Publications by authors named "Shunye Zhang"

4 Publications

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The discrepancy of aromatase expression in epicardial adipose tissue between CHD and non-CHD patients.

Cardiovasc J Afr 2021 Jun 7;32:1-4. Epub 2021 Jun 7.

Department of Cardiovascular Surgery, Shanxi Cardiovascular Hospital, Taiyuan, PR of China. Email:

Objectives: Epicardial adipose tissue (EAT) aromatase converts androstenedione and other adrenal androgens into oestrogens. The locally produced oestradiol (E) may have cardiovascular protective effects. Little is known about the relationship between EAT aromatase level and coronary heart disease (CHD). Here, we compared EAT aromatase levels in CHD versus non-CHD patients and assessed the relationship between EAT aromatase levels and lesion degree in the coronary arteries.

Methods: EAT and blood specimens were obtained from patients undergoing thoracotomy prior to cardiopulmonary bypass. Serum E levels were obtained from our hospital laboratory. EAT aromatase expression was determined by RT-qPCR and ELISA assays. All patients underwent coronary angiography and the level of coronary lesions was evaluated with the SYNTAX score.

Results: Compared with non-CHD patients, CHD patients had lower EAT aromatase mRNA and protein levels. In the CHD patients, EAT aromatase and oestrogen levels negatively correlated with the severity of coronary artery disease.

Conclusions: Our data revealed that reduced EAT aromatase levels correlated with coronary atherosclerotic lesions. Reduced EAT aromatase protein levels may aggravate the severity of atherosclerosis. Future studies should investigate the mechanisms regulating aromatase expression in epicardial fat.
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http://dx.doi.org/10.5830/CVJA-2021-012DOI Listing
June 2021

Carvedilol attenuates CPB-induced apoptosis in dog heart: regulationof Fas/FasL and caspase-3 pathway.

Chin Med J (Engl) 2003 May;116(5):761-6

Department of Cardiovascular Surgery, Shanxi Cardiovascular Hospital, Taiyuan 030024, China.

Objective: To evaluate the effects of Carvedilol on cardiopulmonary bypass (CPB)-induced myocardiocyte apoptosis and its effects on regulation of Fas, FasL expression, caspase-3 activity and oxidative stress in the left ventricle (LV) in this setting.

Methods: Ten adult dogs undergoing conventional hypothermic CPB were randomly divided into control and Carvedilol treated groups (n = 5, respectively). Dogs in Carvedilol treated group received a bolus of Carvedilol (1 mg/kg) intravenously and a maintenance dosage of Carvedilol (3 micro g.min(-1).kg(-1)) for 3 hours after the reperfusion of the heart. Dogs in control group received no Carvediolol. LV samples were obtained before, during and 3 hours after CPB. In situ nick end-labeling (TUNEL) technique was used to detect the apoptotic cells. The expressions of Fas and FasL were detected immunohistochemically and quantified by fluorescence activated cell sorting (FACS). The activity of caspase-3 enzyme and malondialdehyde (MDA) level were measured by cleavage of Z-DEVD-AMC substrate and thiobarbituric acid reactive substance (TBARS) method, respectively.

Results: Before and during CPB, all the parameters were not significantly different intra- or between groups (P > 0.05). After CPB, these parameters in both groups were significantly elevated compared with those of before and during CPB (P < 0.028, respectively). However, the number of apoptotic cells in Carvedilol treated group was significantly decreased compared with that of the control group (P < 0.021). The expressions of Fas and FasL were significantly downregulated by Carvedilol (P < 0.001 and 0.003, respectively). The caspase-3 activity and the content of MDA in the Carvedilol treated group was also significantly reduced (P < 0.026 and 0.005, respectively).

Conclusions: Carvedilol significantly reduces CPB-induced cardiomyocyte apoptosis in dog hearts and the reduction of cardiomyocyte apoptosis is associated with downregulation of Fas and FasL expression, inhibition of caspase-3 activity and oxidative stress in LV.
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May 2003

Regulatory effect of bcl-2 family proteins in CPB-induced cardiomyocyte apoptosis in dog hearts.

J Huazhong Univ Sci Technolog Med Sci 2002 ;22(2):103-6

Department of Cardiovascular Surgery, Xiehe Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022.

Whether conventional hypothermic CPB induces myocyte apoptosis in dog hearts and modulation of bcl-2, bcl-xl, bax, bad, and caspase-3 pathways in this setting was investigated. Ten healthy adult dogs were randomized into sham-operated and CPB groups. Samples of left ventricle were obtained before, during and 3 h after CPB. In situ TUNEL was used to detect apoptotic myocytes. Immunohistochemistry and flow cytometry were employed for detection of expressions of bcl-2, bcl-xl, bax and bad proteins. Z-DEVD-AMC substrate cleavage and TBARS methods were used to measure the activity of caspase-3 and the content of lipid peroxide in LV myocardium, respectively. After CPB, the number of apoptotic myocytes in CPB group was significantly increased. The results of immunohistochemistry demonstrated that bcl-2, bcl-xl, bax and bad proteins were constitutionally present on the sarcolemma of the LV myocytes. FACS results showed that, after CPB, expressions of bax and bad in CPB group were significantly upregulated, while the expressions of bcl-2 and bcl-xl were not significantly changed in both groups. The activity of caspase-3 and the content of lipid peroxide in LV myocardium in CPB group were also significantly increased after CPB. The present study shows that there exists myocardiocyte apoptosis in dog hearts undergoing conventional hypothermic CPB and the myocyte apoptosis is initiated by ischemia and performed during reperfusion. Moreover, the CPB-induced myocyte apoptosis was associated with upregulation of expressions of bax and bad proteins, activation of caspase-3 and increase of oxidative stress.
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http://dx.doi.org/10.1007/BF02857665DOI Listing
July 2004
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