[Protective effect of succinic acid on primary cardiomyocyte hypoxia/reoxygenation injury].
To establish cardiomyocyte hypoxia/reoxygenation injury model by culturing primary cardiomyocytes from suckling SD rats, in order to study the effect of succinic acid on LDH leakage rate cardiomyocyte ischemia/reperfusion injury. Furthermore, flow cytometry and western blot were conducted to detect the effect of succinic acid on cardiomyocyte apoptosis, cleaved caspase-3 and p-Akt, and discuss the protective effect of succinic acid on primary cardiomyocyte hypoxia/reoxygenation injury of primary cardiomyocytes from neonatal SD rats. According to the findings of the study, succinic acid at the concentrations ranging between 31.25 mg x L(-1) and 500 mg x L(-1) had no significant effect on primary cardiomyocyte activity, and succinic acid at the concentrations of 400, 200, 100, 50 mg x L(-1) could notably reduce cardiomyocyte ischemia/reperfusion LDH leakage rate (P < 0.01 or P < 0.05, respectively). Succinic acid at the concentrations of 400 mg x L(-1) and 200 mg x L(-1) could significantly reduce the percentage of cardiomyocyte apoptosis (P < 0.05), and inhibit the protein expression of cleaved caspase-3 caused by cardiomyocyte ischemia/reperfusion (P < 0.05). Succinic acid at the concentration of 400 mg x L(-1) could remarkably increase the protein expression of cardiomyocyte Akt (P < 0.05), while succinic acid at the concentration of 200 mg x L(-1) had no obvious effect on the protein expression of cardiomyocyte Akt. Therefore, this study demonstrated that succinic acid could inhibit necrosis and apoptosis caused by cardiomyocyte hypoxia/reoxygenation by activating Akt phosphorylation.
Experimental Research Center, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China. xilan2013@gmail.com
Xi-Lan
XL
Tang
Experimental Research Center, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China.
Jian-Xun
JX
Liu
Experimental Research Center, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China.
Peng
P
Li
Experimental Research Center, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China.
Wei
W
Dong
Experimental Research Center, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China.
Lei
L
Li
Experimental Research Center, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China.
Yong-Qiu
YQ
Zheng
Experimental Research Center, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China.
Jin-Cai
JC
Hou
D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D053148:Caspase 3 / Q000378:metabolism; D015687:Cell Hypoxia / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D032383:Myocytes, Cardiac / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D010100:Oxygen / Q000378:metabolism; D020011:Protective Agents / Q000494:pharmacology*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D019802:Succinic Acid / Q000494:pharmacology*
D020011:Protective Agents; D019802:Succinic Acid; D051057:Proto-Oncogene Proteins c-akt; D053148:Caspase 3; D010100:Oxygen