Regulation of endothelial nitric oxide synthase and asymmetric dimethylarginine by matrine attenuates isoproterenol-induced acute myocardial injury in rats

Li, Xiaobing; Wang, Xiao; Guo, Yafang; Deng, Ning; Zheng, Ping; Chen, Nansheng; Wu, Yang; Dai, Guidong

doi:10.1111/j.2042-7158.2012.01502.x

Cited by 29 publications

(32 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this study, matrine was given for the longest duration in comparison to previous reports [28,38], and matrine-treated rats appeared to have a significantly lower mean body weight from week 5 to the end of the experiment. These data raise concerns about the toxicity of matrine.…”

Section: Discussionmentioning

confidence: 98%

“…Our previous studies demonstrated that oral administration of matrine (50 and 100 mg/kg) was beneficial for the prevention of isoproterenol-induced myocardial infarction in rats [28,38], which suggests that matrine may offer advantages in terms of cardiovascular events over COX-2 inhibitors. Lubet et al [6] suggested that most or all of the efficacy of chemopreventive compounds occurs later than the initiation phase in this model.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Suppressive Effect of Matrine on Tumor Invasion in N-Butyl-N-(4-Hydroxybutyl)Nitrosamine-Induced Urinary Bladder Carcinogenesis

Gao¹,

Guo

Deng³

et al. 2014

Chemotherapy

Self Cite

View full text Add to dashboard Cite

Aims: This study was designed to investigate the mechanisms and suppressive effects of matrine on the development of urinary bladder cancers induced by N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in rats. Methods: Male Sprague-Dawley rats were given BBN (200 mg/rat) twice a week for a period of 8 weeks. Oral administration of matrine (50 and 100 mg/kg) was started 1 week before BBN exposure for 35 weeks. Half of each bladder was histopathologically analyzed and the remainder was extracted for protein analysis by Western blot. Results: The bladders of BBN-treated rats demonstrated progression from epithelial hyperplasia to papillary urothelial neoplasia and even poorly differentiated invasive cancer. Matrine (50 and 100 mg/kg) treatment decreased the formation of large bladder tumors by 31.6 and 21.1%, respectively. An incidence of cancer cells was detected in rats given BBN [70% (14/20)] and matrine [50 mg/kg: 68.4% (13/19) and 100 mg/kg: 57.9% (11/19), respectively]. The frequency of invasive tumors in the matrine treatment groups [50 mg/kg: 15.4% (2/13), 100 mg/kg: 9.1% (1/11)] was significantly lower than in the BBN-alone group [57% (8/14)]. Furthermore, oral administration of matrine (50 and 100 mg/kg) markedly attenuated the BBN-induced upregulation of bladder cyclooxygenase-2 (COX-2) expression and the elevation of bladder cytosolic phospholipase A2 (cPLA2) levels. Although the contents of 15-prostaglandin dehydrogenase (PGDH), which degrades PGE₂, were dramatically reduced by BBN, matrine exerted no effects on reduced PGDH contents. Conclusion: Our results suggest that matrine suppressed bladder tumor invasion in a rat model, and this might be primarily mediated through regulation of the protein contents, COX-2 and cPLA2 in the bladder.

show abstract

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Suppressive Effect of Matrine on Tumor Invasion in N-Butyl-N-(4-Hydroxybutyl)Nitrosamine-Induced Urinary Bladder Carcinogenesis

Gao¹,

Guo

Deng³

et al. 2014

Chemotherapy

Self Cite

View full text Add to dashboard Cite

show abstract

“…It is well documented that rats treated with low (0.02-3.0 mg/kg) doses of isoproterenol was a useful model to assess the mechanisms of myocardial growth and the progression of cardiac diseases, 28 whereas subcutaneous injection of very large (20-100 mg/kg) doses of isoproterenol to experiment animals were found to induce subendocardial myocardial ischemia, hypoxia, necrosis, and finally fibroblastic hyperplasia, and the pathophysiological and morphologic alterations in the heart of this noncoronary myocardial necrotic rat model were comparable with those taking place in human myocardial infarction. 21,22,28,29 In our study, acute myocardial injury was induced in rats by subcutaneous injection of 85 mg/kg of isoproterenol daily for two consecutive days, [21][22][23][24]29 and the efficacy of betaine on protecting the heart against myocardial infarction were observed on this noninvasive myocardial necrotic rat model.…”

Section: Discussionmentioning

confidence: 99%

“…[21][22][23] Therefore, the aim of this work was to investigate the cardioprotective effects of betaine on the regulation of the STAT3 and apoptotic pathway.…”

Section: Introductionmentioning

confidence: 99%

Regulation of signal transducer and activator of transcription 3 and apoptotic pathways by betaine attenuates isoproterenol-induced acute myocardial injury in rats

et al. 2014

View full text Add to dashboard Cite

The present study was designed to investigate the cardioprotective effects of betaine on acute myocardial ischemia induced experimentally in rats focusing on regulation of signal transducer and activator of transcription 3 (STAT3) and apoptotic pathways as the potential mechanism underlying the drug effect. Male Sprague Dawley rats were treated with betaine (100, 200, and 400 mg/kg) orally for 40 days. Acute myocardial ischemic injury was induced in rats by subcutaneous injection of isoproterenol (85 mg/kg), for two consecutive days. Serum cardiac marker enzyme, histopathological variables and expression of protein levels were analyzed. Oral administration of betaine (200 and 400 mg/kg) significantly reduced the level of cardiac marker enzyme in the serum and prevented left ventricular remodeling. Western blot analysis showed that isoproterenol-induced phosphorylation of STAT3 was maintained or further enhanced by betaine treatment in myocardium. Furthermore, betaine (200 and 400 mg/kg) treatment increased the ventricular expression of Bcl-2 and reduced the level of Bax, therefore causing a significant increase in the ratio of Bcl-2/Bax. The protective role of betaine on myocardial damage was further confirmed by histopathological examination. In summary, our results showed that betaine pretreatment attenuated isoproterenol-induced acute myocardial ischemia via the regulation of STAT3 and apoptotic pathways.

show abstract

“…Therefore, ISOinduced myocardial injury serves as a well-standardized model to study the beneficial effects of many drugs [6]. The mechanism of action of ISO has been linked to its ability to deplete the energy reserve of the myocardium and to induce severe oxidative stress, resulting in necrotic lesions in the myocardium [7,8]. Hence, antioxidative agents may play an important role in ameliorating ISO-induced toxicity.…”

Section: Introductionmentioning

confidence: 99%

Kolaviron, a biflavonoid fraction from Garcinia kola, protects against isoproterenol-induced injury by mitigating cardiac dysfunction and oxidative stress in rats

Adaramoye

Lawal

2014

Journal of Basic and Clinical Physiology and Pharmacology

View full text Add to dashboard Cite

show abstract

Regulation of endothelial nitric oxide synthase and asymmetric dimethylarginine by matrine attenuates isoproterenol-induced acute myocardial injury in rats

Abstract: Our results suggested that matrine protects against isoproterenol-induced myocardial ischaemia via eNOS and ADMA pathway.

Cited by 29 publications

References 45 publications

Suppressive Effect of Matrine on Tumor Invasion in N-Butyl-N-(4-Hydroxybutyl)Nitrosamine-Induced Urinary Bladder Carcinogenesis

Suppressive Effect of Matrine on Tumor Invasion in N-Butyl-N-(4-Hydroxybutyl)Nitrosamine-Induced Urinary Bladder Carcinogenesis

Regulation of signal transducer and activator of transcription 3 and apoptotic pathways by betaine attenuates isoproterenol-induced acute myocardial injury in rats

Kolaviron, a biflavonoid fraction from Garcinia kola, protects against isoproterenol-induced injury by mitigating cardiac dysfunction and oxidative stress in rats

Contact Info

Product

Resources

About