Hebei Academy of Medical science

Shijiazhuang, China

Hebei Academy of Medical science

Shijiazhuang, China
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Xie Y.-H.,Hebei University of Science and Technology | Ma Y.-S.,TCM Hospital of Shijiazhuang City | Zhang N.,Hebei Academy of Medical science | Zhang J.-X.,Hebei Academy of Medical science
Chinese Pharmacological Bulletin | Year: 2014

Aims: To observe the changes of endogenous hydrogen sulfide/cystathionine- γ-lyase (H2S/CSE) system and to study the effects of H 2S on cardiac function, H2S/CSE and myocardial infarct volumes in acute myocardial ischemic injury in isolated hearts of rats. Methods: The myocardial ischemic injury model was established by the ligation of coronary artery. The hemodynamic parameters, such as the left ventricular developed pressure (LVDP), ± dp/dtmax and coronary arterial flow(CF), were respectively recorded to evaluate the cardiac function. The content of H2S and the activity of CSE in cardiac tissue were detected respectively at each time point after ischemia. Infarct volumes in isolated rat hearts were determined by dual staining with Evans-blue and TTC. Results (1) Compared with those of the sham group, LVDP, ± dp/dt max and CF were significantly decreased at 30 min, 1,2,3,4 4 after ischemia(P <0.01), there were no statistically significant differences in the content of H2S and the activity of CSE in cardiac tissue at 30 min after ischemia. But during the periods from 1h to 4h after ischemia, the content of H2S and the activity of CSE in cardiac tissue were significantly decreased, the infarct volumes were greatly increased compared with those of the sham control group (P < 0.05 or P < 0.01). (2) Compared with those of the ischemia 4h group, LVDP, ± dp/dtmax and CF were significantly increased in the NaHS low, middle and high dose groups (P < 0.05 or P < 0.01), the content of H2S and the activity of CSE in cardiac tissue were significantly increased in the NaHS low, middle and high dose groups (P < 0.05 or P < 0.01), and the infarct volumes were significantly decreased in NaHS middle and high dose groups (P < 0.01). Conclusion: H2S and CSE are involved in myocardial ischemic injury in isolated hearts of rats. Administration of NaHS could enhance the activity of CSE, increase the content of H2S, and reduce infarct volumes. It could be suggested that H 2S has cardioprotective effects on acute myocardial ischemic injury.


Xie Y.-H.,Hebei University of Science and Technology | Ma Y.-S.,TCM Hospital of Shijiazhuang | Zhang N.,Hebei Academy of Medical science | Zhang J.-X.,Hebei Academy of Medical science
Chinese Pharmacological Bulletin | Year: 2014

Aim: To investigate whether hydrogen sulfide (H2S) inhibits cardiomyocyte apoptosis induced by acute myocardial ischemia in isolated perfused rat heart.Methods: The myocardial ischemia injury model was replicated with Langendorff isolated perfused rat heart, and the left anterior descending coronary artery was ligated for 4 h. 40 male SD rats were divided into five groups randomly: sham group, ischemia group, and NaHS groups (5, 10, 20 μmol • L-1). The segmental heart samples were used for HE staining. Cardiomyocyte apoptosis was detected with TUNEL assay. The expressions of caspase-3 and Cyt-C in hearts were determined with Western blot analysis.Results: Myocardial cells were found to show serious disorder and coagulated zonal necrosis under light microscope, the apoptotic rate of cardiomyocytes and the expression of caspase-3 and Cyt-C were significantly increased after ischemia for 4h. Perfusion of NaHS resulted in more clear cell morphology and milder pathologic changes of myocardiocytes according to the HE staining a-nalysis, and the significant decrease of expression of Cyt-C. After perfusion of 10, 20 μmol • L-1 NaHS, the apoptotic rate of cardiomyocytes and the expression of caspase-3 were significantly decreased.Conclusion: H2S has certain protective effects on acute myocardial ischemic injury in isolated perfused rat heart via inhibiting cardiomyocyte apoptosis.


Zhang J.-X.,Hebei Academy of Medical science | Ding Y.-Y.,Hebei Academy of Medical science | Li L.-F.,Hebei Academy of Medical science | Liu F.,Hebei Academy of Medical science | And 3 more authors.
Chinese Pharmacological Bulletin | Year: 2012

Aim: To investigate the effect of hydrogen sulfide (H2S) on cardiomyocyte apoptosis in rats with acute myocardial ischemia and to analyze the pathological damage of myocardial tissue. Methods: Forty male rats were randomly divided into five groups: sham group, ischemia group, ischemia + NaHS (Low dose) group, ischemia + NaHS (Middle dose) group, ischemia + NaHS (High dose) group. The acute myocardial ischemia model was established by ligating the left anterior descending coronary (LAD) of the rats. LADs were not ligated but only threaded in the sham operation rats. In ischemia + NaHS Low, Middle and High dose groups the NaHS (0.78, 1.56, 3.12 mg·kg-1) were intraperitoneally administrated respectively 3 hours after ischemia. The rats were respectively killed 6 hours after ischemia. Hearts were quickly removed, and the apoptotic rate of cardiomyocytes was evaluated by Flow Cytometry. The positive expressions of Bcl-2 and Bax in cardiomyocytes were respectively detected by immunohistochemistry. The expression of caspase-3 protein was observed with Western blot analysis. Results: Acute myocardial ischemia significantly increased the apoptotic rate of cardiomyocytes and the expression of Bax and caspase-3 protein, and decreased the expression of bcl-2 and the ratio of bcl-2/Bax. Administration of NaHS reduced the percentage of apoptotic cells, the expression of caspase-3 and Bax protein, improved the expression of bcl-2 protein, the ratio of bcl-2/Bax, and the pathological injury of the myocardial cells induced by acute ischemia in rats. Conclusion: H2S attenuates acute ischemia induced-apoptosis of myocardial cells, whose mechanisms may be involved in the increases in the expression of Bcl-2 and the ratio of bcl-2/Bax and the decreases in the expressions Bax and Cleaved capsase-3.


Xie Y.-H.,Hebei University of Science and Technology | Zhang N.,Hebei Academy of Medical science | Ma Y.-S.,Shijiazhuang Hospital of Traditional Chinese Medicine | Zhang J.-X.,Hebei Academy of Medical science
Chinese Journal of Pharmacology and Toxicology | Year: 2015

OBJECTIVE To investigate the mitochondrial pathway and possible molecular mechanism of sodium hydrosulfide (NaHS) in acute myocardial ischemia injury in isolated hearts of rats. METHODS The myocardial ischemia injury model was established by ligating of coronary artery. After 2 h ischemia, hearts in model group were sequentially subjected to K-H solution for 2 h, while hearts in NaHS groups received 2 h of NaHS 5, 10 and 20 μmol L-1 containing buffer, respectively. The ultrastructural alterations of mitochondria were observed under an electric microscopy. Mitochondria were separated by homogenization and differential centrifugation before their swelling and activity of mitochondria were determined. The activities of ATPase, glutathione peroxidase (GSH-Px), superoxide dis- mutase (SOD) and lactate dehydrogenase (LDH), and the content of malondialdehyde(MDA), were respectively measured by spectrophotometry. RESULTS Compared with the sham group, the swelling of mitochondria was distinctly increased in model group. The activities of ATPase, GSH-Px and SOD in myocardial mitochondria of the NaHS group were 4.76±0.25,68.59±2.00 and (23.37±1.13) kU g-1 protein, respectively, which were significantly lower than in the sham group (11.23±0.65, 133.37±3.47 and (74.42±1.97) kU-g-1 protein, respectively, P<0.01]. The content of MDA in myocardial mitochondria of the model group was (1.45±0.09)μmol-g-1 protein, which was significantly higher than in the sham group C(0.85±0.05)nmol-g-1 protein, P<0.01 ], and the activity of LDH in perfusate was (104±6)U-L-1, which was significantly higher than in the sham group (50±3)U-L-1(P<0.01). Compared with the model group, the swelling of mitochondria was distinctly inhibited in NaHS 5, 10 and 20 nmol-L-1 groups(P< 0.01), but the activity of ATPase(5.06±0.22, 7.72±0.37 and (10.57+0.44 )kU-g-1 protein, respectively], GSH-Px[87.94±1.65, 106.66±2.14 and (125.57±2.12) kU-g-1 protein, respectively] and SOD[39.00± 1.00, 57.46±1.21 and (69.56±1.56) kU g-1 protein, respectively] in myocardial mitochondria was significantly increased, the content of MDA [1.28±0.09, 1.06±0.06 and (0.89±0.04)pmol-g-1 protein, respectively] in myocardial mitochondria was significantly decreased in NaHS 5, 10 and 20 pmol L-1 groups (P<0.05 or P<0.01), and the activity of LDH[83±3, 70±4 and (60±4)U-L-1, respectively] in perfusate was significantly decreased in NaHS 5, 10 and 20 μmol-L-1 groups (P<0.01). CONCLUSION NaHS prevents acute myocardial ischemia injury in isolated hearts of rats presumably by improving antioxidant defense and attenuating oxidative damage to mitochondria.


Li G.-F.,Hebei Medical University | Luo H.-K.,Hebei Medical University | Li L.-F.,Hebei Academy of Medical science | Zhang Q.-Z.,Hebei Academy of Medical science | And 7 more authors.
Clinical and Experimental Pharmacology and Physiology | Year: 2012

Hydrogen sulphide (H2S), one of three signalling gasotransmitters, plays an important role in oxidative stress and apoptosis. However, the effects of H2S on oxidative stress-induced apoptosis in focal cerebral ischaemic injury in rats have not been clarified. In the present study, sodium hydrosulphide (NaHS) was used as the H2S donor. Eighty-four Sprague-Dawley rats were randomly divided into six groups: sham, sham + low-dose (2.8 mg/kg) NaHS, sham + high-dose (11.2 mg/kg) NaHS, infarct, infarct + low-dose NaHS and infarct + high-dose NaHS. The focal cerebral ischaemic model was created by cranially inserting a nylon thread with a rounded tip into an internal carotid artery. Rats were killed 21 h after administration of NaHS. In the infarct + low-dose NaHS compared with infarct group, infarct volume was significantly decreased and injury to the mitochondria in nerve cells was mitigated. Furthermore, significant increases were seen in mitochondrial superoxide dismutase and glutathione peroxidase activity and neuronal bcl-2 protein levels, whereas mitochondrial malondialdehyde content and neuronal bax and caspase 3 protein levels were significantly decreased, in the infarct + low-dose NaHS compared with infarct group. The effects seen in the infarct group were significantly aggravated in the infarct + high-dose NaHS group. The findings of the present study provide novel evidence for the dual effects of H2S on focal cerebral ischaemic injury via modulation of oxidative stress-induced apoptosis. © 2012 The Authors Clinical and Experimental Pharmacology and Physiology © 2012 Wiley Publishing Asia Pty Ltd.


Xie Y.-H.,Hebei Medical University | Zhang N.,Hebei Medical University | Li L.-F.,Hebei Academy of Medical science | Zhang Q.-Z.,Hebei Academy of Medical science | And 6 more authors.
Molecular Medicine Reports | Year: 2014

Hydrogen sulfide (H2S) is a signaling gasotransmitter, involved in various physiological and pathological processes. H2S-donating drugs have been tested to conjugate the beneficial effects of H2S with other pharmaceutical properties. It has been shown that the endogenous cystathionine-γ-lyase (CSE)/H2S pathway participates in myocardial ischemia injury in isolated hearts in rats. The present study aimed to investigate the cytoprotective action of H2S against acute myocardial ischemia injury in rats. Isolated rat hearts were perfused and subjected to ischemic conditions for 4 h. The hearts were assigned to five groups: Sham, model, infarct plus low-dose (5 μmol/l) NaHS, infarct plus middle-dose (10 μmol/l) NaHS and infarct plus high-dose (20 μmol/l) NaHS. The administration of NaHS enhanced the activity of CSE, increased the content of H2S and reduced infarct volumes following myocardial ischemia injury. Furthermore, the administration of NaHS attenuated the injury to organelles (including the mitochondria, nucleus and myofilaments) by reducing lactate dehydrogenase activity, decreasing the level of mitochondrial malondialdehyde and increasing the activities of superoxide dismutase and glutathione peroxidase in the ischemic myocardial mitochondria. These protective effects of H2S against myocardial ischemia injury appeared to be mediated by its antioxidant activities and the preservation of mitochondrial function.


PubMed | Hebei Medical University and Hebei Academy of Medical science
Type: Journal Article | Journal: International journal of molecular medicine | Year: 2016

The endogenous signaling gasotransmitter, hydrosulfide (H2S), has been shown to exert cardioprotective effects against acute myocardial infarction (AMI) due to ischemic injury. However, the mechanisms responsible for these effects are not yet fully understood. In this study, we investigated whether sodium hydrogen sulfide (NaHS), an H2S donor, attenuates acute myocardial ischemic injury through glycogen synthase kinase-3 (GSK-3)/-catenin signaling. For this purpose, we utilized an in vivo rat model of AMI by occluding the left anterior descending coronary artery. NaHS (0.39, 0.78 or 1.56 mg/kg, intraperitoneally), the GSK-3 inhibitor, SB216763 (0.6 mg/kg, intravenously), or 1% dimethylsulfoxide (2 ml/kg, intravenously) were administered to the rats. The results demonstrated that the administration of medium- and high-dose NaHS and SB216763 significantly improved rat cardiac function, as evidenced by an increase in the mean arterial pressure, left ventricular developed pressure, contraction and relaxation rates, as well as a decrease in left ventricular end-diastolic pressure. In addition, the administration of NaHS and SB216763 attenuated myocardial injury as reflected by a decrease in apoptotic cell death and in the serum lactate dehydrogenase concentrations, and prevented myocardial structural changes. The administration of NaHS and SB216763 increased the concentrations of phosphorylated (p-)GSK-3, the p-GSK-3/t-GSK-3 ratio and downstream protein -catenin. Moreover, western blot and immunohistochemical analyses of apoptotic signaling pathway proteins further established the cardioprotective potential of NaHS, as reflected by the upregulation of Bcl-2 expression, the downregulation of Bax expression, and a decrease in the number of TUNEL-positive stained cells. These findings suggest that hydrosulfide exerts cardioprotective effects against AMI-induced apoptosis through the GSK-3/-catenin signaling pathway.


PubMed | Peoples Hospital of Dingzhou, Hebei Medical University and Hebei Academy of Medical science
Type: Journal Article | Journal: Experimental and therapeutic medicine | Year: 2015

Hydrogen sulfide (H


Marcus N.J.,University of Nebraska Medical Center | Del Rio R.,University of Nebraska Medical Center | Schultz E.P.,University of Nebraska - Lincoln | Xia X.-H.,Hebei Academy of Medical Science | Schultz H.D.,University of Nebraska Medical Center
Journal of Physiology | Year: 2014

In congestive heart failure (CHF), carotid body (CB) chemoreceptor activity is enhanced and is associated with oscillatory (Cheyne-Stokes) breathing patterns, increased sympathetic nerve activity (SNA) and increased arrhythmia incidence. We hypothesized that denervation of the CB (CBD) chemoreceptors would reduce SNA, reduce apnoea and arrhythmia incidence and improve ventricular function in pacing-induced CHF rabbits. Resting breathing, renal SNA (RSNA) and arrhythmia incidence were measured in three groups of animals: (1) sham CHF/sham-CBD (sham-sham); (2) CHF/sham-CBD (CHF-sham); and (3) CHF/CBD (CHF-CBD). Chemoreflex sensitivity was measured as the RSNA and minute ventilatory (V̇E) responses to hypoxia and hypercapnia. Respiratory pattern was measured by plethysmography and quantified by an apnoea-hypopnoea index, respiratory rate variability index and the coefficient of variation of tidal volume. Sympatho-respiratory coupling (SRC) was assessed using power spectral analysis and the magnitude of the peak coherence function between tidal volume and RSNA frequency spectra. Arrhythmia incidence and low frequency/high frequency ratio of heart rate variability were assessed using ECG and blood pressure waveforms, respectively. RSNA and V̇E responses to hypoxia were augmented in CHF-sham and abolished in CHF-CBD animals. Resting RSNA was greater in CHF-sham compared to sham-sham animals (43 ± 5% max vs. 23 ± 2% max, P < 0.05), and this increase was not found in CHF-CBD animals (25 ± 1% max, P < 0.05 vs. CHF-sham). Low frequency/high frequency heart rate variability ratio was similarly increased in CHF and reduced by CBD (P < 0.05). Respiratory rate variability index, coefficient of variation of tidal volume and apnoea-hypopnoea index were increased in CHF-sham animals and reduced in CHF-CBD animals (P < 0.05). SRC (peak coherence) was increased in CHF-sham animals (sham-sham 0.49 ± 0.05; CHF-sham 0.79 ± 0.06), and was attenuated in CHF-CBD animals (0.59 ± 0.05) (P < 0.05 for all comparisons). Arrhythmia incidence was increased in CHF-sham and reduced in CHF-CBD animals (213 ± 58 events h-1 CHF, 108 ± 48 events h-1 CHF-CBD, P < 0.05). Furthermore, ventricular systolic (3.8 ± 0.7 vs. 6.3 ± 0.5 ml, P < 0.05) and diastolic (6.3 ± 1.0 vs. 9.1 ± 0.5 ml, P < 0.05) volumes were reduced, and ejection fraction preserved (41 ± 5% vs. 54 ± 2% reduction from pre-pace, P < 0.05) in CHF-CBD compared to CHF-sham rabbits. Similar patterns of changes were observed longitudinally within the CHF-CBD group before and after CBD. In conclusion, CBD is effective in reducing RSNA, SRC and arrhythmia incidence, while improving breathing stability and cardiac function in pacing-induced CHF rabbits. © 2013 The Physiological Society.


Liu F.,Hebei Academy of Medical science
Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology | Year: 2011

To investigate the effect of hydrogen sulfide (H2S) on mitochondrial function in acute myocardial ischemia in rats. Acute myocardial ischemia models were established by ligating the left anterior descending coronary artery (LADC) of rats. Fourty-eight male SD rats were randomly divided into 6 groups (n = 8): sham operation group, ischemia group, ischemia + sodium hydrosulfide (NaHS) low, middle and high dose groups and ischemia + DL-proparglycine(PPG) group. The ultrastructures of myocardial mitochondria were observed with electron microscope. The content of H2S in plasma and the activity of cystathionine-gamma-lyase (CSE) in myocardial tissue of rats were respectively detected. The swelling and activity of myocardial mitochondria were determined. The activities of ATPase, GSH-Px, SOD and the content of malondial-dehyde (MDA) in myocardial mitochondria of rats were also measured. Compared with those of the sham operation group, the content of H2S in plasma, the activity of CSE in myocardial tissue and the activity of myocardium mitochondria were significantly decreased. The activities of ATPase, SOD, GSH-Px in myocardial mitochondria were significantly decreased, The content of malondial dehyde(MDA) in myocardial mitochondria and the swelling of mitochondria were distinctly increased in the ischemia group (P < 0.01). Compared with those of the ischemia group, the content of H2S in plasma and the activity of CSE in myocardial tissue were increased, and the activities of mitochondria, ATPase, SOD, and GSH-Px in myocardial mitochondria were significantly increased in ischemia + NaHS low, middle and high-dose groups; the swelling of mitochondria and the content of MDA in myocardial mitochondria were significantly decreased in ischemia + NaHS middle and high-dose groups (P < 0.05 or P < 0.01). The administration of PPG could partially reduce the myocardial protection of hydrogen sulfide (P < 0.05 or P < 0.01). It could be concluded that the administration of hydrogen sulfide could enhance the activities of mitochondrial ATPase, SOD, GSH-Px, decrease the level of mitochondrial lipid peroxidation, and play a protective effect against acute myocardial ischemia.

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