scholarly journals Olmesartan, an AT1 Antagonist, Attenuates Oxidative Stress, Endoplasmic Reticulum Stress and Cardiac Inflammatory Mediators in Rats with Heart Failure Induced by Experimental Autoimmune Myocarditis

2011 ◽  
Vol 7 (2) ◽  
pp. 154-167 ◽  
Author(s):  
Vijayakumar Sukumaran ◽  
Kenichi Watanabe ◽  
Punniyakoti T. Veeraveedu ◽  
Narasimman Gurusamy ◽  
Meilei Ma ◽  
...  
2012 ◽  
Vol 50 (2) ◽  
pp. 139-144 ◽  
Author(s):  
Somasundaram Arumugam ◽  
Rajarajan A. Thandavarayan ◽  
Punniyakoti T. Veeraveedu ◽  
Meilei Ma ◽  
Vijayasree V. Giridharan ◽  
...  

2017 ◽  
Vol 23 (1) ◽  
pp. 89-97 ◽  
Author(s):  
Monika Skrzypiec-Spring ◽  
Katarzyna Haczkiewicz ◽  
Agnieszka Sapa ◽  
Tomasz Piasecki ◽  
Joanna Kwiatkowska ◽  
...  

Aims: Acute myocarditis is a potentially lethal inflammatory heart disease that frequently precedes the development of dilated cardiomyopathy and subsequent heart failure. At present, there is no effective standardized therapy for acute myocarditis, besides the optimal care of heart failure and arrhythmias in accordance with evidence-based guidelines and specific etiology-driven therapy for infectious myocarditis. Carvedilol has been shown to be cardioprotective by reducing cardiac pro-inflammatory cytokines present in oxidative stress in certain heart diseases. However, effects of carvedilol administration in acute myocarditis with its impact on matrix metalloproteinases’ (MMPs) activation have not been elucidated. Methods and Results: Carvedilol in 3 doses (2, 10, and 30 mg/kg) was given daily to 3 study groups of rats (n = 8) with experimental autoimmune myocarditis by gastric gavage for 3 weeks. In comparison to untreated rats (n = 8) with induced myocarditis, carvedilol significantly prevented the left ventricle enlargement and/or systolic dysfunction depending on the dose in study groups. Performed zymography showed enhanced MMP-2 activity in untreated rats, while carvedilol administration reduced alterations. This was accompanied by prevention of troponin I release and myofilaments degradation in cardiac muscle tissue. Additionally, severe inflammatory cell infiltration was detected in the nontreated group. Carvedilol in all doses tested, had no impact on severity of inflammation. The severity of inflammation did not differ between study groups and in relation to the untreated group. Conclusions: The protective effects of carvedilol on heart function observed in the acute phase of experimental autoimmune myocarditis seem to be associated with its ability to decrease MMP-2 activity and subsequently prevent degradation of myofilaments and release of troponin I while not related to suppression of inflammation.


2013 ◽  
Vol 31 (6) ◽  
pp. 352-362 ◽  
Author(s):  
Somasundaram Arumugam ◽  
Sayaka Mito ◽  
Rajarajan A. Thandavarayan ◽  
Vijayasree V. Giridharan ◽  
Vigneshwaran Pitchaimani ◽  
...  

2010 ◽  
Vol 33 (3) ◽  
pp. 477-486 ◽  
Author(s):  
Yoshiki Sanzen ◽  
Minami Ito ◽  
Yoshimi Ohta ◽  
Yutaka Yoshida ◽  
Tomie Kawada ◽  
...  

2012 ◽  
Vol 351 (2) ◽  
pp. 208-219 ◽  
Author(s):  
Vijayakumar Sukumaran ◽  
Punniyakoti T. Veeraveedu ◽  
Narasimman Gurusamy ◽  
Arun Prasath Lakshmanan ◽  
Ken’ichi Yamaguchi ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Yuanyang Chen ◽  
Sihao Zheng ◽  
Zhiwei Wang ◽  
Xin Cai ◽  
Yanjia Che ◽  
...  

Background. Heart transplantation (HT) is the only effective treatment for end-stage heart failure because it can effectively improve the survival rate and quality of life of patients with heart failure. Artesunate (ART) is an artemisinin derivative, with good water solubility and higher oral bioavailability. The main aim of this study was to determine the role of ART in HT mice. Methods. In animal experiments, mice were divided into the control group, HT group, low ART+HT group, and high ART+HT group. Next, inflammatory cell infiltration, oxidative stress injury, and myocardial cell apoptosis were determined in heart tissue. The proportion of multiple lymphocytes in spleen and lymph nodes was then determined using flow cytometry. In addition, cell experiments were conducted to determine the changes in expression of surface maturation markers of BMDC and changes in intracellular reactive oxygen species after LPS stimulation. Finally, western blot analysis was performed to determine the levels of endoplasmic reticulum stress-related proteins (CHOP/ATF4/PERK). Results. The survival time of mice in the ART treatment group was significantly prolonged and was positively correlated with the dose. In animal experiments, ART significantly reduced inflammatory cell infiltration in heart tissue and the proportion of CD4+CD8+ T cells in spleens and lymph nodes. Moreover, ART treatment lowered the 8-OHdg in hearts and myocardial apoptosis. In cell experiments, ART treatment slowed down the development and maturation of BMDCs by inhibiting the expression of endoplasmic reticulum stress-related proteins. Furthermore, the treatment alleviated the oxidative stress damage of BMDCs. Conclusion. ART can inhibit maturation of dendritic cells through the endoplasmic reticulum stress signaling pathway, thereby alleviating acute rejection in mice after heart transplantation.


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