Da-wei Zhang

307 Hospital of the Chinese People's Liberation Army, Peping, Beijing, China

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Publications (4)0 Total impact

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    ABSTRACT: To explore the change of phospho-p38 (P-p38) mitogen activated protein kinase(MAPK) and its influence on myocardial apoptosis in reperfusion injury in postconditioning. Totally 60 rats were equally and randomly divided into six groups: Sham group,reperfusion injury (R/I) group, postconditioning (Post) group, SB203580 (I_p38) group, anisomycin plus postconditioning (Ani+post) group,and anisomycin (Ani) group. After the model of acute myocardial infarction was established,placebo solution (DMSO), SB203580 (1 mg/kg), or anisomycin (2 mg/kg) was injected through jugular vein 5 minutes before reperfusion. Six hours later, 3 rats in each group were executed and the hearts were separated to measure the signaling molecules including phospho-p38,tumor necrosis factor-alpha (TNF-α), Caspase-8, Bcl-2/Bax, and cytochrome-c (Cyt-c). Twenty-four hours later,the hemodynamic data were measured in the remaining rats,and then blood was collected to determine the serum markers of cardiac damage. After that,hearts were separated to measure the infarction area and apoptosis. Six hours after reperfusion,the expressions of P-p38 in Post and I_p38 group were significantly lower than those in R/I group (P<0.05), significantly higher in Ani+post and Ani group than in Post group (P<0.05), and significantly lower in Ani+post group than in R/I group (P<0.05). The expressions of TNF-α and Caspase-8 were significantly lower in Post and I_p38 group than in R/I group (P<.05) and significantly higher in Ani+post and Ani group than in Post group (P<0.05). The expression of TNF-α was significantly lower in Ani+post group than in R/I group (P<0.05). The expression of Bcl-2 was significantly higher in Post and I_p38 groups than in R/I group (P<0.05) and significantly lower in Ani+post and Ani groups than in Post group (P<0.05). The expression of Bax was significantly lower in Post and I_p38 groups than in R/I group (P<0.05) and were significantly higher in Ani+post and Ani group than in Post group (P<0.05). The expression of Cyt-c after the removal of the cytoplasm mitochondria was significantly lower in Post and I_p38 group than in R/I group (P<0.05) and was significantly higher in Ani+post and Ani group than in Post group (P<0.05). Twenty-four hours after reperfusion,the values of rate-pressure product and ±delta pressure/delta time max were significantly lower in R/I group than in Post and I_p38 groups (P<0.05) and was significantly higher in Post group than in Ani+post and Ani group (P<0.05). The apoptotic index (AI) was significantly lower in Post and I_p38 groups than in R/I group (P<0.05) and was significantly higher in Ani+post and Ani groups than in Post group (P<0.05). The values of creatine kinase and creatine kinase-MB were significantly lower in Post,Ani+post, and I_p38 groups than in R/I group (P<0.05) and were significantly higher in Ani+post and Ani group than in Post group (P<0.05). The area of necrosis/area at risk ratio was significantly lower in Post and I_p38 groups than in R/I group (P<0.05) and was significantly higher in Ani+post and Ani groups than in Post group (P<0.05). Postconditioning can inhibit the phosphorylation of p38 MAPK,through which it can attenuate cardiocyte apoptosis by both extrinsic and mitochondria pathways.
    Zhongguo yi xue ke xue yuan xue bao. Acta Academiae Medicinae Sinicae 10/2010; 32(5):526-32.
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    ABSTRACT: The effects of various postconditioning algorithm on reperfusion injury and the role of mitochondrion pathway were investigated in a rat model of reperfusion/injury. Rats were divided into 5 groups: sham, reperfusion/injury (R/I group), reverse algorithm of postconditioning (R-Post, 30/10-25/15-15/25-10/30 s of reperfusion/re-occlusion), standard algorithm of postconditioning (S-Post, 4 cycles of 20/20 s of reperfusion/re-occlusion), and gradual algorithm of postconditioning (G-Post, 10/30-15/25-25/15-30/10 s of reperfusion/re-occlusion). The levels of Bax, Cytochrome-c, Caspase-9, serum marker of myocardium and apoptosis index were significantly lower while the level of Bcl-2 was significantly higher in the three postconditioning groups than those in R/I group (all P < 0.05). The levels of Bax (0.35 +/- 0.10 vs. 0.50 +/- 0.02, P < 0.05), Cytochrome-c (0.66 +/- 0.16 vs. 1.68 +/- 0.22, P < 0.05), Caspase-9 (0.61 +/- 0.17 vs. 1.66 +/- 0.55, P < 0.05), serum marker of myocardium [CK: (251.00 +/- 45.16) U/L vs. (388.56 +/- 75.01) U/L, P < 0.05; CK-MB: (146.00 +/- 60.12) U/L vs. (291.16 +/- 52.41) U/L, P < 0.05] and apoptosis index [(4.32 +/- 1.16)% vs. (8.58 +/- 1.12)% , P < 0.05] were all significantly lower while Bcl-2 level (2.00 +/- 0.34 vs. 1.40 +/- 0.18, P < 0.05) was significantly higher in G-Post group than those in S-Post group. Moreover, above mentioned cardiac protective effects were significantly stronger in the G-Post group compared to R-Post group (all P < 0.05). In conclusion, gradual algorithm of postconditioning could attenuate reperfusion injury more significantly than standard algorithm, and mitochondrion pathway plays an important role in this cardioprotective process.
    Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 06/2010; 38(6):539-44.
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    ABSTRACT: To test whether postconditioning could inhibit the expression of phospho-JNK (P-JNK) mitogen activated protein kinase (MAPK) and study its relation to apoptosis of cardiocyte. Sixty rats were randomly divided into six groups: sham, reperfusion injury (R/I), postconditioning (Post), SP600125 (I_JNK), anisomycin and postconditioning (Ani+Post) and anisomycin (Ani) groups. After acute myocardial infarction was induced in rats, placebo solution (DMSO), SP600125 (6 mg/kg) or anisomycin (2 mg/kg) was injected through jugular vein 5 min before reperfusion; 6 h later 3 rats of each group were executed and the hearts were separated to measure the signaling molecules (phospho-JNK, TNF alpha, Caspase-8, Bcl-2/Bax, cytochrome-c). Twenty-two hours later hemodynamic data were measured in the left rats, and then blood samples were taken to determine serum markers of cardiac damage, and hearts were separated to measure the infarction area and cardiocyte apoptosis. Postconditioning improved +/-DP/DTmax of left ventricle, limited infarct area, relieved apoptosis and necrosis of cardiocytes, and inhibited the expression of P-JNK (1.12 +/-0.21 Compared with 1.90 +/-0.32, P<0.05). At the same time the levels of TNFalpha Caspase-8, Bax and Cyt-c were lower in Post group than those in R/I group, but Bcl-2 expression levels were higher. I_JNK group presented the similar protection effect of postconditioning [TUNEL index: (6.23 +/-2.43)% Compared with (18.22 +/-5.10)%, P<0.05; Infarct area: (23.44 +/-6.34)% Compared with (42.31 +/-8.21)%, P<0.05]. On the other hand, Ani+Post group partially lost cardioprotection effect [TUNEL index: (14.12 +/-2.00)% Compared with (18.22 +/-5.10)%,P>0.05; Infarct area: (35.27 +/-5.28)% Compared with (42.31+/-8.21)%,P>0.05], because of the activation of JNK MAPK. Postconditioning can inhibit phosphorylation of JNK MAPK, which attenuates cardiocyte apoptosis by both extrinsic and mitochondria pathway.
    Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences 11/2009; 38(6):611-9.
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    ABSTRACT: To evaluate the influence of pharmacological postconditioning with edaravone, a new free radical scavenger, on myocardial ischemia/reperfusion injury and the mechanism thereof. Forty Wistar rats underwent ligation of the left anterior descending coronary artery (LAD) with PTCA balloon to establish ischemia/reperfusion models, with the LAD occluded for 45 min and reperfused for 180 min. The rats were randomly divided into 5 equal groups : (1) I/R group undergoing occlusion of the LAD for 45 min and reperfusion for 180 min; (2) I-postC group undergoing ischemia for 45 min, 3 cycles of balloon air relief-aeration (30s reperfusion and 30s ischemia), and then reperfusion for 180 min, (3) iA-1 group undergoing injection of edaravone, 3 mg/kg into the aorta root 1 min before reperfusion; (4) iA-2 group undergoing injection of edaravone 10 mg/kg into the aorta root 1 min before reperfusion; and (5) iV group undergoing intravenous injection of edaravone 10 mg/kg 1 min before reperfusion. Another 8 rats underwent sham operation. By the end of experiment arterial blood was collected to measure the dynamic parameters and serum biochemical markers: MB isoenzyme of creatine kinase (CK-MB), malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO). Then the rats were killed. The ischemic size and Infarct size of myocardium were measured by Evans blue and TTC staining respectively. The myocardial infarct size and levels of serum CK-MB, MDA, and NO were all significantly reduced in the I-postC, iA-1, and iA-2 groups compared with the I/R group (all P < 0.01), and the activity levels of SOD of these groups were all enhanced (all P < 0.05). The MI size and levels of serum CK-MB and MDA of the iV group were all reduced, the activity level of SOD was enhanced compared with the I/R group (all P < 0.05), and the NO level was decreased, but not significantly. Edaravone pharmacological postconditioning applied just before the onset of coronary reperfusion provides potent myocardial infarct size reduction, an effect similar to the cardio-protective effect of dynamic postconditioning. The common potential mechanism of both practices may be associated with decreasing the injury by reactive oxygen species and strengthening the resistance to oxidation stress. Intra aorta root-coronary injection may be a more effective pharmacological postconditioning pathway than intravenous pathway.
    Zhonghua yi xue za zhi 09/2008; 88(36):2558-61.