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tnf myocardial infarction

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https://www.readbyqxmd.com/read/28293100/adenosine-a2a-receptor-agonist-prevents-cardiac-remodeling-and-dysfunction-in-spontaneously-hypertensive-male-rats-after-myocardial-infarction
#1
Jaqueline S da Silva, Daniele Gabriel-Costa, Roberto T Sudo, Hao Wang, Leanne Groban, Emanuele B Ferraz, José Hamilton M Nascimento, Carlos Alberto M Fraga, Eliezer J Barreiro, Gisele Zapata-Sudo
BACKGROUND: This work evaluated the hypothesis that 3,4-methylenedioxybenzoyl-2-thienylhydrazone (LASSBio-294), an agonist of adenosine A2A receptor, could be beneficial for preventing cardiac dysfunction due to hypertension associated with myocardial infarction (MI). METHODS: Male spontaneously hypertensive rats (SHR) were randomly divided into four groups (six animals per group): sham-operation (SHR-Sham), and myocardial infarction rats (SHR-MI) were treated orally either with vehicle or LASSBio-294 (10 and 20 mg...
2017: Drug Design, Development and Therapy
https://www.readbyqxmd.com/read/28281187/mir-145-5p-regulates-hypoxia-induced-inflammatory-response-and-apoptosis-in-cardiomyocytes-by-targeting-cd40
#2
Ming Yuan, Liwei Zhang, Fei You, Jingyu Zhou, Yongjiang Ma, Feifei Yang, Ling Tao
An increasing body of evidence indicates that inflammation and apoptosis are involved in the development of acute myocardial infarction (AMI). In this study, we sought to investigate the specific role and the underlying regulatory mechanism of miR-145-5p in myocardial ischemic injury. H9c2 cardiac cells were exposed to hypoxia to establish a model of myocardial hypoxic/ischemic injury. We found that miR-145-5p was notably down-regulated, while CD40 expression was highly elevated in H9c2 cells following exposure to acute hypoxia...
March 9, 2017: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/28266659/sequential-activation-of-different-pathway-networks-in-ischemia-affected-and-non-affected-myocardium-inducing-intrinsic-remote-conditioning-to-prevent-left-ventricular-remodeling
#3
Noemi Pavo, Dominika Lukovic, Katrin Zlabinger, Abelina Zimba, David Lorant, Georg Goliasch, Johannes Winkler, Dietmar Pils, Katharina Auer, Hendrik Jan Ankersmit, Zoltán Giricz, Tamas Baranyai, Márta Sárközy, András Jakab, Rita Garamvölgyi, Maximilian Y Emmert, Simon P Hoerstrup, Derek J Hausenloy, Péter Ferdinandy, Gerald Maurer, Mariann Gyöngyösi
We have analyzed the pathway networks of ischemia-affected and remote myocardial areas after repetitive ischemia/reperfusion (r-I/R) injury without ensuing myocardial infarction (MI) to elaborate a spatial- and chronologic model of cardioprotective gene networks to prevent left ventricular (LV) adverse remodeling. Domestic pigs underwent three cycles of 10/10 min r-I/R by percutaneous intracoronary balloon inflation/deflation in the mid left anterior descending artery, without consecutive MI. Sham interventions (n = 8) served as controls...
March 7, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28261301/cardiomyocyte-mitochondria-as-targets-of-humoral-factors-released-by-remote-ischemic-preconditioning
#4
Nilguen Gedik, Leonardo Maciel, Christiane Schulte, Andreas Skyschally, Gerd Heusch, Petra Kleinbongard
INTRODUCTION: Remote ischemic preconditioning (RIPC) reduces myocardial infarct size, and protection can be transferred with plasma to other individuals, even across species. Mitochondria are the end-effectors of cardioprotection by local ischemic conditioning maneuvers. We have now analyzed mitochondrial function in response to RIPC. MATERIAL AND METHODS: Plasma from pigs undergoing placebo or RIPC (infarct size reduction by 67% in RIPC pigs compared to placebo) was transferred to isolated perfused rat hearts subjected to 30 min global ischemia followed by 120 min reperfusion for infarct size measurement...
March 1, 2017: Archives of Medical Science: AMS
https://www.readbyqxmd.com/read/28261283/biochemical-markers-of-type-2-diabetes-as-a-late-complication-of-myocardial-infarction-a-case-control-study
#5
Olga Barbarash, Olga Gruzdeva, Evgenya Uchasova, Ekaterina Belik, Yulia Dyleva, Victoria Karetnikova
INTRODUCTION: On average, 19-23% of patients with acute myocardial infarction (MI) suffer from type 2 diabetes mellitus, which is newly diagnosed in a significant number of patients. Both classic carbohydrate metabolism and lipid metabolism may be promising diagnostic markers for insulin resistance in acute coronary syndrome. MATERIAL AND METHODS: Two hundred patients (130 males and 70 females aged 61.4 ±1.12 years) with ST-segment elevation MI were included in the study...
March 1, 2017: Archives of Medical Science: AMS
https://www.readbyqxmd.com/read/28245350/cardiovascular-safety-of-tocilizumab-versus-tumor-necrosis-factor-inhibitors-in-patients-with-rheumatoid-arthritis-a-multi-database-cohort-study
#6
Seoyoung C Kim, Daniel H Solomon, James R Rogers, Sara Gale, Micki Klearman, Khaled Sarsour, Sebastian Schneeweiss
OBJECTIVE: While tocilizumab (TCZ) is known to increase LDL cholesterol, it is unclear whether TCZ increases cardiovascular (CV) risks in patients with rheumatoid arthritis (RA). METHODS: To examine comparative CV safety, we conducted a cohort study of RA patients who newly started TCZ or TNFi using claims data from Medicare, IMS PharMetrics and MarketScan. All patients were required to have previously used a different TNFi, abatacept, or tofacitinib. The primary outcome was a composite CV endpoint of hospitalization for myocardial infarction (MI) or stroke...
February 28, 2017: Arthritis & Rheumatology
https://www.readbyqxmd.com/read/28222157/dexmedetomidine-preconditioning-may-attenuate-myocardial-ischemia-reperfusion-injury-by-down-regulating-the-hmgb1-tlr4-myd88-nf-%C3%B0%C2%BAb-signaling-pathway
#7
Jing-Jing Zhang, Ke Peng, Juan Zhang, Xiao-Wen Meng, Fu-Hai Ji
AIMS: To investigate whether dexmedetomidine (DEX) preconditioning could alleviate the inflammation caused by myocardial ischemia/reperfusion (I/R) injury by reducing HMGB1-TLR4-MyD88-NF-кB signaling. METHODS: Seventy rats were randomly assigned into five groups: sham group, myocardial I/R group (I/R), DEX+I/R group (DEX), DEX+yohimbine+I/R group (DEX/YOH), and yohimbine+I/R group (YOH). Animals were subjected to 30 min of ischemia induced by occluding the left anterior descending artery followed by 120 min of reperfusion...
2017: PloS One
https://www.readbyqxmd.com/read/28214843/metabolites-of-hypoxic-cardiomyocytes-induce-the-migration-of-cardiac-fibroblasts
#8
Huairui Shi, Xuehong Zhang, Zekun He, Zhiyong Wu, Liya Rao, Yushu Li
BACKGROUND: The migration of cardiac fibroblasts to the infarct region plays a major role in the repair process after myocardial necrosis or damage. However, few studies investigated whether early hypoxia in cardiomyocytes induces the migration of cardiac fibroblasts. The purpose of this study was to assess the role of metabolites of early hypoxic cardiomyocytes in the induction of cardiac fibroblast migration. METHODS: Neonatal rat heart tissue was digested with a mixture of trypsin and collagenase at an appropriate ratio...
January 27, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28209739/myocardial-ischemic-tolerance-in-rats-subjected-to-endurance-exercise-training-during-adaptation-to-chronic-hypoxia
#9
Petra Alánová, Anna Chytilová, Jan Neckář, Jaroslav Hrdlička, Petra Míčová, Kristýna Holzerová, Markéta Hlaváčková, Kristýna Macháčková, František Papoušek, Jana Vašinová, Daniel Benák, Olga Nováková, František Kolář
Chronic hypoxia and exercise are natural stimuli that confer sustainable cardioprotection against ischemia/reperfusion (I/R) injury but it is unknown whether they can act in synergy to enhance ischemic resistance. Inflammatory response mediated by tumor necrosis factor-α (TNF-α) plays a role in the infarct size-limitation by continuous normobaric hypoxia (CNH) whereas exercise is associated with anti-inflammatory effects. This study was conducted to determine whether exercise training performed under conditions of CNH (12% O2) affects myocardial ischemic resistance with respect to inflammatory and redox status...
February 16, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28204966/inhibition-of-the-renin-angiotensin-system-post-myocardial-infarction-prevents-inflammation-associated-acute-cardiac-rupture
#10
Xiao-Ming Gao, Alan Tsai, Annas Al-Sharea, Yidan Su, Shirley Moore, Li-Ping Han, Helen Kiriazis, Anthony M Dart, Andrew J Murphy, Xiao-Jun Du
PURPOSE: Inhibition of the renin-angiotensin system (RAS) is beneficial in patient management after myocardial infarction (MI). However, whether RAS inhibition also provides cardiac protection in the acute phase of MI is unclear. METHODS: Male 129sv mice underwent coronary artery occlusion to induce MI, followed by treatment with losartan (L, 20 and 60 mg/kg), perindopril (P, 2 and 6 mg/kg), amlodipine (20 mg/kg as a BP-lowering agent) or vehicle as control. Drug effects on hemodynamics were examined...
February 15, 2017: Cardiovascular Drugs and Therapy
https://www.readbyqxmd.com/read/28183800/tnfsf15-inhibits-vegf-stimulated-vascular-hyperpermeability-by-inducing-vegfr2-dephosphorylation
#11
Gui-Li Yang, Zilong Zhao, Ting-Ting Qin, Dong Wang, Lijuan Chen, Rong Xiang, Zhen Xi, Rongcai Jiang, Zhi-Song Zhang, Jianning Zhang, Lu-Yuan Li
Vascular hyperpermeability is critical in ischemic diseases, including stroke and myocardial infarction, as well as in inflammation and cancer. It is well known that the VEGF-VEGFR2 signaling pathways are pivotal in promoting vascular permeability; however, counterbalancing mechanisms that restrict vascular permeability to maintain the integrity of blood vessels, are not yet fully understood. We report that TNF superfamily member 15 (TNFSF15), a cytokine largely produced by vascular endothelial cells and a specific inhibitor of the proliferation of these same cells, can inhibit VEGF-induced vascular permeability in vitro and in vivo, and that death receptor 3 (DR3), a cell surface receptor of TNFSF15, mediates TNFSF15-induced dephosphorylation of VEGFR2...
February 9, 2017: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28177670/effect-of-vitamin-d-on-isoprenaline-induced-myocardial-infarction-in-rats-possible-role-of-peroxisome-proliferator-activated-receptor-%C3%A9-ppar-%C3%A9
#12
Ola Ahmed El-Gohary, Mona Maher Allam
Infarct-like lesion induced by isoprenaline is a well-known model to study myocardial infarction (MI). Vitamin D has been shown to have anti-inflammatory and antioxidant effects. Recent studies highlighted cross talk between vitamin D and peroxisome proliferator-activated receptor gamma (PPAR- ɣ). The present study was designed to investigate the effect of pretreatment with vitamin D on the isoprenaline-induced infarct-like lesion in rats and the role of PPAR- ɣ as a novel mechanism in vitamin D-mediated cardio protective effect...
January 22, 2017: Canadian Journal of Physiology and Pharmacology
https://www.readbyqxmd.com/read/28174192/infarcted-myocardium-primed-dendritic-cells-improve-remodeling-and-cardiac-function-after-myocardial-infarction-by-modulating-the-treg-and-macrophage-polarization
#13
Eun Ho Choo, Jun-Ho Lee, Eun-Hye Park, Hyo Eun Park, Nam-Chul Jung, Tae-Hoon Kim, Yoon-Seok Koh, Eunmin Kim, Ki-Bae Seung, Cheongsoo Park, Kwan-Soo Hong, Kwonyoon Kang, Jie-Young Song, Han Geuk Seo, Dae-Seog Lim, Kiyuk Chang
BACKGROUND: -Inflammatory responses play a critical role in left ventricular (LV) remodeling after a myocardial infarction (MI). Tolerogenic dendritic cells (tDCs) can modulate immune responses inducing regulatory T cells (Tregs) in a number of inflammatory diseases. METHODS: -We generated tDCs by treating bone marrow-derived dendritic cells with TNF-α and cardiac lysate from MI mice. We injected MI mice, which were induced by a ligation of the left anterior descending coronary artery in C57BL/6 mice, twice with tDCs within 24 hours and at 7 days after the ligation...
February 7, 2017: Circulation
https://www.readbyqxmd.com/read/28142118/dang-gui-bu-xue-tang-ameliorates-coronary-artery-ligation-induced-myocardial-ischemia-in-rats
#14
Ma Chunhua, Long Hongyan, Zhu Weina, He Xiaoli, Zhang Yajie, Ruan Jie
Dang The present study was designed to investigate cardioprotective effects of Dang Gui Bu Xue Tang (DGBUT) on coronary artery ligation-induced myocardial ischemia. Myocardial ischemia (MI) model was induced in SD rats by surgical ligation of the left anterior descending coronary artery. ST segment elevation of Electrocardiograph (ECG) infarct size, levels of lactate dehydrogenase (LDH), creatine kinase (CK), glutathione (GSH) and catalase (CAT), catalase (SOD), malondialdehyde (MDA), and inflammatory cytokines and phosphorylation of extracellular signal-regulated kinase (ERK) 1/2, p38, c-Jun NH2 terminal kinases (JNK), nuclear factor (NF)-κBp65, inhibitory kappa B (IκB) α, IκB kinase (IKK) α and IKKβ were evaluated in rats treated with or without DGBUT...
April 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28135708/remote-ischaemic-preconditioning-and-sevoflurane-postconditioning-synergistically-protect-rats-from-myocardial-injury-induced-by-ischemia-and-reperfusion-partly-via-inhibition-tlr4-myd88-nf-%C3%AE%C2%BAb-signaling-pathway
#15
Jiru Zhang, Jing Zhang, Peng Yu, Min Chen, Qingfeng Peng, Zhiqiang Wang, Nan Dong
BACKGROUND/AIMS: A combination sevoflurane postconditioning (SPC) and remote ischemic preconditioning (RIPC) is proved effective in an ex vivo rat heart perfusion model. However, the combined effect of those two interventions is not tested in rat myocardial ischemia/reperfusion (I/R) model, and the underlying mechanisms remain to be elucidated. This study aimed to investigate the effect in vivo using a rat myocardial I/R model and illuminate the related mechanisms. METHODS: Forty male Sprague-Dawley rats were randomly divided into the following 5 groups: i) sham-operated control; ii) I/R; iii) I/R + RIPC; iv) I/R + SPC; v) I/R + RIPC + SPC...
January 16, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28110194/the-cardioprotective-effect-of-total-flavonoids-on-myocardial-ischemia-reperfusion-in-rats
#16
Dongling Lv, Xiaohu Cheng, Lingyi Tang, Meng Jiang
The flowers of Abelmoschus manihot (L.) Medic is a traditional Chinese medicine used for the treatment of ischemic diseases. The present study is to investigate whether total flavones (TA) of extracted from Abelmoschus manihot L. Medic has the potential cardioprotective effect on myocardial ischemia/reperfusion (I/R) damage in rats. The index of myocardial injury, inflammatory biomarkers and NLRP3-related parameters were measured, respectively. The results demonstrated that compared to I/R group, TA reduced myocardial infarction area, declined serum creatinine kinase (CK), lactate dehydrogenase (LDH) levels, attenuated serum interleukin-6 (IL-6), IL-1β and tumour necrosis factor (TNF-α) production...
April 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/28109806/momordica-charantia-polysaccharides-ameliorate-oxidative-stress-hyperlipidemia-inflammation-and-apoptosis-during-myocardial-infarction-by-inhibiting-the-nf-%C3%AE%C2%BAb-signaling-pathway
#17
Mohammad Raish
The polysaccharide extract of Momordica charantia has various biological activities; however, its effect on endothelial dysfunction in myocardial infarction remains unclear. To elucidate this, myocardial infarction was induced in rats using isoproterenol (ISP). Pretreatment with M. charantia polysaccharides (MCP; 150 or 300mg/kg) for 25days significantly inhibited increases in heart weight, the heart-weight-to-body-weight ratio, and infarction size, and ameliorated the increased serum levels of aspartate transaminase, creatine kinase, lactate dehydrogenase, total cholesterol, triglycerides, very-low-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol...
April 2017: International Journal of Biological Macromolecules
https://www.readbyqxmd.com/read/28105124/cardioprotective-effects-of-traditional-chinese-medicine-guanmaitong-on-acute-myocardial-infarction
#18
Xing-Hua Wang, Guang-Ping Li, Wan-Song Yang, Zhan-Quan Jiao, Hong-Mei Liu, Yan-Ping Ni
Guanmaitong (GMT) is a traditional Chinese herbal compound that has been used for the treatment of coronary heart disease (CHD) and other cardiovascular diseases. However, the efficacy of GMT in treating cardiovascular diseases remains unclear. The aim of the present study was to investigate the protective mechanisms and identify the targeted proteins and signaling networks associated with the physiological activity of GMT in a rat model of acute myocardial infarction (AMI). Sprague-Dawley rats were randomly allocated into five groups: Control group (sham-operated), the model group, and small, medium, and large dosage GMT groups...
December 2016: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/28104751/exercise-training-decreases-nadph-oxidase-activity-and-restores-skeletal-muscle-mass-in-heart-failure-rats
#19
Telma F Cunha, Luiz Roberto Grassman Bechara, Aline V N Bacurau, Paulo R Jannig, Vanessa Azevedo Voltarelli, Paulo M Dourado, Andrea R Vasconcelos, Cristóforo Scavone, Julio C B Ferreira, Patricia C Brum
We have recently demonstrated that NADPH oxidase hyperactivity, NF-κB activation and increased p38 phosphorylation lead to atrophy of glycolytic muscle in heart failure (HF). Aerobic exercise training (AET) is an efficient strategy to counteract skeletal muscle atrophy in this syndrome. Therefore, we tested whether AET would regulate muscle redox balance and protein degradation by decreasing NADPH oxidase hyperactivity, reestablishing NF-κB signaling, p38 phosphorylation and proteasome activity in plantaris muscle of myocardial infarcted-induced HF (MI) rats...
January 19, 2017: Journal of Applied Physiology
https://www.readbyqxmd.com/read/28077321/camkii%C3%AE-subtypes-differentially-regulate-infarct-formation-following-ex-vivo-myocardial-ischemia-reperfusion-through-nf-%C3%AE%C2%BAb-and-tnf-%C3%AE
#20
Charles B B Gray, Takeshi Suetomi, Sunny Xiang, Shikha Mishra, Erik A Blackwood, Christopher C Glembotski, Shigeki Miyamoto, B Daan Westenbrink, Joan Heller Brown
Deletion of Ca(2+)/calmodulin-dependent protein kinase II delta (CaMKIIδ) has been shown to protect against in vivo ischemia/reperfusion (I/R) injury. It remains unclear which CaMKIIδ isoforms and downstream mechanisms are responsible for the salutary effects of CaMKIIδ gene deletion. In this study we sought to compare the roles of the CaMKIIδB and CaMKIIδC subtypes and the mechanisms by which they contribute to ex vivo I/R damage. WT, CaMKIIδKO, and mice expressing only CaMKIIδB or δC were subjected to ex vivo global ischemia for 25min followed by reperfusion...
February 2017: Journal of Molecular and Cellular Cardiology
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