6 results on '"Cao CM"'
Search Results
2. [Mitochondrial calcium uniporter participates in TNF-alpha induced cardioprotection in isolated rat hearts subjected to ischemia/reperfusion].
- Author
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Gao Q, Zhang SZ, Mao HH, Li QS, Cao CM, and Xia Q
- Subjects
- Animals, Calcium Channels drug effects, In Vitro Techniques, Ischemic Preconditioning, Myocardial methods, Male, Mitochondrial Permeability Transition Pore, Rats, Rats, Sprague-Dawley, Spermine pharmacology, Calcium Channels metabolism, Cardiotonic Agents pharmacology, Mitochondrial Membrane Transport Proteins drug effects, Myocardial Reperfusion Injury prevention & control, Tumor Necrosis Factor-alpha pharmacology
- Abstract
Aim: To investigate whether mitochondrial calcium uniporter participates in the cardioprotection of tumor necrosis factor alpha (TNFalpha) pretreatment in isolated rat hearts subjected to ischemia/reperfusion., Methods: Isolated perfused rat hearts were subjected to 30 min regional ischemia (occlusion of left anterior descending artery) and 120 min reperfusion. The infarct size, coronary flow (CF) and lactate dehydrogenase (LDH) release during reperfusion were measured. The mitochondria of the heart were isolated and suspended in the swelling buffer for measurement of absorbance at 520 nm., Results: Pretreatment with TNFa at 10 U/ml for 7 min followed by 10 min washout reduced the infarct size and LDH release, and improved the recovery of CF during reperfusion. Administration of spermine (20 micromol/L), an opener of mitochondrial calcium uniporter, for 10 min during early reperfusion attenuated the reduction of infarct size and LDH release, and improvement of CF induced by TNFalpha. In isolated mitochondria of the heart pretreated with TNFalpha, the absorbance at 520 nm decreased less than that of mitochondria without TNFalpha pretreatment. Administration of spermine (50 micromol/L) attenuated the change of the absorbance induced by TNFalpha., Conclusion: The findings indicate that TNFalpha protects myocardium against ischemia/reperfusion injury via inhibiting mitochondrial calcium uniporter opening as well as mitochondrial permeability transition pore opening. more...
- Published
- 2006
Catalog
3. The mitochondrial permeability transition pore and the Ca2+-activated K+ channel contribute to the cardioprotection conferred by tumor necrosis factor-alpha.
- Author
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Gao Q, Zhang SZ, Cao CM, Bruce IC, and Xia Q
- Subjects
- Animals, Atractyloside pharmacology, Coronary Circulation physiology, Cyclosporine pharmacology, In Vitro Techniques, Ion Channels drug effects, L-Lactate Dehydrogenase biosynthesis, Male, Mitochondria, Heart drug effects, Mitochondrial Membrane Transport Proteins, Mitochondrial Permeability Transition Pore, Myocardial Contraction drug effects, Myocardial Ischemia physiopathology, Permeability, Potassium Channel Blockers pharmacology, Potassium Channels, Calcium-Activated drug effects, Rats, Rats, Sprague-Dawley, Ion Channels physiology, Mitochondria, Heart physiology, Myocardial Infarction prevention & control, Myocardial Ischemia drug therapy, Myocardial Reperfusion Injury prevention & control, Potassium Channels, Calcium-Activated physiology, Tumor Necrosis Factor-alpha pharmacology
- Abstract
Pretreatment with tumor necrosis factor-alpha (TNF-alpha) is known to trigger cardioprotection and it can activate multiple downstream signaling cascades. However, it is not known whether the mitochondrial permeability transition pore and the Ca(2+)-activated K(+) channel (K(Ca) channel) are involved in the TNF-alpha-induced cardioprotection. In the present study, we examined whether TNF-alpha inhibits pore opening and activates the K(Ca) channel in the cardioprotection. In isolated rat hearts subjected to 30 min of regional ischemia and 120 min of reperfusion, pretreatment with 10 U/ml TNF-alpha for 7 min followed by 10 min washout improved the recovery of rate-pressure product (RPP=left ventricular developed pressure x heart rate) and coronary flow (CF) during reperfusion, and reduced the infarct size and release of lactate dehydrogenase (LDH). Administration of 20 micromol/L atractyloside, a pore opener, for the last 5 min of ischemia and first 15 min of reperfusion, and pretreatment with 1 micromol/L paxilline, an inhibitor of the K(Ca) channel, for 5 min before ischemia, attenuated the recovery of RPP and CF, and the reductions of infarct size and release of LDH induced by TNF-alpha. On the other hand, administration of 10 micromol/L NS 1619, an opener of the K(Ca) channel, for 10 min before ischemia, decreased the infarct size and LDH release, and improved contractile functions and CF; these effects were attenuated by atractyloside. Pretreatment with 0.2 micromol/L cyclosporin A for the last 5 min of ischemia and first 15 min of reperfusion showed similar effects to those of TNF-alpha, and they were not attenuated by paxilline. In mitochondria isolated from hearts pretreated with 10 U/ml TNF-alpha for 7 min, a significant inhibition of Ca(2+)-induced swelling was observed. Furthermore, paxilline attenuated the inhibition of Ca(2+)-induced mitochondrial swelling by TNF-alpha. These findings indicate that TNF-alpha protects the myocardium against ischemia and reperfusion injury by inhibiting mitochondrial permeability transition pore opening as well as activating K(Ca) channels, probably the mitochondrial K(Ca) channel, which is upstream from the pore. more...
- Published
- 2005
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4. [Role of reactive oxygen species, nitric oxide and mitochondrial K(ATP) channels in TNF-alpha induced cardioprotection].
- Author
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Fu C, Xia Q, Cao CM, Gao Q, Yao H, and Jin HF
- Subjects
- Animals, Cardiotonic Agents therapeutic use, Heart drug effects, In Vitro Techniques, Male, Mitochondria, Heart metabolism, Myocardium metabolism, Rats, Rats, Sprague-Dawley, Ischemic Preconditioning, Myocardial methods, Nitric Oxide metabolism, Potassium Channels metabolism, Reactive Oxygen Species metabolism, Tumor Necrosis Factor-alpha therapeutic use
- Abstract
Aim: To explore the cardiac effect of TNF-alpha in postischemic heart and the possible mechanism., Methods: Langendorff perfused rat heart was used to evaluate the contractile properties of myocardium by intraventricular pressure measurement. The isolated rat heart underwent 20 min of global ischemia followed by 20 min of reperfusion. The level of lactate dehydrogenase (LDH) in the coronary effluent was measured to evaluate the cardiac injury. And the activity of manganese superoxide dismutase (Mn-SOD) in myocardium was measured., Results: Perfusion with TNF-alpha (104 U/L) attenuated the inhibitory effects induced by ischemia/reperfusion on left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure(LVEDP), maximal rise/fall rate of left ventricular pressure (+/- dP/dtmax) and rate pressure product (LVDP multiplied by heart rate, LVDP x HR). TNF-alpha significantly decreased the release of LDH (P < 0.05) and increased the activity of Mn-SOD in the myocardium (P < 0.05). Antioxidant 2-MPG (0.3 mmol/L), NOS inhibitor L-NAME (0.5 mmol/L) or mitochondrial selective KATP channel inhibitor 5-HD (100 micromol/L) attenuated the increase in LVDP, +/- dP/dtmax and LVDP x HR, and decrease in LVEDP induced by TNF-alpha in ischemia/reperfusion heart, respectively. And the effects of TNF-alpha in reducing the levels of LDH and increasing the Mn-SOD activity were also attenuated by 2-MPG, L-NAME or 5-HD, respectively., Conclusion: TNF-alpha pretreatment attenuates the myocardial injury induced by ischemia/reperfusion, which coincides with the increasing of myocardial Mn-SOD activity. Reactive oxygen species, nitric oxide and mitochondrial KATP channels are involved in the cardioprotection induced by TNF-alpha. more...
- Published
- 2005
5. [Reactive oxygen species and mitochondrial KATP-sensitive channels mediated cardioprotection induced by TNF-alpha during hypoxia and reoxygenation].
- Author
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Fu C, Cao CM, Xia Q, Yang J, and Lu Y
- Subjects
- Animals, Animals, Newborn, Cell Hypoxia, Cells, Cultured, Heart Ventricles cytology, Mitochondria, Heart physiology, Myocardial Ischemia metabolism, Myocardial Reperfusion Injury prevention & control, Oxygen metabolism, Rats, Rats, Sprague-Dawley, KATP Channels metabolism, Mitochondria, Heart metabolism, Myocardial Reperfusion Injury physiopathology, Myocytes, Cardiac cytology, Reactive Oxygen Species metabolism, Tumor Necrosis Factor-alpha pharmacology
- Abstract
The aim of the present study was to testify whether the reactive oxygen species and mitochondrial ATP-sensitive potassium (K(ATP)) channels were involved in the cardioprotection induced by tumor necrosis factor alpha (TNF-alpha) in the cultured neonatal ventricular myocytes suffered from 12 h of hypoxia and 6 h of reoxygenation. We tested the release of lactate dihydrogenase (LDH) and manganese superoxide dismutase (Mn-SOD) with spectrophotometry. It was shown that pretreatment with TNF-alpha (10, 50, 100, or 500 U/ml) significantly increased the Mn-SOD activity and reduced LDH release in the neonatal ventricular myocytes subjected to hypoxia and reoxygenation. Pretreatment with NAC (1 mmol/L), antimycin A (50 micromol/L), 2-MPG (400 micromol/L), DDC (100 nmol/L) or 5-HD (100 micromol/L), respectively, attenuated the increase in Mn-SOD activity and reduction of LDH level induced by TNF-alpha in ventricular myocytes. Diazoxide (50 micromol/L), a selective opener of the mitochondrial K(ATP) channel, decreased the LDH release of the myocytes subjected to hypoxia and reoxygenation, which could be abolished by pretreatment with NAC (1 mmol/L) or 5-HD (100 micromol/L). These results suggest that oxygen radical signals and mitochondrial K(ATP) channels are involved in the cardioprotection induced by TNF-alpha. more...
- Published
- 2003
6. [Mechanism of negative inotropic effect of tumor necrosis factor-alpha on rat myocardium].
- Author
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Fu C, Cao CM, Zhang J, and Xia Q
- Subjects
- Animals, Calcium metabolism, Calcium-Transporting ATPases metabolism, Depression, Chemical, In Vitro Techniques, Male, Myocardium metabolism, Rats, Rats, Sprague-Dawley, Sodium-Potassium-Exchanging ATPase metabolism, Myocardial Contraction drug effects, Tumor Necrosis Factor-alpha pharmacology
- Abstract
Objective: To investigate the mechanism of the negative inotropic effect of tumor necrosis factor-alpha (TNF-alpha) in cardiomyocytes., Methods: The spectrofluorometric method was used to verify the calcium handling of the single myocyte. The activities of Ca(2+)-ATPase of sarcoplasmic reticulum (SR) and the activities of Ca(2+)-ATPase and Na(+)/K(+)-ATPase of plasma membrane were measured with colorimetric methods., Results: TNF-alpha at 20 U/ml and 200 U/ml depressed the contractility of ventricular papillary muscle to 91% and 76% of control (P<0.01) respectively, but had no effect on the amplitude of electrically induced calcium transient in single myocyte. TNF-alpha inhibited the responsiveness of SR Ca(2+)ATPase activity to ATP (0.1 - 4 mmol/L) and Ca(2+) (1 - 40 micromol/L). TNF-alpha did not alter the activities of Ca(2+)-ATPase and Na(+)/K(+)-ATPase of plasma membrane compared with control group., Conclusion: TNF-alpha decreases the myocardial contractility, at least partly, by inhibiting the activity of SR Ca(2+)- ATPase. more...
- Published
- 2003
- Full Text
- View/download PDF
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