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Recombinant expressed vasoactive intestinal peptide analogue ameliorates TNBS-induced colitis in rats.

To investigate the modulatory effect of recombinant-expressed vasoactive intestinal peptide (VIP) analogue (rVIPa) on trinitrobenzene sulfonic acid (TNBS)-induced colitis in rats.

1030 related Products with: Recombinant expressed vasoactive intestinal peptide analogue ameliorates TNBS-induced colitis in rats.

Rabbit Anti-Human Vasoact Recombinant Human Interfe Recombinant Human Interle Recombinant Human Interle Recombinant Human Interle Recombinant Human Interle Recombinant Human Insulin Recombinant Human Insulin Recombinant Human Insulin GLP 1 ELISA Kit, Rat Gluc Trefoil factor 3 (Intesti Anti AGO2 Human, Monoclon

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Clusterin Reduces Cold Ischemia-Reperfusion Injury in Heart Transplantation Through Regulation of NF-kB Signaling and Bax/Bcl-xL Expression.

Ischemia-reperfusion (I/R) injury is an unavoidable event occurring during heart transplantation and is a key factor in graft failure and the long-term survival rate of recipients. Therefore, there is an urgent need for the development of new therapies to prevent I/R injury. Clusterin is a hetero-dimeric glycoprotein with an antiapoptotic function. In this study, we investigated whether clusterin was cardioprotective in heart transplantation against I/R injury using an in vivo rat model and an in vitro cell culture system, and examined the underlying mechanisms of I/R injury.

2944 related Products with: Clusterin Reduces Cold Ischemia-Reperfusion Injury in Heart Transplantation Through Regulation of NF-kB Signaling and Bax/Bcl-xL Expression.

NF-kB II Phospho-Specific DNA (cytosine 5) methyltr NF-kB Phospho-Specific Ar GLP 2 ELISA Kit, Rat Prog Anti beta3 AR Human, Poly ABT-263 Mechanisms: Bcl-2 ABT-737 Mechanisms: Bcl-2 XL-147 Mechanisms: PI3K i XL-765 (SAR-245409) Mecha XL-184 (Cabozantinib) Mec GDC-0973 (XL-518) Mechani ABT-199 Mechanisms: Bcl-2

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[Effect of neuregulin-1 on heart function and inflammatory mediators in rats with sepsis].

To explore the protective effect of neuregulin-1 (NRG-1) on heart function and myocardium in rats with sepsis and its mechanism.

2010 related Products with: [Effect of neuregulin-1 on heart function and inflammatory mediators in rats with sepsis].

Anti beta3 AR Human, Poly Rabbit Anti-FGF3 Oncogene Bcl-2 Oncoprotein; Clone Bcl-2 Oncoprotein; Clone Bcl-2 Oncoprotein; Clone BCIP INT Solution Sterile filtered goat se Sterile filtered rat ser Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon anti HCMV IE pp65 IgG1 (m anti HCMV gB IgG1 (monocl

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Targeting Chondroitin Sulfate Glycosaminoglycans to Treat Cardiac Fibrosis in Pathological Remodeling.

-Heart failure (HF) is a leading cause of mortality and morbidity, and the search for novel therapeutic approaches continues. In the monogenic disease mucopolysaccharidosis (MPS) VI, loss of function mutations in arylsulfatase B (ASB) leads to myocardial accumulation of chondroitin sulfate (CS) glycosaminoglycans (GAGs), manifesting as a myriad of cardiac symptoms. Here, we studied changes in myocardial CS in non-MPS failing hearts, and assessed its generic role in pathological cardiac remodeling.-Healthy and diseased human and rat left ventricles were subjected to histological and immuno-staining methods to analyze for GAG distribution. GAGs were extracted and analyzed for quantitative and compositional changes using Alcian Blue assay and liquid chromatography mass spectrometry. Expression changes in 20 CS-related genes were studied in three primary human cardiac cell types and THP-1 derived macrophages under each of 9stimulatory conditions. In two rat models of pathological remodeling induced by transverse aortic constriction (TAC) or isoprenaline infusion, recombinant human arylsulfatase B (rhASB), clinically used as enzyme replacement therapy (ERT) in MPS VI, was administered intravenously for 7 or 5 weeks respectively. Cardiac function, myocardial fibrosis and inflammation were assessed by echocardiography and histology. CS-interacting molecules were assessed using surface plasmon resonance and a mechanism of action was verified-Failing human hearts displayed significant perivascular and interstitial CS accumulation, particularly in regions of intense fibrosis. Relative composition of CS disaccharides remained unchanged. Transforming growth factor β (TGFβ) induced CS upregulation in cardiac fibroblasts. CS accumulation was also observed in both the pressure-overload and the isoprenaline models of pathological remodeling in rats. Early treatment with rhASB in the TAC model, and delayed treatment in the isoprenaline model, proved rhASB to be effective at preventing cardiac deterioration and augmenting functional recovery. Functional improvement was accompanied by reduced myocardial inflammation and overall fibrosis. Tumor necrosis factor α (TNFα) was identified as a direct binding partner of CS GAG chains, and rhASB reduced TNFα-induced inflammatory gene activationin endothelial cells and macrophages.-CS GAGs accumulate during cardiac pathological remodeling, and mediate myocardial inflammation and fibrosis. RhASB targets CS effectively as a novel therapeutic approach for the treatment of heart failure.

1943 related Products with: Targeting Chondroitin Sulfate Glycosaminoglycans to Treat Cardiac Fibrosis in Pathological Remodeling.

Recombinant Human Interfe Native Influenza HA (A To Native Influenza HA (A To Native Influenza HA (A To Cell Meter™ Fluorimetri Cell Meter™ Fluorimetri T-2 Toxin Mycotoxins ELIS 1-Acetyl-3-indoxyl Sulfat 1-Acetyl-3-indoxyl-d4 Sul Nycodenz, non ionic, non Homogenizer for 24 sample Top five cancer tissue ar

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Analytical performance of a commercial multiplex Luminex-based cytokine panel in the rat.

Multiplex immunoassays are an important tool in biomarker research during preclinical drug development. However, information regarding analytical performance of commercial multiplex assays for animal species is often limited. To be able to correctly interpret study results, a fit-for-purpose validation approach is recommended. The objective of our study was to provide a realistic example of what level of validation can be expected from this type of assay, using a rat cytokine panel.

2191 related Products with: Analytical performance of a commercial multiplex Luminex-based cytokine panel in the rat.

Inflammation (Rat) Quanti Cytokine (Rat) Antibody A Cytokine (Rat) Antibody A Cytokine (Rat) Antibody A Cytokine (Rat) Antibody A Inflammation (Human) Quan Inflammation (Human) Quan Inflammation (Human) Quan Inflammation (Mouse) Quan Cytokine (Rat) Quantitati Cytokine (Rat) Quantitati Cytokine (Rat) Quantitati

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Interfering RNA against PKC-α Inhibits TNF-α-induced IP3R1 Expression and Improves Glomerular Filtration Rate in Rats with Fulminant Hepatic Failure.

We have reported that tumor necrosis factor- (TNF-α) is critical for reduction of glomerular filtration rate (GFR) in rats with fulminant hepatic failure (FHF). The present study aims to evaluate the underlying mechanisms of decreased GFR during acute hepatic failure.

2614 related Products with: Interfering RNA against PKC-α Inhibits TNF-α-induced IP3R1 Expression and Improves Glomerular Filtration Rate in Rats with Fulminant Hepatic Failure.

Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon DNA (cytosine 5) methyltr Human Epstein-Barr Virus Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Mouse Epstein-Barr Virus LPAM-1(Integrin α4, CD49

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Novel Fusion Protein Targeting Mitochondrial DNA Improves Pancreatic Islet Functional Potency and Islet Transplantation Outcomes.

Long-term graft survival is an ongoing challenge in the field of islet transplantation. With the growing demand for transplantable organs, therapies to improve organ quality and reduce the incidence of graft dysfunction are of paramount importance. We evaluated the protective role of a recombinant DNA repair protein targeted to mitochondria (Exscien I-III), as a therapeutic agent using a rodent model of pancreatic islet transplantation. We first investigated the effect of therapy on isolated rat islets cultured with pro-inflammatory cytokines (interleukin-1 β, interferon γ, and tumor necrosis factor α) for 48 h and documented a significant reduction in apoptosis by flow cytometry, improved viability by immunofluorescence, and conserved functional potency in vitro and in vivo in Exscien I-III-treated islets. We then tested the effect of therapy in systemic inflammation using a rat model of donor brain death (BD) sustained for a 6-h period. Donor rats were allocated to 4 groups: (non-BD + vehicle, non-BD + Exscien I-III, BD + vehicle, and BD + Exscien I-III) and treated with Exscien I-III (4 mg/kg) or vehicle 30 min after BD induction. Sham (non-BD)-operated animals receiving either Exscien I-III or vehicle served as controls. Islets purified from BD + Exscien I-III-treated donors showed a significant increase in glucose-stimulated insulin release in vitro when compared to islets from vehicle-treated counterparts. In addition, donor treatment with Exscien I-III attenuated the effects of BD and significantly improved the functional potency of transplanted islets in vivo. Our data indicate that mitochondrially targeted antioxidant therapy is a novel strategy to protect pancreas and islet quality from the deleterious effects of cytokines in culture and during the inflammatory response associated with donation after BD. The potential for rapid translation into clinical practice makes Exscien I-III an attractive therapeutic option for the management of brain-dead donors or as an additive to islets in culture after isolation setting.

2272 related Products with: Novel Fusion Protein Targeting Mitochondrial DNA Improves Pancreatic Islet Functional Potency and Islet Transplantation Outcomes.

Glucokinase, islet isofor Glucokinase, islet isofor Glucokinase, islet isofor Glucokinase, islet isofor Glucokinase, islet isofor Glucokinase, islet isofor Glucokinase, islet isofor Glucokinase, islet isofor E. coli SSB (Single Stran E. coli SSB (Single Stran E. coli SSB (Single Stran E. coli SSB (Single Stran

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IL-33 Provides Neuroprotection through Suppressing Apoptotic, Autophagic and NF-κB-Mediated Inflammatory Pathways in a Rat Model of Recurrent Neonatal Seizure.

Interleukin-33 (IL-33) is a novel identified chromatin-associated cytokine of IL-1 family cytokines. It signals through a heterodimer comprised of ST2L and IL-1RAcp, and plays a crucial role in many diseases. However, very little is known about the role and underlying intricate mechanisms of IL-33 in recurrent neonatal seizure (RNS). To determine whether IL-33 plays an important regulatory role, we established a neonatal seizure model in this study. Rats were subjected to recurrent seizures induced by inhaling volatile flurothyl. Recombinant IL-33 or PBS were also administered by intraperitoneally (IP) before surgery, respectively. Here, our current results indicated that RNS contributed to a significant reduction in IL-33 and its specific receptor (ST2L) expressions in cortex. While, in hippocampus, RNS induced an increase in IL-33 and ST2L evidently, compared with Sham group. After injection with IL-33, however, a remarkable increase in total IL-33 was detected both in brain cortex and hippocampus. In addition, IL-33 was mainly co-localized in the nuclear of GFAPastrocytes and the cytoplasm of the Iba-1microglia and IL-33/NeuNmerged cells. In parallel, ST2L was expressed mainly in the membrane of GFAPastrocytes, Iba-1microglia and NeuNneurons, respectively. Furthermore, administration of IL-33 improved RNS-induced behavioral deficits, promoted bodyweight gain, and ameliorated spatial learning and memory ability. Moreover, IL-33 pretreatment blocked the activation of NF-κB, resisted inflammatory cytokines IL-1β and TNF-α increase, as well as suppressed apoptosis and autophagy activation after RNS. Collectively, IL-33 provides potential neuroprotection through suppressing apoptosis, autophagy and at least in part by NF-κB-mediated inflammatory pathways after RNS.

2932 related Products with: IL-33 Provides Neuroprotection through Suppressing Apoptotic, Autophagic and NF-κB-Mediated Inflammatory Pathways in a Rat Model of Recurrent Neonatal Seizure.

Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Rat Anti-Mouse Interleuki Recombinant Rat Interleuk Recombinant Rat Interleuk Rat Macrophage Inflammato

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Overexpression of SIRT2 Alleviates Neuropathic Pain and Neuroinflammation Through Deacetylation of Transcription Factor Nuclear Factor-Kappa B.

Sirtuin 2 (SIRT2), a member of the mammalian sirtuin family, plays an important role in the pathogenesis of various neurological diseases. However, whether SIRT2 is involved in the regulation of neuropathic pain remains unclear. In this study, we aimed to investigate the potential role of SIRT2 in regulating neuropathic pain in a rat model induced by chronic constriction injury (CCI). We found that SIRT2 was downregulated in the dorsal root ganglion (DRG) in CCI rats. Intrathecal injection of a recombinant adenovirus expressing SIRT2 markedly alleviated mechanical allodynia and thermal hyperalgesia in CCI rats. This also inhibited the expression of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 in the DRG of CCI rats. Moreover, our results showed that overexpression of SIRT2 inhibited the acetylation of the nuclear factor-kappa B (NF-κB) p65 protein in the DRG of CCI rats. Additionally, treatment with a SIRT2 specific inhibitor significantly aggravated neuropathic pain and attenuated the inhibitory effect of SIRT2 overexpression on neuropathic pain development. Taken together, these results suggest that overexpression of SIRT2 alleviates neuropathic pain associated with inhibition of NF-κB signaling and neuroinflammation. Therefore, SIRT2 may serve as a potential therapeutic target for treatment of neuropathic pain.

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RANK Ligand Soluble, Huma Transcription factor E3 a Anti PDX1 Polyclonal Anti HSF EMSA Kit: Heat shock Procarta Transcription Fa Activating Transcription Activating Transcription Activating Transcription Activating Transcription Factor VIII Related Anti Factor VIII Related Anti Factor VIII Related Anti

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Axl activation attenuates neuroinflammation by inhibiting the TLR/TRAF/NF-κB pathway after MCAO in rats.

Ischemic stroke activates Toll-like receptors (TLRs), triggering rapid inflammatory cytokine production. Axl signaling has multiple roles, including regulating cytokine secretion, clearing apoptotic cells, and maintaining cell survival, however, its role in inflammation after ischemic stroke has not been examined. We hypothesized that activation of Axl by recombinant Growth-arrest-specific protein 6 (rGas6) attenuates neuroinflammation by inhibiting the TLR/TRAF/NF-κB pathway after middle cerebral artery occlusion (MCAO) in rats. METH: Sprague-Dawley rats were subjected to 2h of MCAO. One hour after reperfusion, the rats were given an intranasal injection of rGas6, vehicle, or R428 (Axl receptor inhibitor). Neurological scores, infarct volumes, immunofluorescence staining, Morris Water Maze, rotarod test and histology alterations were analyzed. The expressions of proinflammatory cytokines, including IL-1β, IL-6, TNF-α, and Gas6, Axl, STAT1, SOCS1, SOCS3 and the TLR/TRAF/NF-κB pathway were quantified using Western blot.

1934 related Products with: Axl activation attenuates neuroinflammation by inhibiting the TLR/TRAF/NF-κB pathway after MCAO in rats.

NF-kB Phospho-Specific Ar NF-kB II Phospho-Specific Stat3 Activation Inhibito EtBr Destaining Bag Kit A BYL-719 Mechanisms: PI3K- Apoptosis antibody array Cell cycle antibody array Cytokine antibody array i Signal transduction antib AKT Phospho-Specific Arra AKT PKB Signaling Phospho AMPK Signaling Phospho-Sp

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