caspase-3 expressions among groups. Results: Epithelial and Brunner’s gland damage, mononuclear cell infiltration, hemorrhage, and TNF-α and Caspase-3 expressions significantly increased in the LPS group. However, NRG administrations exerted a strong protective effect on the small intestine tissues in terms of these parameters in LPS+NRG group. Conclusion: This study demonstrated that 100 mg/kg NRG injection can be regarded as a protective agent against negative effects of endotoxin-induced infection on the intestinal mucosa and that it should not be disregarded in further clinical trials. [ABSTRACT FROM AUTHOR]