scholarly journals Protective Effect of Salvia miltiorrhiza on Angiotensin II-Induced Hypertrophic Responses in Neonatal Rat Cardiac Cells

2001 ◽  
Vol 87 (4) ◽  
pp. 289-296 ◽  
Author(s):  
XinShou Ouyang ◽  
Kyoko Takahashi ◽  
Katsuko Komatsu ◽  
Norio Nakamura ◽  
Masao Hattori ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Protective Effect ◽  
Salvia Miltiorrhiza ◽  
Cardiac Cells ◽  
Neonatal Rat

Effect of Taurine on Angiotensin II-Induced Hypertrophy of Neonatal Rat Cardiac Cells

1997 ◽  
Vol 30 (6) ◽  
pp. 725-730 ◽  
Author(s):  
Kyoko Takahashi ◽  
Mitsuhiro Azuma ◽  
Koki Taira ◽  
Akemichi Baba ◽  
Isamu Yamamoto ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Cells ◽  
Neonatal Rat

Abstract 152: IL-10 Inhibits Angiotensin II-induced Pathological Autophagy in Myocardium.

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Suresh K Verma ◽  
Prasanna Krishnamurthy ◽  
Tatiana Abramova ◽  
Garikipati Srikanth ◽  
Mohsin Khan ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Fluorescent Protein ◽  
Heart Function ◽  
Cardiac Cells ◽  
Neonatal Rat ◽  
Autophagic Flux ◽  
Protective Effects ◽  
Ang Ii ◽  
Akt Inhibitor

Background: In heart, persistent pressure overload causes pathological autophagy leading to cardiac cell death and heart failure. The role IL-10, a pleiotropic anti-inflammatory cytokine, on pathological autophagy is largely unknown. Here we hypothesized that IL-10 inhibits stress-induced pathological autophagy and therefore attenuates cardiac cells death and improve heart function. Method and Results: Cardiac stress was induced in C57 BL/6 mice by Angiotensin II treatment (Ang II-1.2mg.kg b.wt/day for 28 days) using mini osmotic pumps. Ang II treatment markedly induced autophagy in mice as measured by electron microscopy (autophagosome numbers) and Western blotting (Becline1 and LC3II proteins expression). Interestingly, systemic recombinant mouse IL-10 administration markedly inhibited Ang II-induced autophagy. To further understand the mechanism of IL-10 protection, neonatal rat ventricular myocytes (NRCM) were transfected with monomeric Red Fluorescent Protein-Enhanced Green Fluorescent Protein (mRFP-EGFP) tandem fluorescent-tagged LC3 (tfLC3) adenovirus (to measure autophagic flux) and then treated with AngII (1μM) and/or IL-10 (20ng/mL), in vitro. Ang II treatment significantly increased the numbers of both yellow (merged EGFP and mRFP signals) and red puncta, indicating active formation of both autophagosomes and autolysosomes, however, this flux was strongly inhibited by IL-10. Furthermore, Ang II significantly increased the Beclin1 and LC3II proteins expression, which was markedly reduced by IL-10 as measured by Western blot analysis. In addition, Ang II-inhibited AKT signaling (anti-autophagic signaling component) was strongly enhanced by IL-10. Ang II-induced autophagic signaling was mimicked by AKT inhibitor, suggesting AKT as the downstream target of IL-10 effects. Conclusion: Inhibition of pathological autophagy is a novel mechanism for cardio-protective effects of IL-10.

scholarly journals Angiotensin II-induced protein tyrosine phosphorylation in neonatal rat cardiac fibroblasts.

1994 ◽  
Vol 269 (30) ◽  
pp. 19626-19632
Author(s):  
W. Schorb ◽  
T.C. Peeler ◽  
N.N. Madigan ◽  
K.M. Conrad ◽  
K.M. Baker
Keyword(s):  
Angiotensin Ii ◽  
Tyrosine Phosphorylation ◽  
Cardiac Fibroblasts ◽  
Neonatal Rat ◽  
Protein Tyrosine Phosphorylation ◽  
Protein Tyrosine

scholarly journals Protective effect of Salvia miltiorrhiza Bunge on 5-fluorouracil-induced oral mucositis

2017 ◽  
Vol 40 (1) ◽  
pp. 39-46 ◽  
Author(s):  
Do Rim Kim ◽  
Jinsung Kim ◽  
Ja Young Oh ◽  
Ha Young Kim ◽  
Young Joo Kim ◽  
...  
Keyword(s):  
Protective Effect ◽  
Oral Mucositis ◽  
Salvia Miltiorrhiza ◽  
Salvia Miltiorrhiza Bunge

Abstract 180: Synergistic Salutary Effects of HMG-CoA Reductase Inhibitor and Angiotensin II Receptor Blocker on Load-induced Heart Failure

2014 ◽  
Vol 115 (suppl_1) ◽  
Author(s):  
Yasuhiro Maejima ◽  
Mitsuaki Isobe
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Reductase Inhibitor ◽  
Neonatal Rat ◽  
Receptor Blocker ◽  
Angiotensin Ii Receptor Blocker ◽  
Angiotensin Ii Receptor ◽  
Hmg Coa Reductase ◽  
Hmg Coa Reductase Inhibitor ◽  
Coa Reductase

We have shown previously that combined HMG-CoA reductase inhibitor (statin) and angiotensin II receptor blocker (ARB) therapy significantly improves both symptoms and left ventricular (LV) function over time in patients with heart failure (HF) by a clinical study [ HF-COSTAR Trial]. We elucidated the mechanisms of combination therapy with the ARB (losartan, LOS) and long-acting and statin (simvastatin, SIM) for the treatment of load-induced heart failure. Salt-loaded Dahl salt-sensitive (DS) rats were treated with vehicle, LOS (5mg/kg/day), SIM (2mg/kg/day) and LOS + SIM for 16 weeks. LOS and SIM in combination improved LV dysfunction (ΔLV fractional shortening; LOS = 60%, SIM = 42%, LOS + SIM = 24%, p <0.05), limited LV hypertrophy (ΔLV septal thickness; LOS = −21%, SIM = −18%, LOS + SIM = −13%, p <0.05) and reduced cardiac fibrosis (ΔLV collagen density; LOS = −26%, SIM = −16%, LOS + SIM = −28%, p <0.05) more than LOS or SIM alone. Both Rho and matrix metalloprotease-9 (MMP-9) activity in LV tissue were increased in untreated DS rats, and LOS and SIM in combination decreased these changes more than did LOS and SIM monotherapies. We confirmed that the plasma level of Exp-3174 (E3174), a LOS metabolite and a potent inverse agonist of angiotensin II receptor type 1, was higher in rats treated with LOS and SIM in combination than in those treated with LOS alone (E3174/LOS ratio; LOS = 2.6 ± 0.3 vs. LOS + SIM = 3.2 ± 0.2, p <0.05). Next, to mimic the response of volume-overload heart failure in vitro , cultured neonatal rat cardiomyocytes (CMs) were cyclically stretched. Stretch-induced increased CM hypertrophy was suppressed by pretreatment with both SIM and E3174 more than by pretreatment with LOS, E3174, SIM, or LOS and SIM in combination. Mechanical stretch also induced activation of extracellular signal regulated kinase (ERK) and the stretch-induced ERK activation of CMs was also significantly suppressed by SIM + E3174. In conclusion, LOS and SIM had beneficial myocardial effects in rats with salt-sensitive hypertension, partly through promoting the accumulation of plasma E3174. SIM enhanced the myocardial protective effects of LOS through suppression of Rho and MMP-9 activity. Thus, a combination of ARB with statin has a promising potential as a therapeutic strategy for HF.

scholarly journals Preparation and Biological Activity of the Monoclonal Antibody against the Second Extracellular Loop of the Angiotensin II Type 1 Receptor

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Mingming Wei ◽  
Chengrui Zhao ◽  
Suli Zhang ◽  
Li Wang ◽  
Huirong Liu ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Biological Activity ◽  
Angiotensin Ii ◽  
Abdominal Cavity ◽  
Beat Frequency ◽  
Neonatal Rat ◽  
Logarithmic Phase ◽  
Extracellular Loop ◽  
Mouse Ascites

The current study was to prepare a mouse-derived antibody against the angiotensin II type 1 receptor (AT1-mAb) based on monoclonal antibody technology, to provide a foundation for research on AT1-AA-positive diseases. Balb/C mice were actively immunized with the second extracellular loop of the angiotensin II type 1 receptor (AT1R-ECII). Then, mouse spleen lymphocytes were fused with myeloma cells and monoclonal hybridomas that secreted AT1-mAb were generated and cultured, after which those in logarithmic-phase were injected into the abdominal cavity of mice to retrieve the ascites. Highly purified AT1-mAb was isolated from mouse ascites after injection with 1 × 107hybridomas. A greater amount of AT1-mAb was purified from mouse ascites compared to the cell supernatant of hybridomas. AT1-mAb purified from mouse ascites constricted the thoracic aorta of mice and increased the beat frequency of neonatal rat myocardial cells via the AT1R, identical to the effects of AT1-AA extracted from patients’ sera. Murine blood pressure increased after intravenous injection of AT1-mAb via the tail vein. High purity and good biological activity of AT1-mAb can be obtained from mouse ascites after intraperitoneal injection of monoclonal hybridomas that secrete AT1-mAb. These data provide a simple tool for studying AT1-AA-positive diseases.

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