Only in Titles

           Search results for: Caspase 3, rat recombinant   

paperclip

#28992627   2017/10/09 Save this To Up

H3 Relaxin Protects Against Myocardial Injury in Experimental Diabetic Cardiomyopathy by Inhibiting Myocardial Apoptosis, Fibrosis and Inflammation.

Apoptosis, fibrosis and NLRP3 inflammasome activation are involved in the development of diabetic cardiomyopathy (DCM). Human recombinant relaxin-3 (H3 relaxin) is a novel bioactive peptide that inhibits cardiac injury; however, whether H3 relaxin prevents cardiac injury in rats with DCM and the underlying mechanisms are unknown.

1030 related Products with: H3 Relaxin Protects Against Myocardial Injury in Experimental Diabetic Cardiomyopathy by Inhibiting Myocardial Apoptosis, Fibrosis and Inflammation.

Influenza A H3N2 Viral Ly Rabbit Anti-Influenza-A H Rabbit Anti-Influenza-A H Rabbit Anti-Influenza-A H Mouse Anti-Influenza-A HA Mouse Anti-Influenza-A He Mouse Anti-Influenza-A He Native Influenza A Virus Native Influenza A Virus Native Influenza A Virus Recombinant Influenza A V Recombinant Influenza A V

Related Pathways

paperclip

#28903487   2017/09/14 Save this To Up

From the Cover: Arsenic Induces Hippocampal Neuronal Apoptosis and Cognitive Impairments via an Up-Regulated BMP2/Smad-Dependent Reduced BDNF/TrkB Signaling in Rats.

Arsenic promotes hippocampal neuronal damage inducing cognitive impairments. However, mechanism arbitrating arsenic-mediated cognitive deficits remains less-known. Here, we identified that chronic exposure to environmentally relevant doses of arsenic increased apoptosis, characterized by caspase-3 activation, poly(ADP-ribose) polymerase cleavage and Terminal deoxynucleotidyl transferase dUTP nick-end labeling of rat hippocampal neurons, marked by NeuN. Investigating apoptotic mechanism through invivo and invitro studies revealed that arsenic promoted bone morphogenetic protein-2 (BMP2) expression, supported by increased BMP-receptor2 (BMPR2) and p-Smad1/5 in hippocampal neurons. BMP2-silencing and treatment with BMP antagonist, noggin, attenuated the arsenic-induced apoptosis and loss in hippocampal neurons. We then investigated whether BMP2/Smad signaling stimulated neuronal apoptosis independently or required other intermediate pathways. We hypothesized participation of brain-derived neurotrophic factor (BDNF) that promotes neuronal survival. We identified an arsenic-mediated attenuation of BDNF-dependent TrkB signaling, and observed that co-treatment with recombinant-BDNF reinstated BDNF/TrkB and reduced neuronal apoptosis. To probe whether BMP2/Smad and BDNF/TrkB pathways could be linked, we co-treated arsenic with noggin or recombinant BDNF. We detected a noggin-mediated restored BDNF/TrkB, while recombinant-BDNF failed to affect BMP2/Smad signaling. In addition, we found that TrkB-inhibitor, K252a, nullified noggin-induced protection, proving the necessity of a downstream reduced BDNF/TrKB signaling for BMP2/Smad-mediated apoptosis in arsenic-treated neurons. We further related our observations with cognitive performances, and detected noggin-mediated restoration of transfer latency time and learning-memory ability for passive avoidance and Y-Maze tests respectively in arsenic-treated rats. Overall, our study proves that arsenic promotes hippocampal neuronal apoptosis through an up-regulated BMP2/Smad-dependent attenuation of BDNF/TrkB pathway, inducing cognitive deficits.

2006 related Products with: From the Cover: Arsenic Induces Hippocampal Neuronal Apoptosis and Cognitive Impairments via an Up-Regulated BMP2/Smad-Dependent Reduced BDNF/TrkB Signaling in Rats.

anti H inh human blood an Apoptosis antibody array AKT PKB Signaling Phospho AMPK Signaling Phospho-Sp Apoptosis Phospho-Specifi Cancer Apoptosis Phospho- ErbB Her Signaling Phosph ERK Signaling Phospho-Spe GPCR Signaling to MAPK ER IGF-1R Signaling Phospho- NF-kB II Phospho-Specific p53 Signaling Phospho-Spe

Related Pathways

paperclip

#28881749   2017/09/08 Save this To Up

Effects of microRNA-126 on cell proliferation, apoptosis and tumor angiogenesis via the down-regulating ERK signaling pathway by targeting EGFL7 in hepatocellular carcinoma.

This study intends to explore the effects of microRNA-126 (miR-126) on cell proliferation, apoptosis, and tumor angiogenesis in hepatocellular carcinoma (HCC) by regulating epidermal growth factor-like domain 7 (EGFL7) through extracellular signal-regulated kinase (ERK) signaling. HCC tissues and adjacent normal tissues were obtained from 184 HCC patients. HCC cells were separately transfected with recombinant plasmids. Western blotting and qRT-PCR were applied to detect miR-126 and EGFL7, ERK, Fas/FasL, Bcl-2, Caspase mRNA and protein levels. CCK8 and TUNEL were performed to determinate cell proliferation and apoptosis. Flow cytometry was used to analyze cell cycle distribution. Rats model of HCC was constructed, and tumor weight and the number of new blood vessels were recorded after 3 weeks of tumor transplantation. Compared with the adjacent normal tissues, HCC tissues exhibited lower miR-126 expression, and higher EGFL7, and ERK mRNA and protein levels. Overexpression of miR-126 in HCC cell lines suppressed EGFL7, ERK, Bcl-2, and P-ERK, and increased apoptotic-associated proteins Fas/FasL and Caspase-3, and it inhibited cell proliferation and induced cell apoptosis. Overexpression of miR-126 in nude mice resulted in reduced tumor weight and less new blood vessels in tumors. The inhibition of miR-126 decreased cell apoptosis, and enhanced cell proliferation and tumor angiogenesis. This study demonstrates that miR-126 might decrease cell proliferation, induce apoptosis, and inhibit tumor angiogenesis in HCC by inhibiting EGFL7 via down-regulating the ERK signaling pathway.

1851 related Products with: Effects of microRNA-126 on cell proliferation, apoptosis and tumor angiogenesis via the down-regulating ERK signaling pathway by targeting EGFL7 in hepatocellular carcinoma.

ERK Signaling Phospho-Spe GPCR Signaling to MAPK ER T-Cell Receptor Signaling Cultrex In Vitro Angiogen AP-1 Reporter – HEK293 SRE Reporter - HEK293 Cel Wnt Signaling Pathway TCF Apoptosis antibody array Cell cycle antibody array AKT PKB Signaling Phospho AMPK Signaling Phospho-Sp Apoptosis Phospho-Specifi

Related Pathways

paperclip

#28754618   2017/07/29 Save this To Up

Hepatoprotective effect of hesperidin in hepatocellular carcinoma: Involvement of Wnt signaling pathways.

Wnt3a and Wnt5a are ligands orchestrating the canonical and non-canonical pathways, respectively, with involvement in hepatocellular carcinoma (HCC). Hesperidin (HP) is a natural product found in citrus fruits and reputed for its antitumor activity. The present study aims to investigate the potential hepatoprotective effect of HP against thioacetamide (TAA)-induced HCC focusing on its potential role on Wnt3a and Wnt5a signaling pathways.

1977 related Products with: Hepatoprotective effect of hesperidin in hepatocellular carcinoma: Involvement of Wnt signaling pathways.

Liver hepatocellular carc Liver cancer (hepatocellu Hepatocellular carcinoma Hepatocellular carcinoma Hepatocellular carcinoma Hepatocellular carcinoma Normal liver and hepatoce Recombinant Human WNT Inh Recombinant Human WNT Inh Recombinant Human WNT Inh Wnt Signaling Pathway TCF AKT PKB Signaling Phospho

Related Pathways

paperclip

#28728173   2017/07/20 Save this To Up

Glucocorticoid-Induced Leucine Zipper Protects the Retina From Light-Induced Retinal Degeneration by Inducing Bcl-xL in Rats.

The aim of the present study was to investigate the neuroprotective effects of glucocorticoid-induced leucine zipper (GILZ) in a light-induced retinal degeneration model and to explore the underlying mechanisms.

2985 related Products with: Glucocorticoid-Induced Leucine Zipper Protects the Retina From Light-Induced Retinal Degeneration by Inducing Bcl-xL in Rats.

Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Human Epstein-Barr Virus Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Mouse Epstein-Barr Virus TGF beta induced factor 2 Bovine prolactin-induced

Related Pathways

paperclip

#28698029   2017/07/12 Save this To Up

Critical role of EphA4 in early brain injury after subarachnoid hemorrhage in rat.

Early brain injury (EBI) is reported as a primary cause of mortality in subarachnoid hemorrhage (SAH) patients. Eph receptor A4 (EphA4) has been associated with blood-brain barrier integrity and pro-apoptosis. We aimed to investigate a role of EphA4 in EBI after SAH. One hundred and seventy-nine male adult Sprague-Dawley rats were randomly divided into sham versus endovascular perforation model of SAH groups. SAH grade, neurological score, Evans blue dye extravasation, brain water content, mortality, Fluoro-Jade staining, immunofluorescence staining, and western blot experiments were performed after SAH. Small interfering RNA (siRNA) for EphA4, recombinant Ephexin-1 (rEphx-1), and Fasudil, a potent ROCK2 inhibitor, were used for intervention to study a role of EphA4 on EBI after SAH. The expression of EphA4, Ephexin-1, RhoA, and ROCK2 significantly increased after SAH. Knockdown of EphA4 using EphA4 siRNA injection intracerebroventricularly (i.c.v) reduced Evans blue extravasation, decreased brain water content, and alleviated neurobehavioral dysfunction after SAH. Additionally, the expression of Ephexin-1, RhoA, ROCK2 and cleaved caspase-3 were decreased. Tight junction proteins increased, and apoptotic neuron death decreased. The effects of EphA4 siRNA were abolished by rEphx-1. In contrast, Fasudil abolished the effects of rEphx-1. These results suggest that EphA4, a novel and promising target for treatment, exacerbates EBI through an Ephexin-1/ROCK2 pathway after SAH.

2062 related Products with: Critical role of EphA4 in early brain injury after subarachnoid hemorrhage in rat.

Rat TGF-beta-inducible ea Rat TGF-beta-inducible ea Beta Amyloid (42) ELISA K Beta Amyloid (40) ELISA K 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

Related Pathways

paperclip

#28645823   2017/06/24 Save this To Up

Recombinant human soluble thrombomodulin prevents acute lung injury in a rat cardiopulmonary bypass model.

Cardiopulmonary bypass (CPB) may induce systemic inflammatory responses causing acute lung injury. Recombinant human soluble thrombomodulin (rTM) is reported to attenuate the secretion of inflammatory cytokines and the high-mobility group box 1 (HMGB1) protein, which is critical in controlling systemic inflammation and apoptosis. We investigated the protective effects of rTM on CPB-induced lung injury in a rat model.

2728 related Products with: Recombinant human soluble thrombomodulin prevents acute lung injury in a rat cardiopulmonary bypass model.

anti FAS IgG1 (monoclonal Goat Anti-Human, Mouse, R Goat Anti-Human, Mouse, R Goat Anti-Human, Rat CHRN RANK Ligand Soluble, Huma RANK Ligand Soluble, Huma RANK Ligand Soluble, Huma Integrin β1 (CD29) Antib Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe

Related Pathways

paperclip

#28639431   2017/06/22 Save this To Up

Decrease in Oxidative Stress Parameters after Post-Ischaemic Recombinant Human Erythropoietin Administration in the Hippocampus of Rats Exposed to Focal Cerebral Ischaemia.

Recombinant human erythropoietin (rhEpo) is a multi-functional drug with antioxidant potential. However, the underlying molecular mechanisms of its action are still unclear. The purpose of this study was to investigate the effects of rhEpo on the brain infarct volume as well as on the levels of the neuronal damage, oxidative stress parameters and active caspase-3, nuclear factor erythroid 2-related factor 2 (Nrf2) and haemeoxygenase-1 (HO-1) expressions in the hippocampi of rats exposed to the right middle cerebral artery occlusion (MCAO) for 1 hr. Ischaemic animals received either vehicle or rhEpo (5000 IU/kg, i.p.) immediately or 3 hr after the induction of ischaemia. Sham-operated, vehicle-treated animals served as the control group. Rats were killed 24 hr after the onset of the ischaemic or sham experimental procedure. MCAO caused ipsilateral brain infarction within the striatum and cortex. In the CA1 region of the hippocampi, we did not find significant neuronal loss, but a statistically significant rise in the active caspase-3 and Nrf2 protein expressions was registered. We detected also significant increases in the hippocampal levels of oxidative stress parameters (thiobarbituric acid-reactive substances, superoxide dismutase, glutathione peroxidase). Post-ischaemic administration of rhEpo significantly reduced the brain infarct volume, decreased levels of all tested oxidative stress parameters and increased the Nrf2 expression level. These findings suggest that decrease in oxidative stress parameters in the hippocampus could be an early indicator of post-ischaemic neuroprotective effect of rhEpo in rats exposed to focal cerebral ischaemia and that this effect could be attributable to additional post-ischaemic activation of Nrf2 endogenous antioxidant system.

2109 related Products with: Decrease in Oxidative Stress Parameters after Post-Ischaemic Recombinant Human Erythropoietin Administration in the Hippocampus of Rats Exposed to Focal Cerebral Ischaemia.

Recombinant Human Interfe Macrophage Colony Stimula Macrophage Colony Stimula Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interfe Recombinant Human Interle Recombinant Human Interle Recombinant Human Interle

Related Pathways

paperclip

#28495827   2017/05/12 Save this To Up

Hyperbaric Oxygen Reduces Infarction Volume and Hemorrhagic Transformation Through ATP/NAD(+)/Sirt1 Pathway in Hyperglycemic Middle Cerebral Artery Occlusion Rats.

Energy depletion is a critical factor leading to cell death and brain dysfunction after ischemic stroke. In this study, we investigated whether energy depletion is involved in hyperglycemia-induced hemorrhagic transformation after ischemic stroke and determined the pathway underlying the beneficial effects of hyperbaric oxygen (HBO).

2403 related Products with: Hyperbaric Oxygen Reduces Infarction Volume and Hemorrhagic Transformation Through ATP/NAD(+)/Sirt1 Pathway in Hyperglycemic Middle Cerebral Artery Occlusion Rats.

SIRT1 Inhibitor, EX 527 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 Cancer Apoptosis Phospho- Cell Cycle Phospho-Specif Chromatin Transcription P CREB Phospho-Specific Arr

Related Pathways

paperclip

#28465353   2017/05/03 Save this To Up

TRIM24 protein promotes and TRIM32 protein inhibits cardiomyocyte hypertrophy via regulation of dysbindin protein levels.

We have previously shown that dysbindin is a potent inducer of cardiomyocyte hypertrophy via activation of Rho-dependent serum-response factor (SRF) signaling. We have now performed a yeast two-hybrid screen using dysbindin as bait against a cardiac cDNA library to identify the cardiac dysbindin interactome. Among several putative binding proteins, we identified tripartite motif-containing protein 24 (TRIM24) and confirmed this interaction by co-immunoprecipitation and co-immunostaining. Another tripartite motif (TRIM) family protein, TRIM32, has been reported earlier as an E3 ubiquitin ligase for dysbindin in skeletal muscle. Consistently, we found that TRIM32 also degraded dysbindin in neonatal rat ventricular cardiomyocytes as well. Surprisingly, however, TRIM24 did not promote dysbindin decay but rather protected dysbindin against degradation by TRIM32. Correspondingly, TRIM32 attenuated the activation of SRF signaling and hypertrophy due to dysbindin, whereas TRIM24 promoted these effects in neonatal rat ventricular cardiomyocytes. This study also implies that TRIM32 is a key regulator of cell viability and apoptosis in cardiomyocytes via simultaneous activation of p53 and caspase-3/-7 and inhibition of X-linked inhibitor of apoptosis. In conclusion, we provide here a novel mechanism of post-translational regulation of dysbindin and hypertrophy via TRIM24 and TRIM32 and show the importance of TRIM32 in cardiomyocyte apoptosis in vitro.

2634 related Products with: TRIM24 protein promotes and TRIM32 protein inhibits cardiomyocyte hypertrophy via regulation of dysbindin protein levels.

HTLV 1 gp21 recombinant p Allergens, Phospholipase anti FAS IgG1 (monoclonal Viral antibodies, anti-H Anti PDX1 Polyclonal Anti Rabbit Anti-Rat Androgen Recombinant Human Androge Myelin Basic Protein Heat Shock Protein 70 (H Heat Shock Protein 70 (H nm23 (NDPK-A Protein); C nm23 (NDPK-A Protein); C

Related Pathways