Baicalein pretreatment confers cardioprotection against acute myocardial infarction by activating the endothelial nitric oxide synthase signaling pathway and inhibiting oxidative stress

Tan,Shengyu; Zhou,Shenghua; Luo,Yingquan

doi:10.3892/mmr.2014.2091

Baicalein pretreatment confers cardioprotection against acute myocardial infarction by activating the endothelial nitric oxide synthase signaling pathway and inhibiting oxidative stress

Authors:
- Shengyu Tan
- Shenghua Zhou
- Yingquan Luo
View Affiliations

Affiliations: Department of Geriatrics, Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China, Department of Cardiology, Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China
Published online on: March 28, 2014 https://doi.org/10.3892/mmr.2014.2091
Pages: 2429-2434

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )

Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )

Cited By (CrossRef): 0 citations Loading Articles...

Abstract

Baicalein, a flavonoid purified from the root of Scutellaria baicalensis Georgi, is well known for its anti‑inflammatory and anti‑oxidative properties. The present study aimed to evaluate the cardioprotective effect of baicalein in a rat model of acute myocardial infarction and investigate the potential molecular mechanisms of this effect. The acute myocardial infarction model was prepared by permanently occluding the left anterior descending artery. Baicalein and/or the endothelial nitric oxide synthase (eNOS) inhibitor L‑NAME was injected prior to the induction of acute myocardial infarction. In the vehicle‑treated group, acute myocardial infarction resulted in a markedly increased infarction size and elevated levels of plasma cardiac enzymes, including creatine kinase, the MB isoenzyme of creatine kinase, lactate dehydrogenase and cardiac troponin T, compared with those in the sham‑surgery group. In the baicalein treatment group, the infarcted area and plasma levels of the cardiac enzymes were significantly decreased compared with those in the vehicle‑treated group. In addition, pretreatment with baicalein potently increased the levels of eNOS protein and nitric oxide production in the infarcted rats. Furthermore, myocardial oxidative stress was attenuated by baicalein preconditioning following acute myocardial infarction. However, L‑NAME inihibted the cardioprotective effects of baicalein. These data indicate that baicalein protects against acute myocardial infarction‑induced injury by activating eNOS signaling and inhibiting oxidative stress.

View Figures

View References

1	Bulhak AA, Sjöquist PO, Xu CB, Edvinsson L and Pernow J: Protection against myocardial ischaemia/reperfusion injury by PPAR-alpha activation is related to production of nitric oxide and endothelin-1. Basic Res Cardiol. 101:244–252. 2006. View Article : Google Scholar
2	Gourine AV, Bulhak AA, Gonon AT, Pernow J and Sjöquist PO: Cardioprotective effect induced by brief exposure to nitric oxide before myocardial ischemia-reperfusion in vivo. Nitric Oxide. 7:210–216. 2002. View Article : Google Scholar : PubMed/NCBI
3	Andelová E, Barteková M, Pancza D, Styk J and Ravingerová T: The role of NO in ischemia/reperfusion injury in isolated rat heart. Gen Physiol Biophys. 24:411–426. 2005.PubMed/NCBI
4	Balligand JL and Cannon PJ: Nitric oxide synthases and cardiac muscle. Autocrine and paracrine influences. Arterioscler Thromb Vasc Biol. 17:1846–1858. 1997. View Article : Google Scholar : PubMed/NCBI
5	Jones SP, Greer JJ, van Haperen R, Duncker DJ, de Crom R and Lefer DJ: Endothelial nitric oxide synthase overexpression attenuates congestive heart failure in mice. Proc Natl Acad Sci USA. 100:4891–4896. 2003. View Article : Google Scholar : PubMed/NCBI
6	Sumeray MS, Rees DD and Yellon DM: Infarct size and nitric oxide synthase in murine myocardium. J Mol Cell Cardiol. 32:35–42. 2000. View Article : Google Scholar : PubMed/NCBI
7	Jones SP, Girod WG, Palazzo AJ, et al: Myocardial ischemia-reperfusion injury is exacerbated in absence of endothelial cell nitric oxide synthase. Am J Physiol. 276:H1567–H1573. 1999.PubMed/NCBI
8	Carden DL and Granger DN: Pathophysiology of ischaemia-reperfusion injury. J Pathol. 190:255–266. 2000. View Article : Google Scholar : PubMed/NCBI
9	Collard CD and Gelman S: Pathophysiology, clinical manifestations, and prevention of ischemia-reperfusion injury. Anesthesiology. 94:1133–1138. 2001. View Article : Google Scholar : PubMed/NCBI
10	Panda VS and Naik SR: Cardioprotective activity of Ginkgo biloba Phytosomes in isoproterenol-induced myocardial necrosis in rats: a biochemical and histoarchitectural evaluation. Exp Toxicol Pathol. 60:397–404. 2008.
11	Priscilla DH and Prince PS: Cardioprotective effect of gallic acid on cardiac troponin-T, cardiac marker enzymes, lipid peroxidation products and antioxidants in experimentally induced myocardial infarction in Wistar rats. Chem Biol Interact. 179:118–124. 2009. View Article : Google Scholar
12	Lin CC and Shieh DE: The anti-inflammatory activity of Scutellaria rivularis extracts and its active components, baicalin, baicalein and wogonin. Am J Chin Med. 24:31–36. 1996.
13	Gabrielska J, Oszmiański J, Zyłka R and Komorowska M: Antioxidant activity of flavones from Scutellaria baicalensis in lecithin liposomes. Z Naturforsch C. 52:817–823. 1997.
14	Shao ZH, Vanden Hoek TL, Qin Y, et al: Baicalein attenuates oxidant stress in cardiomyocytes. Am J Physiol Heart Circ Physiol. 282:H999–H1006. 2002.PubMed/NCBI
15	Woo AY, Cheng CH and Waye MM: Baicalein protects rat cardiomyocytes from hypoxia/reoxygenation damage via a prooxidant mechanism. Cardiovasc Res. 65:244–253. 2005. View Article : Google Scholar : PubMed/NCBI
16	Yu W, Liu Q and Zhu S: Carvacrol protects against acute myocardial infarction of rats via anti-oxidative and anti-apoptotic pathways. Biol Pharm Bull. 36:579–584. 2013. View Article : Google Scholar : PubMed/NCBI
17	Kuo CP, Wen LL, Chen CM, et al: Attenuation of neurological injury with early baicalein treatment following subarachnoid hemorrhage in rats. J Neurosurg. 199:1028–1037. 2013.PubMed/NCBI
18	Maslov LN, Lishmanov YB, Oeltgen PR, et al: Activation of peripheral delta2 opioid receptors increases cardiac tolerance to ischemia/reperfusion injury: Involvement of protein kinase C, NO-synthase, KATP channels and the autonomic nervous system. Life Sci. 84:657–663. 2009. View Article : Google Scholar
19	Papazzo A, Conlan X, Lexis L and Lewandowski P: The effect of short-term canola oil ingestion on oxidative stress in the vasculature of stroke-prone spontaneously hypertensive rats. Lipids Health Dis. 10:1802011. View Article : Google Scholar : PubMed/NCBI
20	Guo J, Li HZ, Wang LC, et al: Increased expression of calcium-sensing receptors in atherosclerosis confers hypersensitivity to acute myocardial infarction in rats. Mol Cell Biochem. 366:345–354. 2012. View Article : Google Scholar : PubMed/NCBI
21	Ming X, Tongshen W, Delin W and Ronghua Z: Cardioprotective effect of the compound yangshen granule in rat models with acute myocardial infarction. Evid Based Complement Alternat Med. 2012:7171232012.PubMed/NCBI
22	Katus HA, Remppis A, Scheffold T, Diederich KW and Kuebler W: Intracellular compartmentation of cardiac troponin T and its release kinetics in patients with reperfused and nonreperfused myocardial infarction. Am J Cardiol. 67:1360–1367. 1991. View Article : Google Scholar : PubMed/NCBI
23	Wolfrum S, Dendorfer A, Schutt M, et al: Simvastatin acutely reduces myocardial reperfusion injury in vivo by activating the phosphatidylinositide 3-kinase/Akt pathway. J Cardiovasc Pharmacol. 44:348–355. 2004. View Article : Google Scholar : PubMed/NCBI
24	Pipaliya H and Vaghasiya J: Cardio protective effect of vitamin A against isoproterenol-induced myocardial infarction. J Nutr Sci Vitaminol (Tokyo). 58:402–407. 2012. View Article : Google Scholar : PubMed/NCBI
25	Chang WT, Li J, Vanden Hoek MS, et al: Baicalein preconditioning protects cardiomyocytes from ischemia-reperfusion injury via mitochondrial oxidant signaling. Am J Chin Med. 41:315–331. 2013. View Article : Google Scholar : PubMed/NCBI