Search results for: Rat TNF-alpha ELISA ELISA
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Minocycline an antimicrobial agent attenuates the mitochondrial dependent cell death and stabilizes the expression of HIF-1α in spinal cord injury.One of the crucial mechanisms following spinal cord injury is mitochondria associated cell death. Minocycline, an anti-inflammatory drug is well known to impede the mitochondrial cell death. However, there has been no study on the effect of minocycline linking FAS-mediated cell death and hypoxia inducible factor (HIF-1α), the targets involved in mitochondrial cell death. Male Sprague Drawley rats (N = 18, divided into three groups) were subjected to traumatic spinal cord injury and were injected with minocycline (n = 6) (90 mg/kg, and later 45 mg/kg dose two times a day (every 12 h). Injection with sterile PBS in injured animals served as vehicle (n = 6) and another group comprised of healthy animals (n = 6). TUNEL assay was used to quantify the cell death. The release of Smac/Diablo, cytochrome-c, HIF-1α, FASL and tumour necrosis factor-α (TNFα) was measured using enzyme linked immunosorbent assay (ELISA). Expression of HIF-1α, FASL and other cell-death associated factors were quantified at the mRNA and protein level and confirmed with immunohistochemistry. There was a marked reduction in the HIF-1α and FASL expression levels in minocycline treated group compared to the vehicle. The reduction of HIF-1α and FASL has been associated with other factors associated with cell death (Smac/Diablo, cytochrome-c, TNFα, p53, caspase-8, BID). The present study focuses on the investigation of minocycline in inhibiting the mitochondria associated cell death by modulating FASL and HIF-1α expression, which are seemingly interlinked mechanisms contributing cell death.
2670 related Products with: Minocycline an antimicrobial agent attenuates the mitochondrial dependent cell death and stabilizes the expression of HIF-1α in spinal cord injury.Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in Rabbit Anti-Cell death in
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[Effect of sucralfate on cytokines in rat with paraquat poisoning].To explore the effect of sucralfate on cytokines in rats with paraquat (PQ) poisoning.
Inflammation (Rat) Quanti Rat Inflammation ELISA St Sterile filtered rat ser Insulin 1 (Rat), syntheti Goat Anti-Rat MARCH10, (i Goat Anti-Mouse, Rat DLL1 Goat Anti-Human, Mouse, R Goat Anti-Human, Mouse, R Goat Anti-Rat Connexin 43 Goat Anti-Human, Rat CHRN Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki
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[Effects of heme oxygenase-1/carbon monoxide pathway on the mitochondrial fusion in rat alveolar epithelial type II cells stimulated by lipopolysaccharide].To investigate the effects of heme oxygenase-1/carbon monoxide (HO-1/CO) pathway on mitochondrial fusion in rat alveolar epithelial type II cells (AEC II) stimulated by lipopolysaccharide (LPS).
1211 related Products with: [Effects of heme oxygenase-1/carbon monoxide pathway on the mitochondrial fusion in rat alveolar epithelial type II cells stimulated by lipopolysaccharide].anti HSV (II) gB IgG1 (mo Immunization grade rat ty IMRII Immunization grade IMRII Immunization grade Immunization grade rat ty IMRII SOL Immunization gr IMRII SOL Immunization gr ELISA grade rat type II c ELRII ELISA grade rat typ ELRII ELISA grade rat typ T-cell proliferation grad TCRII T cell proliferatio
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[Effect of different concentrations of hypertonic sodium fluid resuscitation on intestine injury in rats at the early stage of severe burn].To investigate the effect of different concentrations of hypertonic saline solution (HS) on intestine injury in rats at the early stage of severe burn.
2699 related Products with: [Effect of different concentrations of hypertonic sodium fluid resuscitation on intestine injury in rats at the early stage of severe burn].Colon well differentiated Colon moderately differen Colon poorly differentiat Ofloxacin CAS Number [824 Multiple organ tumor tiss Small intestine cancer, m Small intestine disease s Stomach poorly differenti Small intestine cancer te Caspase-12 Inhibitor Z-AT Caspase-12 Inhibitor Z-AT Caspase 12 Inhibitor Z AT
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Evaluation of antioxidant and anti-inflammatory efficacy of caffeine in rat model of neurotoxicity.The present study aims to investigate the neuroprotective effect of caffeine against aluminum chloride (AlCl)-induced neurotoxicity in rats.
1719 related Products with: Evaluation of antioxidant and anti-inflammatory efficacy of caffeine in rat model of neurotoxicity.Goat Anti-Rat MARCH10, (i Goat Anti-Mouse, Rat DLL1 Goat Anti-Human, Mouse, R Goat Anti-Human, Mouse, R Goat Anti-Rat Connexin 43 Goat Anti-Human, Rat CHRN Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki
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RP105 alleviates myocardial ischemia reperfusion injury via inhibiting TLR4/TRIF signaling pathways.The Toll-like receptor 4 (TLR4) signal pathway- induced inflammation is considered to be a crucial link to myocardial ischemia reperfusion injury (MIRI). Our previous study proved that radioprotective 105 kDa protein (RP105), a negative regulator of TLR4, performed a protective role in MIRI by anti-apoptosis approach. However, the mechanism of RP105 cardioprotection of anti-inflammation is still unclear. This study aimed to explore the underlying mechanism of RP105 anti-inflammation effect in MIRI. We established a rat model of MIRI induced by ligation of the left anterior descending coronary artery for 30 min followed by 2 h reperfusion. Animals were pre-infected with Ad-EGFP-RP105, Ad-EGFP or saline at the apex of the heart. All rats were sacrificed to collect blood samples and myocardial tissue and assessed by immunofluorescence, blood biochemical analysis, Evans blue/triphenyltetrazolium chloride (TTC), hematoxylin and eosin (H&E) staining, enzyme-linked immuno sorbent assay (ELISA), western blot analysis, quantitative PCR and electrophoretic mobility shift assay (EMSA). RP105 overexpression with adenovirus vectors reduced serum myocardial enzyme (CK-MB and LDH) activities, decreased myocardial infarct size, mitigated inflammatory factors interferon-β and tumor necrosis factor-α during MIRI. We also found that Ad-RP105 group exerted distinct repression of TLR4/TRIF signal pathway related proteins and mRNAs (TRIF, TBK-1, IRF3 and p-IRF3) with a low transcriptional activity of IRF3. These findings first expounded that RP105 could alleviate the ischemia reperfusion induced inflammatory status in heart via inhibiting TLR4/TRIF signaling pathway and provided a theoretical foundation of RP105 gene in MIRI.
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IL-33 Treatment Attenuates the Systemic Inflammation Reaction in Acinetobacter baumannii Pneumonia by Suppressing TLR4/NF-κB Signaling.Interleukin (IL)-33 treatment has been reported to reduce mortality in a rat model of sepsis, and the present study aimed to determine whether this effect of IL-33 is achieved through a reduction in the systemic inflammatory response in Acinetobacter baumannii pneumonia. After induction of pneumonia, rats were treated with normal saline or IL-33, and mortality over 5 days was recorded. Inflammation within lung tissues was evaluated by hematoxylin and eosin staining as well as measurement of the concentrations of IL-8 and tumor necrosis factor alpha (TNF-α) in the bronchoalveolar lavage fluid (BALF) and plasma by enzyme-linked immunosorbent assay. In addition, the expression of Toll-like receptor 4 (TLR4), ST2, and nuclear factor kappa B (NF-κB) in rat lung tissues was assessed by western blotting. The result showed that the mortality rate and systemic inflammation were significantly increased in rats upon infection with A. baumannii, as evidenced by significant increases in the IL-8 and TNF-α levels in BALF and plasma as well as increased NF-κB activity and TLR4 expression in rat lung tissues. Importantly, IL-33 (1 μg/kg) treatment significantly decreased mortality and pulmonary inflammation in A. baumannii-infected rats. Moreover, IL-33 treatment suppressed the elevation of IL-8 and TNF-α levels and inhibited TLR4 expression and NF-κB activation. Overall, these results suggest that IL-33 may decrease the mortality and inhibit the systematic inflammatory response associated with A. baumannii pneumonia by suppressing TLR4/NF-κB signaling.
2303 related Products with: IL-33 Treatment Attenuates the Systemic Inflammation Reaction in Acinetobacter baumannii Pneumonia by Suppressing TLR4/NF-κB Signaling.Human Interleukin-33 IL-3 Recombinant Mouse Interle NF-kB II Phospho-Specific CELLKINES Natural Human I ACINETOBACTER BAUMANNII 3 BACTERIOLOGY ACINETOBACTE Human Interleukin-4 IL-4 Human Interleukin-6 IL-6 Human Interleukin-7 IL-7 Human Interleukin-2 IL-2 Human Interleukin-16 IL-1 Human Interleukin-17E (IL
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β-Amyrin, the cannabinoid receptors agonist, abrogates mice brain microglial cells inflammation induced by lipopolysaccharide/interferon-γ and regulates Mφ/Mφbalances.Inflammation is a primary response to infection that can pathologically lead to various diseases including neurodegenerative diseases. The purpose of this study was to evaluate the effect of β-Amyrin, a naturally occurring pentacyclic triterpenoid compound, on inflammation induced by lipopolysaccharide (LPS) and interferone-γ (IFN-γ) in rat microglial cells.
2838 related Products with: β-Amyrin, the cannabinoid receptors agonist, abrogates mice brain microglial cells inflammation induced by lipopolysaccharide/interferon-γ and regulates Mφ/Mφbalances.Anti C Reactive Protein A Human Brain Microvascular GFP Expressing Human Brai Mouse Brain Microvascular GFP Expressing Mouse Brai Fontana-Masson Stain Kit Fontana-Masson Stain Kit Interferon γ Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon
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Hypouricemic and Nephroprotective Effects of an Active Fraction from Polyrhachis Vicina Roger On Potassium Oxonate-Induced Hyperuricemia in Rats.The objective of this study is to evaluate the hypouricemic and nephroprotective effects of an active fraction from Polyrhachis vicina Roger (AFPR) in potassium oxonate-induced hyperuricemic rats.
1864 related Products with: Hypouricemic and Nephroprotective Effects of an Active Fraction from Polyrhachis Vicina Roger On Potassium Oxonate-Induced Hyperuricemia in Rats.Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon TGF beta induced factor 2 Rabbit Anti-FGF3 Oncogene CAR,CAR,Constitutive acti Anti-Infectious Pancreati Anti-Infectious Pancreati Anti-Infectious Pancreati Anti-Infectious Pancreati Proteins and Antibodies H
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Curcumin Attenuates Pulmonary Inflammation in Lipopolysaccharide Induced Acute Lung Injury in Neonatal Rat Model by Activating Peroxisome Proliferator-Activated Receptor γ (PPARγ) Pathway.BACKGROUND This study aimed to investigate the therapeutic effect of curcumin in lipopolysaccharide (LPS) induced neonatal acute lung injury (ALI) and the possibly associated molecular mechanisms. MATERIAL AND METHODS ALI neonatal animal model was established by using LPS. Curcumin and/or peroxisome proliferator-activated receptor γ (PPARγ) inhibitor BADGE (bisphenol A diglycidyl ether) were administrated to animals. Lung edema was evaluated by PaO2 and lung wet/dry weight ratio (W/D) measurements. EMSA was used to determine the PPARγ activity. Levels of high-mobility group box 1 (HMGB1), secretory receptor for advanced glycation end products (RAGE), tumor necrosis factor α (TNFα), interleukin 6 (IL6), and transforming growth factor b1 (TGFβ1) in bronchoalveolar lavage fluid (BALF) were examined by ELISA. Western blotting was used to evaluate the expression levels of HMGB1, RAGE, heme oxygenase 1 (HO1), TNFα, IL6, and TGFβ1 in lung tissue. RESULTS Curcumin administration significantly improved lung function by increasing PaO2 and decreasing W/D in neonatal ALI rats. Curcumin treatment upregulated the PPARγ activity and expression level of HO1 which were suppressed in lung tissue of neonatal ALI rats. Elevated levels of HMGB1, RAGE, TNFα, IL6, and TGFβ1 in both lung tissue and BALF from neonatal ALI rats were decreased dramatically by curcumin treatment. PPARγ inhibitor BADGE administration impaired curcumin's alleviation on lung edema, inhibitory effects on inflammatory cytokine expression and recovery of PPARg/HO1 signaling activation. CONCLUSIONS Curcumin alleviated lung edema in LPS-induced ALI by inhibiting inflammation which was induced by PPARγ/HO1 regulated-HMGB1/RAGE pro-inflammatory pathway.
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