Methane attenuates myocardial ischemia injury in rats through anti-oxidative, anti-apoptotic and anti-inflammatory actions

Chen, Ouyang; Ye, Zhouheng; Cao, Zhiyong; Manaenko, Anatol; Ning, Ke; Zhai, Xiao; Zhang, Rongjia; Zhang, Ting; Chen, Xiao; Liu, Wenwu; Sun, Xuejun

doi:10.1016/j.freeradbiomed.2015.11.017

Cited by 96 publications

(82 citation statements)

References 22 publications

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“…However, there is little knowledge about the function of methane in disease treatment. Some studies reported that methane had positive effects on diabetic retinopathy [23], animal intestinal IR injury [24], and liver IRI [17] via its antioxidative, anti-inflammatory, and antiapoptotic activities [25]. It was first demonstrated in our study that i.p.…”

Section: Discussionsupporting

confidence: 51%

Protective Effects of Methane‐Rich Saline on Rats with Lipopolysaccharide‐Induced Acute Lung Injury

Sun

Wang

et al. 2017

Oxidative Medicine and Cellular Longevity

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Objective. The aim of this research is to evaluate the protective effects of methane-rich saline (MS) on lipopolysaccharide- (LPS-) induced acute lung injury (ALI) and investigate its potential antioxidative, anti-inflammatory, and antiapoptotic activities. Methods. LPS-induced (20 mg/kg) ALI rats were injected with MS (2 ml/kg and 20 ml/kg) before the initiation of LPS induction. Survival rate was determined until 96 h after LPS was induced. Lung injury was assayed by oxygenation index, lung permeability index (LPI), wet-to-dry weight (W/D), and histology. The cells in the bronchoalveolar lavage fluid (BALF) were counted. Oxidative stress was examined by the level of malondialdehyde (MDA) and superoxide dismutase (SOD). Inflammatory factors including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in BALF were determined by ELISA. Lung tissue apoptosis was detected by TUNEL staining and western blotting of caspase-3. Results. It was found that methane significantly prolonged the rat survival, decreased the lung W/D ratio and the content of the inflammatory factors, and reduced the amount of caspase-3 and apoptotic index. In addition, MS increased the level of SOD and decreased the level of MDA significantly. Conclusions. MS protects the LPS-challenged ALI via antioxidative, anti-inflammatory, and antiapoptotic effect, which may prove to be a novel therapy for the clinical management of ALI.

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Section: Discussionsupporting

confidence: 51%

Protective Effects of Methane‐Rich Saline on Rats with Lipopolysaccharide‐Induced Acute Lung Injury

Sun

Wang

et al. 2017

Oxidative Medicine and Cellular Longevity

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“…After a left thoracotomy at the fourth intercostal space, the heart was exposed, the pericardium was opened, and the left anterior descending coronary artery (LAD) was ligated. Rats in the sham group underwent the same surgical procedures, with the exception that the LAD was not ligated, in accordance with previous reports [1]. …”

Section: Methodsmentioning

confidence: 69%

“…Myocardial infarction (MI), the most common cardiovascular complaint, is an acute and fatal condition of the cardiovascular system that threatens human health [1]. The ischemic heart experiences cardiomyocyte loss, with subsequent reparative fibrotic healing, decreased cardiac function, which plays an important role in progression of cardiac hypertrophy, and arrhythmia [2].…”

Section: Introductionmentioning

confidence: 99%

Dl-3-n-butylphthalide protects the heart against ischemic injury and H9c2 cardiomyoblasts against oxidative stress: involvement of mitochondrial function and biogenesis

Tian

Yang

et al. 2017

J Biomed Sci

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BackgroundMyocardial infarction (MI) is an acute and fatal condition that threatens human health. Dl-3-n-butylphthalide (NBP) has been used for the treatment of acute ischemic stroke. Mitochondria may play a protective role in MI injury. However, there are few reports on the cardioprotective effect of NBP or the potential mitochondrial mechanism for the NBP-induced protection against cardiac ischemia injury. We investigated the therapeutic effects of NBP in an in vivo MI model and an in vitro oxidative stress model, as well as the potential mitochondrial mechanism.MethodsThis study comprised two different experiments. The aim of experiment 1 was to determine the protective effects of NBP on MI and the underlying mechanisms in vivo. In part 1, myocardial infarct size was measured by staining with 2,3,5-triphenyltetrazoliumchloride (TTC). Myocardial enzymes and mitochondrial enzymes were assayed. The aim of experiment 2 was to investigate the role of NBP in H2O2-induced myocardial ischemic injury in H9c2 cells and to determine the potential mechanism. In part 2, H9c2 cell viability was evaluated. ROS levels, mitochondrial morphology, and mitochondrial membrane potential of H9c2 cells were measured. ATP levels were evaluated using an assay kit; mitochondrial DNA (mtDNA), the expressions of NRF-1 and TFAM, and mitochondrial biogenesis factors were determined.ResultsNBP treatment significantly reduced the infarct ratio, as observed by TTC staining, decreased serum myocardial enzymes in MI, and restored heart mitochondrial enzymes (isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH), malate dehydrogenase (MDH), and a-ketoglutarate dehydrogenase (a-KGDH) activities after MI. Moreover, in in vitro studies, NBP significantly increased the viability of H9c2 cells in a dose-dependent manner, reduced cell apoptosis, protected mitochondrial functions, elevated the cellular ATP levels, and promoted H2O2-induced mitochondrial biogenesis in H9c2 cardiomyoblasts.ConclusionCollectively, the results from both the in vivo and in vitro experiments suggested that NBP exerted a cardioprotective effect on cardiac ischemic injury via the regulation of mitochondrial function and biogenesis.

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“…• NO), carbon monoxide (CO), and methane, H 2 S belongs to a group of gaseous messengers whose importance in different pathophysiological processes has rapidly increased over the years (11,23,24,30,34).…”

Section: Introductionmentioning

confidence: 99%

The role of hydrogen sulfide in homocysteine-induced cardiodynamic effects and oxidative stress markers in the isolated rat heart

et al. 2016

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This study aimed to assess the role of H 2 S in homocysteine-induced cardiodynamic effects in the isolated rat heart. The hearts were retrogradely perfused according to the Langendorff technique. The maximum and minimum rates of pressure in the left ventricle (dp/dt max, dp/dt min), systolic and diastolic left ventricular pressures (SLVP, DLVP), heart rate (HR), and coronary flow (CF) were measured. A spectrophotometrical method was used to measure the following oxidative stress markers: index of lipid peroxidation (thiobarbituric acid reactive substances, TBARS), nitrite level (NO 2 − ), superoxide anion radicals (O 2• − ), and hydrogen peroxide (H 2 O 2 ) concentrations. The administration of 10 μmol/l DL-homocysteine (DL-Hcy) alone decreased dp/dt max, SLVP, and CF but did not change any oxidative stress parameters. The administration of 10 μmol/l DL-propargylglycine (DL-PAG) decreased all cardiodynamic parameters and increased the concentration of O 2• − .The co-administration of DL-Hcy and DL-PAG induced a significant decrease in all estimated cardiodynamic parameters and decreased the concentration of NO 2 − and O 2 • − but increased the levels of TBARS and H 2 O 2 .Homocysteine shows a lower pro-oxidative effect in the presence of hydrogen sulfide (H 2 S), which indicates a potential anti-oxidative capacity of H 2 S.

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Methane attenuates myocardial ischemia injury in rats through anti-oxidative, anti-apoptotic and anti-inflammatory actions

Cited by 96 publications

References 22 publications

Protective Effects of Methane‐Rich Saline on Rats with Lipopolysaccharide‐Induced Acute Lung Injury

Protective Effects of Methane‐Rich Saline on Rats with Lipopolysaccharide‐Induced Acute Lung Injury

Dl-3-n-butylphthalide protects the heart against ischemic injury and H9c2 cardiomyoblasts against oxidative stress: involvement of mitochondrial function and biogenesis

The role of hydrogen sulfide in homocysteine-induced cardiodynamic effects and oxidative stress markers in the isolated rat heart

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