Tao‐Hong‐Si‐Wu decoction reduces ischemia reperfusion rat myoblast cells calcium overloading and inflammation through the Wnt/IP3R/CAMKII pathway

2019 ◽  
Vol 120 (8) ◽  
pp. 13095-13106 ◽  
Author(s):  
Zhu Fuping ◽  
Li Wuping ◽  
Wang Linhua ◽  
Pan Chengxi ◽  
Zhou Fuqiang ◽  
...  
Keyword(s):  
Ischemia Reperfusion ◽  
Myoblast Cells ◽  
Calcium Overloading

Abstract 254: 14, 15-EET Protects Heart Pericytes by Delaying I/R Injury-induced Calcium Overloading

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Zhiping Cao ◽  
Catherine M Davis ◽  
Sanjiv Kaul ◽  
Nabil J Alkayed
Keyword(s):  
Cell Death ◽  
Intracellular Calcium ◽  
Structural Integrity ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Control Group ◽  
Calcium Signal ◽  
Mouse Heart ◽  
Oxygen And Glucose Deprivation ◽  
Calcium Overloading

Background - Pericytes are an important cellular component of the blood vessel wall of the arteries, arterioles, and microvessels of the heart; they provide structural integrity and regulate vessel diameter by contracting and relaxing dynamically in response to vasoactive stimuli. It has been suggested that pericytes contribute to coronary no-flow due to pericyte constriction following myocardial infarction, thus worsening outcome. It has also been demonstrated that intracellular calcium is involved in perciyte constriction. Our previous findings indicate that cardiomyocytes are protected following ischemia/ reperfusion injury (I/R) by the eicosanoid 14,15-EET. Since 14,15-EET is protective following I/R and a vasodilator, we tested the hypotheses that I/R injury induces calcium overloading, which injures peciytes, and that 14, 15-EET is able to block this process. Methods and Results - We isolated and cultured pericytes from the mouse heart ventricle by 3G5 antibody Dynabead sorting. Pericytes were characterized by multiple immunocytochemical markers for contractile proteins, cytoskeletal protein, and cell surface receptors (alpha-smooth muscle actin, calponin-1, NG2, vimentin, CD31,smoothlin, and fibroblast protein-1). Cultured pericytes were subjected to 5 hours of oxygen and glucose deprivation, with or without 14,15-EET, followed by 15 hours of re-oxygenation in the absence of 14,15-EET. Calcium imaging and cell death during re-oxygenation were assessed by Fluo-4 and propidium iodide respectively. Digital images were taken with confocal microscope (Nikon Eclipse Tie-A1RSi). The brightness of the green fluorescent signals represents the relative level of intracellular calcium and the red fluorescent signals represent the cell death. We found that calcium signal peak (overloading) occurred during re-oxygenation, immediately followed by cell death. This process was delayed by 14,15-EET treatment during oxygen and glucose deprivation. The cell death at 5h, 10h, and 15h of re-oxygenation was 57.2%, 71.1%, and 85.3% in control group, and 19.9%, 35.3%, and 58.3% in 14,15-EET treated group. Conclusions - Our data suggests that 14,15-EET-induced protection in pericytes is mediated through the calcium signaling pathway.

DJ1 and microRNA-214 act synergistically to rescue myoblast cells after ischemia/reperfusion injury

2018 ◽  
Vol 119 (9) ◽  
pp. 7192-7203 ◽  
Author(s):  
Shahrooz Ghaderi ◽  
Neda Alidadiani ◽  
Jafar SoleimaniRad ◽  
Hamid R. Heidari ◽  
Nafi Dilaver ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Myoblast Cells

Abstract P25: Hypothermia Treatment Inhibits Cardiomyocytes Calcium Overload and Mitochondria Transition Permeability after Hypoxia- Reoxygenation Injuries

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Chien-Hua Huang ◽  
Chiung-Yuan Hsu ◽  
Min-Shan Tsai ◽  
Huei-Wen Chen ◽  
Hsiao-Ju Cheng ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Reductase Activity ◽  
Ischemia Reperfusion ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Rat Cardiomyocytes ◽  
Hypothermia Treatment ◽  
Mitochondria Permeability Transition Pore ◽  
Calcium Overloading ◽  
Hypoxia Reoxygenation

Introduction: Hypothermia treatment can provide cardiac protection against ischemia reperfusion injuries, but underlying mechanisms remain unclear. Hypothesis: Hypothermia-related cardiomyocyte protection is through the mitochondrial dependent pathways. Methods : H9c2 rat cardiomyocytes were cultured in 37°C, 5% CO 2 incubators. After initiation of hypoxia-reoxygenation (H-R) treatment, the H9c2 cells were moved to hypothermia (31°C) or kept in normothermia (37°C) environments until cells harvested. Cell damage, intracellular and mitochondria calcium loads were studies. Mitochondria permeability transition and transmembrane potentials were studies by flowcytometric studies. Results: Hypothermia treatment ameliorates H9c2 cardiomyocytes survival after H-R injuries (68.1±11.8% vs. 85.0±12.7 %, P=0.025). Intracellular and mitochondria calcium overloading after H-R injuries was improved under 31°C environment (153.5±16.4 % vs. 957.1±311.7 %, P<0.01 for intracellular calcium; 101.8±28.5% vs. 159.4±32.5%, P=0.014 for mitochondria calcium). Mitochondria reductase activity were more preserved under hypothermia treatment after H-R injuries (55.7±10.9% vs. 8.5±1.2%, P<0.01). Hypothermia treatment decreased the continuous opening of mitochondria permeability transition pore after H-R damage by less reduction of mitochondria calcein fluorescence (15.6±13.7 % vs. 52.8±28.1 %, P=0.003). Release of cytochrome c into the cytoplasm from mitochondria after H-R injuries was more evident in normothermia condition by confocal microscopy study. Activation of caspase-9, which is down-streaming to cytochrome c, was down-regulated under hypothermia (62.1±21.9% vs. 87.5±7.3%, P=0.019). Loss of mitochondria integrity with decreasing of mitochondria transmembrane potential was less evident in 31°C than 37°C environments (55.9±23.3% vs. 102±20.2%, P=0.016). Conclusion: Hypothermia treatment at 31°C provides cardiomyocyte protection against hypoxia-reoxygenation injuries. The mechanisms are related to the decreasing intracellular and mitochondria calcium overloading, preserving the integrity of mitochondria by reduction of mitochondria permeability transition pore opening and cytochrome c release.

Effects of nitric oxide and hydrogen on isolated heart and cultured myoblast cells under the condition simulating ischemia–reperfusion

Nitric Oxide ◽  
2012 ◽  
Vol 27 ◽  
pp. S34
Author(s):  
Yuri Sato ◽  
Mai Suzuki ◽  
Kenichi Kokubo ◽  
Toshihiro Shinbo ◽  
Ryuji Hataishi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Isolated Heart ◽  
Ischemia Reperfusion ◽  
Myoblast Cells

scholarly journals Tetrahydroxystilbene Glucoside (TSG) Restores the Effect of Transient Hypoxia on Reperfusion Injury in Senescent H9c2 Cells by Regulating Mitochondrial Energy Metabolism

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Yin Cheng ◽  
Jia Song ◽  
Pengfei Hu ◽  
Yun Zhu
Keyword(s):  
Energy Metabolism ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mitochondrial Energy Metabolism ◽  
Metabolic Functions ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Calcium Overloading ◽  
Tetrahydroxystilbene Glucoside

Tetrahydroxystilbene glucoside (TSG) is extracted from a famous Chinese herbal medicine which is widely used as an antiaging agent in history. Lots of studies gave evidence that TSG exhibited benefits to brain, like improvement of learning and memory and synaptic plasticity. Moreover, the polyphenolic structure of TSG enables its capability to prevent cerebral ischemia/reperfusion injury (IRI) by reducing apoptosis and ROS/RNS generation. Due to its antioxidant profile, TSG had been demonstrated to alleviate cardiac toxicity by regulating biochemical indexes and ROS. However, whether TSG exhibited cardioprotective effects via mitochondrial energy metabolic functions, which played crucial role in IRI, remained unclear. Here, we used an in vitro aging model of cardiomyocytes to evaluate the effects of TSG on transient hypoxia-pretreated hypoxia/reoxygenation (H/R) injury and mitochondrial energy metaolism. Our results showed that TSG enhanced cardioprotective effect of transient hypoxia on H/R by reducing excessive ROS production and calcium overloading. Significant improvements of mitochondrial respiratory functions and ketone body metabolism elucidated that TSG restored the effect of transient hypoxia on H/R injury in aging cardiomyocytes via upregulating mitochondrial energy metabolism.

Changes in hepatic and pulmonary leukotriene concentrations following ischemia-reperfusion of rat liver

2001 ◽  
Vol 120 (5) ◽  
pp. A379-A379
Author(s):  
Y TAKAMATSU ◽  
K SHIMADA ◽  
K CHIJIWA ◽  
M TANAKA
Keyword(s):  
Rat Liver ◽  
Ischemia Reperfusion

1618: Real-Time Monitoring of Nitric Oxide and Blood Flow During Ischemia-Reperfusion in the Rat Testis

2006 ◽  
Vol 175 (4S) ◽  
pp. 521-521
Author(s):  
Motoaki Saito ◽  
Tomoharu Kono ◽  
Yukako Kinoshita ◽  
Itaru Satoh ◽  
Keisuke Satoh
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Real Time ◽  
Ischemia Reperfusion ◽  
Real Time Monitoring ◽  
Rat Testis

1843: Role of Cxcr2 in Renal Ischemia/Reperfusion Injury

2004 ◽  
Vol 171 (4S) ◽  
pp. 487-487
Author(s):  
Motoo Araki ◽  
Masayoshi Miura ◽  
Hiromi Kumon ◽  
John Belperio ◽  
Robert Strieter ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Renal Ischemia Reperfusion Injury
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