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Diallyl trisulfide ameliorates myocardial ischemia-reperfusion injury by reducing oxidative stress and endoplasmic reticulum stress-mediated apoptosis in type 1 diabetic rats: role of SIRT1 activation.
Apoptosis 2017; 22(7):942-954A

Abstract

Diallyl trisulfide (DATS) protects against apoptosis during myocardial ischemia-reperfusion (MI/R) injury in diabetic state, although the underlying mechanisms remain poorly defined. Previously, we and others demonstrated that silent information regulator 1 (SIRT1) activation inhibited oxidative stress and endoplasmic reticulum (ER) stress during MI/R injury. We hypothesize that DATS reduces diabetic MI/R injury by activating SIRT1 signaling. Streptozotocin (STZ)-induced type 1 diabetic rats were subjected to MI/R surgery with or without perioperative administration of DATS (40 mg/kg). We found that DATS treatment markedly improved left ventricular systolic pressure and the first derivative of left ventricular pressure, reduced myocardial infarct size as well as serum creatine kinase and lactate dehydrogenase activities. Furthermore, the myocardial apoptosis was also suppressed by DATS as evidenced by reduced apoptotic index and cleaved caspase-3 expression. However, these effects were abolished by EX527 (the inhibitor of SIRT1 signaling, 5 mg/kg). We further found that DATS effectively upregulated SIRT1 expression and its nuclear distribution. Additionally, PERK/eIF2α/ATF4/CHOP-mediated ER stress-induced apoptosis was suppressed by DATS treatment. Moreover, DATS significantly activated Nrf-2/HO-1 antioxidant signaling pathway, thus reducing Nox-2/4 expressions. However, the ameliorative effects of DATS on oxidative stress and ER stress-mediated myocardial apoptosis were inhibited by EX527 administration. Taken together, these data suggest that perioperative DATS treatment effectively ameliorates MI/R injury in type 1 diabetic setting by enhancing cardiac SIRT1 signaling. SIRT1 activation not only upregulated Nrf-2/HO-1-mediated antioxidant signaling pathway but also suppressed PERK/eIF2α/ATF4/CHOP-mediated ER stress level, thus reducing myocardial apoptosis and eventually preserving cardiac function.

Authors+Show Affiliations

Department of Cardiovascular Surgery, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang, 110016, Liaoning, China.Department of Forensic Medicine, National Police University of China, 83 Tawan Road, Shenyang, 110035, Liaoning, China.Department of Thoracic and Cardiovascular Surgery, Affiliated Drum Tower Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing, 210008, Jiangsu, China.Department of Cardiovascular Surgery, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang, 110016, Liaoning, China.Department of Cardiovascular Surgery, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang, 110016, Liaoning, China.Department of Cardiovascular Surgery, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang, 110016, Liaoning, China.Department of Cardiovascular Surgery, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang, 110016, Liaoning, China.Department of Cardiovascular Surgery, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang, 110016, Liaoning, China.Department of Cardiovascular Surgery, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang, 110016, Liaoning, China.Department of Cardiovascular Surgery, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang, 110016, Liaoning, China.Department of Cardiovascular Surgery, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang, 110016, Liaoning, China.Department of Thoracic and Cardiovascular Surgery, Affiliated Drum Tower Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing, 210008, Jiangsu, China. yang200214yy@163.com. Department of Biomedical Engineering, The Fourth Military Medical University, 169 Changle West Road, Xi'an, 710032, China. yang200214yy@163.com. Faculty of Life Science, Northwest University, 229 Taibai North Road, Xi'an, 710069, Shaanxi, China. yang200214yy@163.com.Department of Cardiovascular Surgery, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang, 110016, Liaoning, China. huishanw@126.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

28455824

Citation

Yu, Liming, et al. "Diallyl Trisulfide Ameliorates Myocardial Ischemia-reperfusion Injury By Reducing Oxidative Stress and Endoplasmic Reticulum Stress-mediated Apoptosis in Type 1 Diabetic Rats: Role of SIRT1 Activation." Apoptosis : an International Journal On Programmed Cell Death, vol. 22, no. 7, 2017, pp. 942-954.
Yu L, Li S, Tang X, et al. Diallyl trisulfide ameliorates myocardial ischemia-reperfusion injury by reducing oxidative stress and endoplasmic reticulum stress-mediated apoptosis in type 1 diabetic rats: role of SIRT1 activation. Apoptosis. 2017;22(7):942-954.
Yu, L., Li, S., Tang, X., Li, Z., Zhang, J., Xue, X., ... Wang, H. (2017). Diallyl trisulfide ameliorates myocardial ischemia-reperfusion injury by reducing oxidative stress and endoplasmic reticulum stress-mediated apoptosis in type 1 diabetic rats: role of SIRT1 activation. Apoptosis : an International Journal On Programmed Cell Death, 22(7), pp. 942-954. doi:10.1007/s10495-017-1378-y.
Yu L, et al. Diallyl Trisulfide Ameliorates Myocardial Ischemia-reperfusion Injury By Reducing Oxidative Stress and Endoplasmic Reticulum Stress-mediated Apoptosis in Type 1 Diabetic Rats: Role of SIRT1 Activation. Apoptosis. 2017;22(7):942-954. PubMed PMID: 28455824.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Diallyl trisulfide ameliorates myocardial ischemia-reperfusion injury by reducing oxidative stress and endoplasmic reticulum stress-mediated apoptosis in type 1 diabetic rats: role of SIRT1 activation. AU - Yu,Liming, AU - Li,Shu, AU - Tang,Xinlong, AU - Li,Zhi, AU - Zhang,Jian, AU - Xue,Xiaodong, AU - Han,Jinsong, AU - Liu,Yu, AU - Zhang,Yuji, AU - Zhang,Yong, AU - Xu,Yinli, AU - Yang,Yang, AU - Wang,Huishan, PY - 2017/4/30/pubmed PY - 2018/3/15/medline PY - 2017/4/30/entrez KW - Diallyl trisulfide KW - Endoplasmic reticulum stress KW - Myocardial ischemia-reperfusion KW - Oxidative stress KW - SIRT1 KW - Type 1 diabetes SP - 942 EP - 954 JF - Apoptosis : an international journal on programmed cell death JO - Apoptosis VL - 22 IS - 7 N2 - Diallyl trisulfide (DATS) protects against apoptosis during myocardial ischemia-reperfusion (MI/R) injury in diabetic state, although the underlying mechanisms remain poorly defined. Previously, we and others demonstrated that silent information regulator 1 (SIRT1) activation inhibited oxidative stress and endoplasmic reticulum (ER) stress during MI/R injury. We hypothesize that DATS reduces diabetic MI/R injury by activating SIRT1 signaling. Streptozotocin (STZ)-induced type 1 diabetic rats were subjected to MI/R surgery with or without perioperative administration of DATS (40 mg/kg). We found that DATS treatment markedly improved left ventricular systolic pressure and the first derivative of left ventricular pressure, reduced myocardial infarct size as well as serum creatine kinase and lactate dehydrogenase activities. Furthermore, the myocardial apoptosis was also suppressed by DATS as evidenced by reduced apoptotic index and cleaved caspase-3 expression. However, these effects were abolished by EX527 (the inhibitor of SIRT1 signaling, 5 mg/kg). We further found that DATS effectively upregulated SIRT1 expression and its nuclear distribution. Additionally, PERK/eIF2α/ATF4/CHOP-mediated ER stress-induced apoptosis was suppressed by DATS treatment. Moreover, DATS significantly activated Nrf-2/HO-1 antioxidant signaling pathway, thus reducing Nox-2/4 expressions. However, the ameliorative effects of DATS on oxidative stress and ER stress-mediated myocardial apoptosis were inhibited by EX527 administration. Taken together, these data suggest that perioperative DATS treatment effectively ameliorates MI/R injury in type 1 diabetic setting by enhancing cardiac SIRT1 signaling. SIRT1 activation not only upregulated Nrf-2/HO-1-mediated antioxidant signaling pathway but also suppressed PERK/eIF2α/ATF4/CHOP-mediated ER stress level, thus reducing myocardial apoptosis and eventually preserving cardiac function. SN - 1573-675X UR - https://www.unboundmedicine.com/medline/citation/28455824/Diallyl_trisulfide_ameliorates_myocardial_ischemia_reperfusion_injury_by_reducing_oxidative_stress_and_endoplasmic_reticulum_stress_mediated_apoptosis_in_type_1_diabetic_rats:_role_of_SIRT1_activation_ L2 - https://doi.org/10.1007/s10495-017-1378-y DB - PRIME DP - Unbound Medicine ER -