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Bilirubin may limit heart ischemia and reperfusion injury in diabetic rats
International Journal of Cardiology 214 (2016) 390
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Bilirubin may limit heart ischemia and reperfusion injury in diabetic rats Yao Lu a,⁎, Jun Hu b, Xuesheng Liu a a b
Department of Anesthesiology, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui Province, PR China Department of Anesthesiology, Tongling People's Hospital, Tongling, Anhui Province, PR China
a r t i c l e
i n f o
Article history: Received 24 March 2016 Accepted 27 March 2016 Available online 6 April 2016 Keywords: Bilirubin Diabetes Myocardial ischemia-reperfusion Heme oxygenase-1
can confer cardioprotection against myocardial ischemia and reperfusion injury in diabetes rats via restoring HIF-1α/HO-1 signaling pathway. Thus, from these above studies, we speculate heme oxygenase-1 (HO-1) derived bilirubin may also produce cardioprotection against myocardial ischemia and reperfusion injury in diabetes rats as in non-diabetic rats. In summary, we do agree with the authors' conclusion that antioxidative damage contributes to the cardioprotection of bilirubin. However, the role of heme oxygenase-1 (HO-1) was not determined. Conflict of interest The authors have no conflict of interest to declare.
To the Editor We have greatly read the report of Bakrania et al. [1] “Pre- or postischemic bilirubin ditaurate treatment reduces oxidative tissue damage and improves cardiac function”, the authors showed that pre- and postischemic treatment with bilirubin ditaurate (BDT) significantly limit ischemia injury in isolated Langendorff perfused hearts. And, their study also indicated that post-treatment is particularly effective. Heme oxygenase-1 (HO-1) is the first and rate limiting enzyme in the heme breakdown to generate bilirubin, free ferrous iron and carbon monoxide [2]. Heme oxygenase-1 (HO-1) and its reaction products have been shown to have both anti-oxidant and anti-inflammatory properties, indicating a protective role of HO-1 in myocardial infarction [3]. Moreover, HO-1 may also contribute to why experimental diabetic models are more resistant to ischemic preconditioning induced cardioprotection, since HO-1 protein expression is reduced in diabetic rats [4]. HO-1 inhibition has been shown to exacerbate inflammatory response, thus inducing endothelial cell death in animal models of atherosclerosis [5]. It has been demonstrated that heme oxygenase-1 (HO-1) derived bilirubin can prevent endothelial cells against high glucose-induced damage [6]. Studies have also shown that increased expression of HO-1 attenuated glucosemediated cell growth arrest and apoptosis and decreased endothelial cell sloughing in diabetic rats [3,7]. Hypoxia inducible factor-1 (HIF-1α) is an upstream of HO-1. HIF-1α induced up-regulation of HO-1 can produce cardioprotective effects in non-diabetic rats [8]. Mao et al. [9] found that antioxidants N-acetylcysteine (NAC) and allopurinol (ALP) ⁎ Corresponding author at: Department of Anesthesiology, First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui Province, PR China. E-mail address: [email protected] (Y. Lu).
http://dx.doi.org/10.1016/j.ijcard.2016.03.233 0167-5273/© 2016 Elsevier Ireland Ltd. All rights reserved.
Financial Support National Natural Science Foundation of China (No. 81100105). References [1] B. Bakrania, et al., Pre- or post-ischemic bilirubin ditaurate treatment reduces oxidative tissue damage and improves cardiac function, Int. J. Cardiol. 202 (2016) 27–33. [2] G.M. Trakshel, M.D. Maines, Multiplicity of heme oxygenase isozymes. HO-1 and HO2 are different molecular species in rat and rabbit, J. Biol. Chem. 264 (1989) 1323–1328. [3] S. Quan, P.M. Kaminski, L. Yang, et al., Heme oxygenase-1 prevents superoxide anion associated endothelial cell sloughing in diabetic rats, Biochem. Biophys. Res. Commun. 315 (2004) 509–516. [4] S. Turkseven, A. Krugger, C. Mingone, et al., Antioxidant mechanism of heme oxygenase-1 involves an increase in superoxide dismutase and catalase in experimental diabetes, Am. J. Physiol. Heart Circ. Physiol. 289 (2005) H701–H707. [5] K. Ishikawa, M. Navab, N. Leitinger, et al., Induction of heme oxygenase-1 inhibits the monocyte transmigration induced by mildly oxidized LDL, J. Clin. Invest. 100 (1997) 1209–1216. [6] M. He, M. Nitti, S. Pairas, et al., Heme oxygenase-1-derived bilirubin protects endothelial cells against high glucose-induced damage, Free Radic. Biol. Med. 89 (2015) 91–98. [7] N.G. Abraham, T. Kushida, J. McClung, et al., Heme oxygenase-1 attenuates glucosemediated cell growth arrest and apoptosis in human microvessel endothelial cells, Circ. Res. 93 (2003) 507–514. [8] R. Ockaili, R. Natarajan, F. Salloum, et al., HIF-1 activation attenuates postischemic myocardial injury: role for heme oxygenase-1 in modulating microvascular chemokine generation, Am. J. Physiol. Heart Circ. Physiol. 289 (2005) H542–H548. [9] X. Mao, T. Wang, Y. Liu, et al., N-acetylcysteine and allopurinol confer synergy in attenuating myocardial ischemia injury via restoring HIF-1α/HO-1 signaling in diabetic rats, PLoS One 8 (2013), e68949.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Correspondence
Bilirubin may limit heart ischemia and reperfusion injury in diabetic rats Yao Lu a,⁎, Jun Hu b, Xuesheng Liu a a b
Department of Anesthesiology, First Affiliated Hospital of Anhui Medical University, Hefei, Anhui Province, PR China Department of Anesthesiology, Tongling People's Hospital, Tongling, Anhui Province, PR China
a r t i c l e
i n f o
Article history: Received 24 March 2016 Accepted 27 March 2016 Available online 6 April 2016 Keywords: Bilirubin Diabetes Myocardial ischemia-reperfusion Heme oxygenase-1
can confer cardioprotection against myocardial ischemia and reperfusion injury in diabetes rats via restoring HIF-1α/HO-1 signaling pathway. Thus, from these above studies, we speculate heme oxygenase-1 (HO-1) derived bilirubin may also produce cardioprotection against myocardial ischemia and reperfusion injury in diabetes rats as in non-diabetic rats. In summary, we do agree with the authors' conclusion that antioxidative damage contributes to the cardioprotection of bilirubin. However, the role of heme oxygenase-1 (HO-1) was not determined. Conflict of interest The authors have no conflict of interest to declare.
To the Editor We have greatly read the report of Bakrania et al. [1] “Pre- or postischemic bilirubin ditaurate treatment reduces oxidative tissue damage and improves cardiac function”, the authors showed that pre- and postischemic treatment with bilirubin ditaurate (BDT) significantly limit ischemia injury in isolated Langendorff perfused hearts. And, their study also indicated that post-treatment is particularly effective. Heme oxygenase-1 (HO-1) is the first and rate limiting enzyme in the heme breakdown to generate bilirubin, free ferrous iron and carbon monoxide [2]. Heme oxygenase-1 (HO-1) and its reaction products have been shown to have both anti-oxidant and anti-inflammatory properties, indicating a protective role of HO-1 in myocardial infarction [3]. Moreover, HO-1 may also contribute to why experimental diabetic models are more resistant to ischemic preconditioning induced cardioprotection, since HO-1 protein expression is reduced in diabetic rats [4]. HO-1 inhibition has been shown to exacerbate inflammatory response, thus inducing endothelial cell death in animal models of atherosclerosis [5]. It has been demonstrated that heme oxygenase-1 (HO-1) derived bilirubin can prevent endothelial cells against high glucose-induced damage [6]. Studies have also shown that increased expression of HO-1 attenuated glucosemediated cell growth arrest and apoptosis and decreased endothelial cell sloughing in diabetic rats [3,7]. Hypoxia inducible factor-1 (HIF-1α) is an upstream of HO-1. HIF-1α induced up-regulation of HO-1 can produce cardioprotective effects in non-diabetic rats [8]. Mao et al. [9] found that antioxidants N-acetylcysteine (NAC) and allopurinol (ALP) ⁎ Corresponding author at: Department of Anesthesiology, First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui Province, PR China. E-mail address: [email protected] (Y. Lu).
http://dx.doi.org/10.1016/j.ijcard.2016.03.233 0167-5273/© 2016 Elsevier Ireland Ltd. All rights reserved.
Financial Support National Natural Science Foundation of China (No. 81100105). References [1] B. Bakrania, et al., Pre- or post-ischemic bilirubin ditaurate treatment reduces oxidative tissue damage and improves cardiac function, Int. J. Cardiol. 202 (2016) 27–33. [2] G.M. Trakshel, M.D. Maines, Multiplicity of heme oxygenase isozymes. HO-1 and HO2 are different molecular species in rat and rabbit, J. Biol. Chem. 264 (1989) 1323–1328. [3] S. Quan, P.M. Kaminski, L. Yang, et al., Heme oxygenase-1 prevents superoxide anion associated endothelial cell sloughing in diabetic rats, Biochem. Biophys. Res. Commun. 315 (2004) 509–516. [4] S. Turkseven, A. Krugger, C. Mingone, et al., Antioxidant mechanism of heme oxygenase-1 involves an increase in superoxide dismutase and catalase in experimental diabetes, Am. J. Physiol. Heart Circ. Physiol. 289 (2005) H701–H707. [5] K. Ishikawa, M. Navab, N. Leitinger, et al., Induction of heme oxygenase-1 inhibits the monocyte transmigration induced by mildly oxidized LDL, J. Clin. Invest. 100 (1997) 1209–1216. [6] M. He, M. Nitti, S. Pairas, et al., Heme oxygenase-1-derived bilirubin protects endothelial cells against high glucose-induced damage, Free Radic. Biol. Med. 89 (2015) 91–98. [7] N.G. Abraham, T. Kushida, J. McClung, et al., Heme oxygenase-1 attenuates glucosemediated cell growth arrest and apoptosis in human microvessel endothelial cells, Circ. Res. 93 (2003) 507–514. [8] R. Ockaili, R. Natarajan, F. Salloum, et al., HIF-1 activation attenuates postischemic myocardial injury: role for heme oxygenase-1 in modulating microvascular chemokine generation, Am. J. Physiol. Heart Circ. Physiol. 289 (2005) H542–H548. [9] X. Mao, T. Wang, Y. Liu, et al., N-acetylcysteine and allopurinol confer synergy in attenuating myocardial ischemia injury via restoring HIF-1α/HO-1 signaling in diabetic rats, PLoS One 8 (2013), e68949.