Molecular and biochemical evidence on the protective effects of embelin and carnosic acid in isoproterenol-induced acute myocardial injury in rats

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• 作者：Cengiz Kocak^a ; ^{drcengizkocak@hotmail.com" class="auth_mail" title="E-mail the corresponding author} ; Fatma Emel Kocak^b ; Raziye Akcilar^c ; Ozben Ozden Isiklar^d ; Havva Kocak^b ; Zeynep Bayat^e ; Hasan Simsek^c ; Figen Taser^f ; Irfan Altuntas^b
• 关键词：Carnosic acid (PubChem CID ; 65126) ; Embelin (PubChem CID ; 3218) ; Isoproterenol hydrochloride (PubChem CID ; 5807) ; 2 ; 3 ; 5-Triphenyltetrazolium chloride (PubChem CID ; 9283) ; Tween 80 (PubChem CID ; 5281955)
• 刊名：Life Sciences
• 出版年：2016
• 出版时间：15 February 2016
• 年：2016
• 卷：147
• 期：Complete
• 页码：15-23
• 全文大小：2520 K

文摘

Acute myocardial infarction is a serious acute cardiac disorder and heart disease is still a major public health problem in adults. We investigated the effects of embelin (EMB) and carnosic acid (CA) in animals with isoproterenol (ISO)-induced myocardial injury.

Main methods

Adult male Wistar–Albino rats were divided into four groups: control, ISO, ISO with EMB, and ISO with CA. Before myocardial injury was induced, drugs were administered by oral gavage. Myocardial injury was induced by subcutaneous injection of ISO hydrochloride for 2 consecutive days. Serum cardiac troponin I (cTnI), ischemia modified albumin (IMA), heart fatty acid binding protein (HFABP) levels and paraoxonase-1 (PON-1) activity, tissue total oxidant status (TOS), total antioxidant status (TAS), total thiol (TT), tumor necrosis factor-α (TNF-α) levels, superoxide dismutase (SOD) activity, and glutathione peroxidase (GSH-Px) activity were measured. Tissue mRNA expression levels of nuclear factor-kappa B (NF-κB), P38 mitogen-activated protein kinase (p38 MAPK), and nuclear factor erythroid 2-related factor 2 (Nrf2) were analyzed. In addition, cardiac tissues were evaluated histopathologically and immunohistochemically.

Key findings

All tested compounds reduced myocardial damage, apoptosis, cTnI, IMA, HFABP, TOS, and TNF-α levels, NF-κB, p38 MAPK, and phosphorylated c-Jun N-terminal protein kinase (pJNK 1/2) expressions. All tested compounds increased SOD activity, GSH-Px activity, TAS levels, TT levels, phosphorylated extracellular signal-regulated kinase (pERK 1/2), and Nrf2 expressions.

Significance

Our results suggest that EMB and CA pretreatment could reduce myocardial injury via antiinflammatory, antioxidant, and antiapoptotic effects.