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1.
Journal of Chinese Physician ; (12): 462-465, 2010.
Article in Chinese | WPRIM | ID: wpr-389917

ABSTRACT

Objective To investigate the synthesis of heat shock protein 70 (HSP70) induced by norepinephrine preconditioning on donor heart and its effects on myocardial cell apoptosis and apoptosis related proteins. Methods 18 Wistar rats were random divided into 2 groups, with 9 in each group. The rats in the control group were intraperitoneally injected with 0.5 ml saline. After 24 hours, hearts were isolated and stored with histidine-tryptophan-ketoglutarate (HTK) solution at 4 ℃ for 3 hours to establish Langendorff isolated heart models, and then isolated hearts were perfused by Langendorff model with Krebs-Hense leit (K-H) solution for 2 hours. The rats in the experimental group received intraperitoneally 3. 1 μmol/kg (0. 53 mg/kg) noradrenaline bitartrate that was dissolved in saline and hearts were isolated and stored after 24 hours. Followed process was the same as that in the control group. Myocardial HSP70, Bcl-2, Bax content, apoptosis index were measured, cell structures were observed under light and electron microscope.Results HSP70 in the experimental group were higher [(17.78 ± 1.82)%] than those in control group [(5.22 ± 1.05)%], and biochemical indicators in texperimental group[(41.88 ± 5.09)%, (22.61 ±3. 49 ) %] were better than those in control group [(31.36 ± 3. 27 ) %, ( 40. 52 ± 4. 1 7) %]. There were alleviated ultrastructure injures in experimental group compared with those in control group. Conclusions This study demonstrated that norepinephrine preconditioning could induce high expression of HSP70 and it could play a very important role during ischemia-reperfusion. It could protect the structure and function of myocytes in isolated rat hearts and inhibited myocardial apoptosis.

2.
Journal of Chinese Physician ; (12): 73-76, 2009.
Article in Chinese | WPRIM | ID: wpr-395847

ABSTRACT

Objective To inwst the antagonistic effect of thrombopoietin on adriamycin induced myocardium injury in rats and explore the mechanism.Methods 32 Wistar rats were randomized into four groups(n=8):Control group,ADM group,ADM+TPOL group and ADM+TPOH group.All agents were given by intraperitoneal injection.The control group was given saline.While the other three groups were given adriamycin at the dosage of20mg/kg.TPO group were injected TPO at the dosages of 10μg/kg or 30μg/kg three times on alternale days.ELISA was used to detect the concentration of CK-MB and cTnI in the serum of rats.The change of cardiocyte ultrastructure was observed by the electron microscope,and pathological change Was observed by immunohistochemistry staining.The expression level of 8- hydroxy-2'-deoxyguanosin(8-OHdG)produced by DNA oxidative damage in myocard tissue were detected.IPP6.0 software was used to detect IOD and calculate the 8-OHdG index.Results The energy of CK-MB and cTNI of TPO group was obviously lower than that in ADM group(P<0.01).The ultragtrueture of cardiocyte in the ADM group Wag damaged more severely than that in TPO group.Pathological Score,IOD and 8-OHdG index of TPO groups were lower than ADM group(P<0.05).These indexes had no significant statistics difference between ADM+TPOL group and ADM+TPOH group.Conclusions TPO can provide heart protection by antagonizing oxidative damage of myocardial cell induced by edriamycin.

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