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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]

Objective: Inflammation which is a response of immune system was demonstrated in many disorders such as atherosclerosis, hypertension, diabetes, cancer and rheumatoid arthritis. Metformin, an oral antidiabetic drug, has anti-inflammatory effect apart from blood glucose regulatory effect. However, the mechanism of its antiinflammatory effect is not clearly understood. In this study, the effect of metformin on the release of cytokines (TNF-α and IL-6) from LPS stimulated rat mononuclear blood cells was investigated. Methods: Blood samples (5ml) were taken from healthy, male, 8-12 weeks old rats (n=5, 200-250g) through cardiac puncture under general anesthesia into sterile EDTA containing tubes. Monocytes were separated by centrifugation and were resuspended in RPMI 1640 media (3.3±0.2x105/ml). Cells were then incubated with metformin (2.5 μM, 25 μM, 250 μM) for 2,5 hours followed by addition of LPS (100 ng/ml, 1μg/ml) for further 5 hours. After centrifugation, the supernatant was taken and TNF-α level was measured by ELISA. Results: There was no statistically significant change in the amounts of TNF-α in the LPS + metformin groups compared to the 100 ng/ml LPS group (p>0.05). In LPS+metformin groups, compared to 1 μg/ml LPS, 2.5 μM and 250 μM metformin significantly increased TNF-α levels (p<0.05), while 25 μM metformin did not make a significant difference (p>0.05). The amount of IL-6 was not within measurable range in this study. Conclusion: In summary, metformin increased the amount of released TNF-α rather than decreased in our study. [ABSTRACT FROM AUTHOR]

Objective Despite the advances in medicine, sepsis still remains a major health problem worldwide and brain tissue is one of the structures damaged in the early period of sepsis. Neuroinflammation (NI) is considered as the main mechanism in septic brain injury. Ramelteon (RML) is a non-selective (MT1 / MT2) melatonin receptor agonist and was approved by the FDA in 2005 with the indication of insomnia. RML shows relatively higher affinity for both receptor subtypes among other melatonergic agonist drugs. Material and Method Twenty-eight male Wistar Albino rats were used to investigate the protective effect of RML on lipopolysaccharide (LPS) induced NI. Control, LPS (5 mg/kg, intraperitoneally), RML (8 mg/kg, orally) and LPS + RML (45 minutes before LPS) groups were created. Six hours following the last drug administration, rats were sacrificed. Blood for hemogram analysis and cortical and hippocampal tissues for histopathological evaluation were collected. Results LPS increased white blood cell and neutrophil/ lymphocyte ratio (NLR) while it decreased lymphocyte and platelet counts. RML decreased NLR and increased platelet counts significantly. In histochemical evaluation, marked inflammatory cell infiltration and apoptosis were observed in both hippocampal and cortical areas of LPS group. RML decreased the inflammatory response and apoptotic bodies in these areas. Conclusion RML may be protective on LPS-induced NI observed in hippocampus via anti-inflammatory and anti-apoptotic mechanisms. [ABSTRACT FROM AUTHOR]

Purpose: The aim of this study is to investigate the anti-inflammatory 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- 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- and Caspase-3 expressions among groups. Results: Epithelial and Brunner’s gland damage, mononuclear cell infiltration, hemorrhage, and TNF- 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.

Copyright of Van Tip Dergisi is the property of Yuzuncu Yil University, Faculty of Medicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Cukurova Medical Journal / Çukurova Üniversitesi Tip Fakültesi Dergisi is the property of Cukurova University, Faculty of Medicine and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: In this study, it was aimed to investigate the effects of hesperetin on renal transforming growth factor-beta 1 (TGF-β1) expression and apoptosis in rat lipopolysaccharide (LPS)-induced acute renal injury model. Methods: In the study, 18 adult male Wistar albino rats were used. Rats divided into three groups, respectively (n=6); control, LPS and LPS + hesperetin. Sepsis model was created with a singledose of LPS (Escherichia coli, O26: B6 serotype, Sigma-aldrich). LPS + hesperetin group was administered intragastrically with the aid of hesperetin oral gavage at a dose of 100 mg/kg, after LPS-induction. Twenty four hours after LPS administration, the rats were opened from the midline under ketamine-xylazine anesthesia and kidney tissue and cardiac blood were collected. Kidney tissue was examined with hematoxylin-eosin staining. TGF-β1 expression was determined by indirect immunohistochemical method. TUNEL method was used to determine renal apoptosis. Blood urea nitrogen (BUN) and creatinine levels in blood serum were determined using spectrophotometric methods. Results: Decreased histopathological changes, TGF-β1 expression and apoptosis were determined in the LPS + hesperetin group compared to the LPS group (p<0.05). In addition, a significant decrease in BUN and creatinine levels was observed in the LPS + hesperetin group compared to the LPS group (p<0.05). Conclusion: The data obtained show that in the LPS-induced rat sepsis model, hesperetin suppresses the expression of TGF-β1 in kidney tissue and provides a protective effect. [ABSTRACT FROM AUTHOR]

Copyright of Etlik Veteriner Mikrobiyoloji Dergisi is the property of Veteriner Kontrol Merkez Arastirma Enstitusu and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Osmangazi Journal of Medicine / Osmangazi Tip Dergisi is the property of Eskisehir Osmangazi University and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

In this study, the effect of lactoferrin (LF) on adenosine deaminase (ADA) activity, nitric oxide (NO) and liver enzyme levels were investigated in lipopolysaccharide (LPS)-induced experimental endotoxemia model in rats. Forty Sprague Dawley female rats were divided into four groups as control, LF (20 mg/kg, i.p.), LPS (20 µg/kg, i.p.) (E. coli type 0111:B4) and LF+LPS (20 mg/kg LF+20 µg/kg LPS, i.p.). For a week, LF was given daily, while LPS was given a single dose. Liver adenosine deaminase, nitric oxide and liver enzymes (aspartate aminotransferase 'AST', alanine aminotransferase 'ALT' and gamma glutamyltranspeptidase 'GGT') levels of animals sacrificed six hours after LPS injection were determined. It was found that ADA activity, considered to be a marker of cellular immunity, and NO levels increased in LPS-induced endotoxemia and LF supplementation decreased these levels significantly (P<0.001). There was no statistically significant difference between liver ALT, AST and GGT activity levels of all groups, but serum AST and GGT activity levels were significantly higher (P<0.001 and P<0.05, respectively) in the LPS group than in the other groups, and LF supplementation significantly reduced these enzyme levels. As a result, it can be said that LPS increases ADA synthesis and NO release and LF acts as an anti-inflammatory and immunosuppressor in stimulating immune response. [ABSTRACT FROM AUTHOR]

Latterly, scientists have turned into progressively curious about therapeutic herbs. A lot of Convolvulus taxa display different biologic activities. In this study, we aimed to evaluate nitric oxide (NO) inhibitive effect of Convolvulus aucheri in LPS-induced non-small cell lung cancer (NSCLC) cells, such as HCC78 and H1975 and determine its antioxidant capacity. While Griess assay was applied to determine the nitrite level as an index of NO production, β-carotene/linoleic acid test was used for the determining antioxidant effect. Cytotoxic activity of C. aucheri extract was detected by using CellTiter-Glo assay. The extract induced a bigger cytotoxic activity on H1975 cells than the HCC78 cells and decreased NO production in concentration-dependent manner. The highest inhibitory potential against NO formation was observed to be 113.06 µM nitrite at a concentration of 40 µg/mL in HCC78 cells. As for the antioxidant activity, C. aucheri showed the highest antioxidant activity of 70.89%. These data bring to mind that C. aucheri may be a useful source for exploration new anticancer compounds. [ABSTRACT FROM AUTHOR]

Copyright of Turkish Journal of Trauma & Emergency Surgery / Ulusal Travma ve Acil Cerrahi Dergisi is the property of KARE Publishing and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Aim: Vascular endothelial growth factor production is decreased depending on the alveolar epithelial cell damage. Acute over expression of vascular endothelial growth factor in lung tissue contributes to the formation permeability. Excessive doses of acetylsalicylate (ASA) may induce pulmonary edema by increasing pulmonary vascular permeability. In this study, the effects of acetylsalicylate overdoses were evaluated on bronchoalveolar lavage fluid levels of vascular endothelial growth factor in the presence of lipopolysaccharide-induced lung injury in rats. Materials and Methods: Lung injury was induced by intraperitoneal injection of lipopolysaccharide (LPS). Rats were divided into six different sets consisting of 7 rats each for control, ASA-300, ASA-500, LPS, LPS+ASA-300 and LPS+ASA-500 series. ASA, 300 mg and 500 mg/kg doses were given by gavage. Acetylsalicylate was given 24 hours after lipopolysaccharide injection in LPS+ASA groups. Rats were sacrificed 6 hours after acetylsalicylate administration and bronchoalveolar lavage was performed. Results: In bronchoalveolar lavage fluid, vascular endothelial growth factor, matrix metalloproteinase-2 and nitric oxide levels were increased in group of ASA-500, and were decreased in groups of LPS+ASA. In addition, plasma salicylate half-life was prolonged in LPS+ASA groups. Conlusion: Lipopolysaccharide increases the time of being metabolized of acetylsalicylate. The lung tissue damage increases due to vascular endothelial growth factor, matrix metalloproteinase-2 and nitric oxide related mechanisms and recovery period is affected adversely. Also in humans, severe toxic effects on the lung tissue that can be generated by 300 and 500 mg/kg acetylsalicylate doses in rats showed less toxic effect. [ABSTRACT FROM AUTHOR]

Objectives: Propolis, a bee-product, has attracted researchers' interest in recent years because of several biological and pharmacological properties. Lipopolysaccharide (LPS) is a component of the outer membrane of Gramnegative bacteria and has an important role in the pathogenesis of septic shock and several inflammatory diseases by causing excessive release of inflammatory cytokines. The aim of this study was to investigate the effects of ethanol extract of propolis collected in Kayseri and its surroundings on production of pro-inflammatory cytokines in LPS-stimulated macrophages. Materials and methods: In vitro, U937 human macrophage cells were grown in RPMI-1640 medium supplemented with fetal bovine serum (10%) and penicillinstreptomycin (2%) and divided into: control, LPS treated, and propolis+LPS treated cell groups. After incubation in an atmosphere of 5% CO2 and at 37°C of cells, interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α levels were measured in cell-free supernatants by ELISA. Results: IL-1β, IL-6 and TNF-α levels increased in LPS treated cell group according to control, statistically significant. Each cytokine levels significantly decreased in LPS and propolis treated cell group according to only LPS treated cell group (p<0.05). Conclusion: Propolis is a natural product to be examined for usage when needed the suppression of pro-inflammatory cytokines. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Health Sciences / Sağlık Bilimleri Dergisi is the property of Erciyes Universitesi Saglik Bilimleri Dergisi and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)