NADPH oxidase inhibitor apocynin prevents atrial remodeling in alloxan-induced diabetic rabbits

International Journal of Cardiology

Volumn 221, Issue , 2016, Pages 812-819

  Qiu, Jiuchun ^a   Zhao, Jianping ^a   Li, Jian ^a   Liang, Xue ^a   Yang, Yajuan ^a   Zhang, Zhiwei ^a   Zhang, Xiaowei ^a   Fu, Huaying ^a   Korantzopoulos, Panagiotis ^b   Liu, Tong ^a   Li, Guangping ^a  

^a SECOND HOSPITAL OF TIANJIN MEDICAL UNIVERSITY   (China)

^b UNIVERSITY OF IOANNINA   (Greece)

Author keywords

Apocynin; Atrial remodeling; Diabetes; NADPH oxidase; Oxidative stress

Indexed keywords

APOCYNIN; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; MALONALDEHYDE; MITOGEN ACTIVATED PROTEIN KINASE; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE OXIDASE; STRESS ACTIVATED PROTEIN KINASE; SUPEROXIDE DISMUTASE; SYNAPTOPHYSIN; TRANSFORMING GROWTH FACTOR BETA; ACETOPHENONE DERIVATIVE; ALLOXAN;

ALLOXAN-INDUCED DIABETES MELLITUS; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; ATRIAL INTERSTITIAL FIBROSIS; ATRIAL REFRACTORY EFFECTIVE PERIOD; ATRIAL REFRACTORY EFFECTIVE PERIOD DISPERSION; CARDIOVASCULAR PARAMETERS; CONTROLLED STUDY; DRUG EFFECT; ECHOCARDIOGRAPHY; ENZYME ACTIVITY; FEMALE; FIBROSIS; HEART ATRIUM REMODELING; HEART ELECTROPHYSIOLOGY; HEART HEMODYNAMICS; HEART MUSCLE REFRACTORY PERIOD; HISTOLOGY; INTERATRIAL CONDUCTION TIME; ISOLATED HEART; MALE; NONHUMAN; OXIDATIVE STRESS; PRIORITY JOURNAL; PROTEIN EXPRESSION; RABBIT; WESTERN BLOTTING; ANIMAL; ANTAGONISTS AND INHIBITORS; ATRIAL FIBRILLATION; BLOOD; DIAGNOSTIC IMAGING; DRUG EFFECTS; EXPERIMENTAL DIABETES MELLITUS; LEPORIDAE; METABOLISM; PHYSIOLOGY; RANDOMIZATION;

ACETOPHENONES; ALLOXAN; ANIMALS; ATRIAL FIBRILLATION; ATRIAL REMODELING; DIABETES MELLITUS, EXPERIMENTAL; FEMALE; MALE; NADPH OXIDASES; RABBITS; RANDOM ALLOCATION;

EID: 84978253122     PISSN: 01675273     EISSN: 18741754     Source Type: Journal    
DOI: 10.1016/j.ijcard.2016.07.132     Document Type: Article

References (41)

1. [1] Benjamin, E.J., Wolf, P.A., D'Agostino, R.B., Silbershatz, H., Kannel, W.B., Levy, D., Impact of atrial fibrillation on the risk of death: the Framingham Heart Study. Circulation 98 (1998), 946–952.
2. [2] Kannel, W.B., Wolf, P.A., Benjamin, E.J., Levy, D., Prevalence, incidence, prognosis, and predisposing conditions for atrial fibrillation: population-based estimates. Am. J. Cardiol. 82 (1998), 2N–9N.
3. [3] Movahed, M.R., Hashemzadeh, M., Jamal, M.M., Diabetes mellitus is a strong, independent risk for atrial fibrillation and flutter in addition to other cardiovascular disease. Int. J. Cardiol. 105 (2005), 315–318.
4. [4] Goudis, C.A., Korantzopoulos, P., Ntalas, I.V., Kallergis, E.M., Liu, T., Ketikoglou, D.G., Diabetes mellitus and atrial fibrillation: pathophysiological mechanisms and potential upstream therapies. Int. J. Cardiol. 184 (2015), 617–622.
5. [5] Zhang, Q., Liu, T., Ng, C.Y., Li, G., Diabetes mellitus and atrial remodeling: mechanisms and potential upstream therapies. Cardiovasc. Ther. 32 (2014), 233–241.
6. [6] Mihm, M.J., Yu, F., Carnes, C.A., Reiser, P.J., McCarthy, P.M., Van Wagoner, D.R., Bauer, J.A., Impaired myofibrillar energetics and oxidative injury during human atrial fibrillation. Circulation 104 (2001), 174–180.
7. [7] Kim, Y.M., Guzik, T.J., Zhang, Y.H., Zhang, M.H., Kattach, H., Ratnatunga, C., Pillai, R., Channon, K.M., Casadei, B., A myocardial Nox2 containing NAD(P)H oxidase contributes to oxidative stress in human atrial fibrillation. Circ. Res. 97 (2005), 629–636.
8. [8] Korantzopoulos, P., Kolettis, T.M., Galaris, D., Goudevenos, J.A., The role of oxidative stress in the pathogenesis and perpetuation of atrial fibrillation. Int. J. Cardiol. 115 (2007), 135–143.
9. [9] Fu, H., Liu, C., Li, J., Zhou, C., Cheng, L., Liu, T., Li, G., Impaired atrial electromechanical function and atrial fibrillation promotion in alloxan-induced diabetic rabbits. Cardiol. J. 20 (2013), 59–67.
10. [10] Liu, T., Zhao, H., Li, J., Korantzopoulos, P., Li, G., Rosiglitazone attenuates atrial structural remodeling and atrial fibrillation promotion in alloxan-induced diabetic rabbits. Cardiovasc. Ther. 32 (2014), 178–183.
11. [11] Fu, H., Li, G., Liu, C., Li, J., Wang, X., Cheng, L., Liu, T., Probucol prevents atrial remodeling by inhibiting oxidative stress and TNF-alpha/NF-kappaB/TGF-beta signal transduction pathway in alloxan-induced diabetic rabbits. J. Cardiovasc. Electrophysiol. 26 (2015), 211–222.
12. [12] Cai, Hydrogen peroxide regulation of endothelial function: origins, mechanisms, and consequences. Cardiovasc. Res., 2005, 26–36.
13. [13] Seddon, M., Looi, Y.H., Shah, A.M., Oxidative stress and redox signalling in cardiac hypertrophy and heart failure. Heart 93 (2007), 903–907.
14. [14] Griendling, K.K., Sorescu, D., Ushio-Fukai, M., NAD(P)H oxidase: role in cardiovascular biology and disease. Circ. Res. 86 (2000), 494–501.
15. [15] Li, J.M., Gall, N.P., Grieve, D.J., Chen, M., Shah, A.M., Activation of NADPH oxidase during progression of cardiac hypertrophy to failure. Hypertension 40 (2002), 477–484.
16. [16] Dudley, S.C. Jr., Hoch, N.E., McCann, L.A., Honeycutt, C., Diamandopoulos, L., Fukai, T., Harrison, D.G., Dikalov, S.I., Langberg, J., Atrial fibrillation increases production of superoxide by the left atrium and left atrial appendage: role of the NADPH and xanthine oxidases. Circulation 112 (2005), 1266–1273.
17. [17] Liu, T., Shao, Q., Korantzopoulos, P., Liu, E., Xu, G., Li, G., Serum levels of nicotinamide-adenine dinucleotide phosphate oxidase 4 are associated with non-valvular atrial fibrillation. Biomed. Rep. 3 (2015), 864–868.
18. [18] Youn, J.Y., Zhang, J., Zhang, Y., Chen, H., Liu, D., Ping, P., Weiss, J.N., Cai, H., Oxidative stress in atrial fibrillation: an emerging role of NADPH oxidase. J. Mol. Cell. Cardiol. 62 (2013), 72–79.
19. [19] Stolk, J., Hiltermann, T.J., Dijkman, J.H., Verhoeven, A.J., Characteristics of the inhibition of NADPH oxidase activation in neutrophils by apocynin, a methoxy-substituted catechol. Am. J. Respir. Cell Mol. Biol. 11 (1994), 95–102.
20. [20] Qin, F., Simeone, M., Patel, R., Inhibition of NADPH oxidase reduces myocardial oxidative stress and apoptosis and improves cardiac function in heart failure after myocardial infarction. Free Radic. Biol. Med. 43 (2007), 271–281.
21. [21] Aljofan, M., Ding, H., High glucose increases expression of cyclooxygenase-2, increases oxidative stress and decreases the generation of nitric oxide in mouse microvessel endothelial cells. J. Cell. Physiol. 222 (2010), 669–675.
22. [22] Sayed, A.A., Khalifa, M., el-Latif, F.F.A., Fenugreek attenuation of diabetic nephropathy in alloxan-diabetic rats: attenuation of diabetic nephropathy in rats. J. Physiol. Biochem. 68 (2012), 263–269.
23. [23] Balteau, M., Tajeddine, N., de Meester, C., Ginion, A., Des Rosiers, C., Brady, N.R., Sommereyns, C., Horman, S., Vanoverschelde, J.L., Gailly, P., Hue, L., Bertrand, L., Beauloye, C., NADPH oxidase activation by hyperglycaemia in cardiomyocytes is independent of glucose metabolism but requires SGLT1. Cardiovasc. Res. 92 (2011), 237–246.
24. [24] Lassegue, B., Clempus, R.E., Vascular NAD(P)H oxidases: specific features, expression, and regulation. Am. J. Phys. Regul. Integr. Comp. Phys. 285 (2003), R277–R297.
25. [25] Clempus, R.E., Griendling, K.K., Reactive oxygen species signaling in vascular smooth muscle cells. Cardiovasc. Res. 71 (2006), 216–225.
26. [26] Anilkumar, N., Sirker, A., Shah, A.M., Redox sensitive signaling pathways in cardiac remodeling, hypertrophy and failure. Front Biosci. (Landmark Ed.) 14 (2009), 3168–3187.
27. [27] Maack, C., Kartes, T., Kilter, H., Schafers, H.J., Nickenig, G., Bohm, M., Laufs, U., Oxygen free radical release in human failing myocardium is associated with increased activity of rac1-GTPase and represents a target for statin treatment. Circulation 108 (2003), 1567–1574.
28. [28] Price, M.O., Atkinson, S.J., Knaus, U.G., Dinauer, M.C., Rac activation induces NADPH oxidase activity in transgenic COSphox cells, and the level of superoxide production is exchange factor-dependent. J. Biol. Chem. 277 (2002), 19220–19228.
29. [29] Byrne, J.A., Grieve, D.J., Bendall, J.K., Li, J.M., Gove, C., Lambeth, J.D., Cave, A.C., Shah, A.M., Contrasting roles of NADPH oxidase isoforms in pressure-overload versus angiotensin II-induced cardiac hypertrophy. Circ. Res. 93 (2003), 802–805.
30. [30] Heymes, C., Bendall, J.K., Ratajczak, P., Cave, A.C., Samuel, J.L., Hasenfuss, G., Shah, A.M., Increased myocardial NADPH oxidase activity in human heart failure. J. Am. Coll. Cardiol. 41 (2003), 2164–2171.
31. [31] Zhang, Q., Li, G., Liu, T., Receptor for advanced glycation end products (RAGE): novel biomarker and therapeutic target for atrial fibrillation. Int. J. Cardiol. 168 (2013), 4802–4804.
32. [32] Mahali, S.K., Manna, S.K., Beta-D-glucoside protects against advanced glycation end products (AGEs)-mediated diabetic responses by suppressing ERK and inducing PPAR gamma DNA binding. Biochem. Pharmacol. 84 (2012), 1681–1690.
33. [33] Min, W., Bin, Z.W., Quan, Z.B., Hui, Z.J., Sheng, F.G., The signal transduction pathway of PKC/NF-kappa B/c-fos may be involved in the influence of high glucose on the cardiomyocytes of neonatal rats. Cardiovasc. Diabetol., 8, 2009, 8.
34. [34] Zhao, W., Zhao, T., Chen, Y., Ahokas, R.A., Sun, Y., Oxidative stress mediates cardiac fibrosis by enhancing transforming growth factor-beta1 in hypertensive rats. Mol. Cell. Biochem. 317 (2008), 43–50.
35. [35] Yeh, Y.H., Kuo, C.T., Chan, T.H., Chang, G.J., Qi, X.Y., Tsai, F., Nattel, S., Chen, W.J., Transforming growth factor-beta and oxidative stress mediate tachycardia-induced cellular remodelling in cultured atrial-derived myocytes. Cardiovasc. Res. 91 (2011), 62–70.
36. [36] Kumar, S., Prasad, S., Sitasawad, S.L., Multiple antioxidants improve cardiac complications and inhibit cardiac cell death in streptozotocin-induced diabetic rats. PLoS One, 8, 2013, e67009.
37. [37] Zhang, L., Zalewski, A., Liu, Y., Mazurek, T., Cowan, S., Martin, J.L., Hofmann, S.M., Vlassara, H., Shi, Y., Diabetes-induced oxidative stress and low-grade inflammation in porcine coronary arteries. Circulation 108 (2003), 472–478.
38. [38] Clerk, A., Fuller, S.J., Michael, A., Sugden, P.H., Stimulation of “stress-regulated” mitogen-activated protein kinases (stress-activated protein kinases/c-Jun N-terminal kinases and p38-mitogen-activated protein kinases) in perfused rat hearts by oxidative and other stresses. J. Biol. Chem. 273 (1998), 7228–7234.
39. [39] Sovari, A.A., Morita, N., Karagueuzian, H.S., Apocynin: a potent NADPH oxidase inhibitor for the management of atrial fibrillation. Redox Rep. 13 (2008), 242–245.
40. [40] Tsai, C.T., Tseng, C.D., Hwang, J.J., Wu, C.K., Yu, C.C., Wang, Y.C., Chen, W.P., Lai, L.P., Chiang, F.T., Lin, J.L., Tachycardia of atrial myocytes induces collagen expression in atrial fibroblasts through transforming growth factor beta1. Cardiovasc. Res. 89 (2011), 805–815.
41. [41] Zhang, D.X., Ren, K., Guan, Y., Wang, Y.T., Shan, Z.L., Protective effects of apocynin on atrial electrical remodeling and oxidative stress in a rabbit rapid atrial pacing model. Chin. J. Phys. 57 (2014), 76–82.