Mangiferin protect myocardial insults through modulation of MAPK/TGF-β pathways

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• 作者：Kapil Suchal^a ; ¹ ; Salma Malik^a ; ¹ ; Nanda Gamad^a ; Rajiv Kumar Malhotra^a ; Sameer N. Goyal^b ; Shreesh Ojha^c ; Santosh Kumari^d ; Jagriti Bhatia^a ; Dharamvir Singh Arya^a ; ^{dsarya16@gmail.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：CAT ; catalase ; DAP ; diastolic arterial pressure ; ERK1/2 ; extracellular regulated kinase 1/2 ; GSH ; reduced glutathione ; IL-6 ; interleukin-6 ; IR ; ischemia-reperfusion ; JNK ; c-Jun NH2 terminal kinase ; MNG ; mangiferin ; LVEDP ; left ventricular end diastolic pressure ; ± ; LVdP/dt ; rate of change of pressure development ; MAP ; mean arterial pressure ; MAPK ; mitogen activated protein kinase ; MDA ; malondialdehyde ; SAP ; systolic arterial pressure ; SOD ; superoxide dismutase ; TGF-β ; transforming growth fa
• 刊名：European Journal of Pharmacology
• 出版年：2016
• 出版时间：5 April 2016
• 年：2016
• 卷：776
• 期：Complete
• 页码：34-43
• 全文大小：3413 K

文摘

Mangiferin, a xanthone glycoside isolated from leaves of Mangifera indica (Anacardiaceae) is known to modulate many biological targets in inflammation and oxidative stress. The present study was designed to investigate whether mangiferin exerts protection against myocardial ischemia-reperfusion (IR) injury and possible role of Mitogen Activated Protein Kinase (MAPKs) and Transforming Growth Factor-β (TGF-β) pathways in its cardioprotection. Male albino Wistar rats were treated with mangiferin (40 mg/kg, i.p.) for 15 days. At the end of the treatment protocol, rats were subjected to IR injury consisting of 45 min ischemia followed by 1 h reperfusion. IR-control rats caused significant cardiac dysfunction, increased serum cardiac injury markers, lipid peroxidation and a significant decrease in tissue antioxidants as compared to sham group. Histopathological examination of IR rats revealed myocardial necrosis, edema and infiltration of inflammatory cells. However, pretreatment with mangiferin significantly restored myocardial oxidant-antioxidant status, maintained membrane integrity, and attenuated the levels of proinflammatory cytokines, pro-apoptotic proteins and TGF-β. Furthermore, mangiferin significantly reduced the phosphorylation of p38, and JNK and enhanced phosphorylation of ERK1/2. These results suggest that mangiferin protects against myocardial IR injury by modulating MAPK mediated inflammation and apoptosis.