TY - JOUR
T1 - Cardioprotective effect of Shenxiong glucose injection on acute myocardial infarction in rats via reduction in myocardial intracellular calcium ion overload
AU - Wang, Zhi-Hua
AU - Pan, Jian Hao
AU - Ma, Xian Peng
AU - Xu, Xiao Yun
AU - Yu, Wen Hui
AU - Fu, Wen Juan
AU - Ke, Jian
AU - Bi, Chang Qiong
AU - Wei, Wei
AU - Zhao, Qu
AU - Wang, Feng
AU - Tang, Dan
AU - Ye, Kaihe
AU - Yi, Zhixian
AU - Nie, Hong
N1 - Includes bibliographical references.
PY - 2017
Y1 - 2017
N2 - Purpose: To explore the cardioprotective effects and potential mechanisms of Shenxiong Glucose Injection (SGI) in rat acute myocardial infarction (AMI). Methods: AMI model was created by ligating left anterior descending coronary artery. After 7 days’ consecutive intravenous administration of SGI, serum samples were used to conduct biochemical analysis while hearts were excised and processed for infraction size, enzyme activity, histopathology and qPCR studies. Intracellular Ca2+ {(Ca2+)i} overload in H9c2 cells was measured by laser scanning confocal microscope (LSCM). Results: In AMI rats, pretreatment with SGI significantly ameliorated myocardial histopathologic damage. It exerted cardioprotective effect by decreasing myocardial infarct size, electrocardiogram (ECG) ST segment elevation, and CK, cTnI, BNP levels in serum. In addition, SGI significantly decreased calmodulin (CaM) and calmodulin-dependent protein kinase II (CaMK II) mRNA expression, but increased Ca2+-Mg2+-ATPase and Na+-K+-ATPase activities in myocardium. In doxorubicin (DOX)-induced H9c2 cells injury model, SGI reversed (Ca2+)i overload to protect cells. Conclusion: The results demonstrate SGI exerts cardioprotective effect by decreasing myocardial infarct size, restoring ST segment and reversing (Ca2+)i overload. It suggests that SGI may be a new clinical candidate to treat myocardial infarction.
AB - Purpose: To explore the cardioprotective effects and potential mechanisms of Shenxiong Glucose Injection (SGI) in rat acute myocardial infarction (AMI). Methods: AMI model was created by ligating left anterior descending coronary artery. After 7 days’ consecutive intravenous administration of SGI, serum samples were used to conduct biochemical analysis while hearts were excised and processed for infraction size, enzyme activity, histopathology and qPCR studies. Intracellular Ca2+ {(Ca2+)i} overload in H9c2 cells was measured by laser scanning confocal microscope (LSCM). Results: In AMI rats, pretreatment with SGI significantly ameliorated myocardial histopathologic damage. It exerted cardioprotective effect by decreasing myocardial infarct size, electrocardiogram (ECG) ST segment elevation, and CK, cTnI, BNP levels in serum. In addition, SGI significantly decreased calmodulin (CaM) and calmodulin-dependent protein kinase II (CaMK II) mRNA expression, but increased Ca2+-Mg2+-ATPase and Na+-K+-ATPase activities in myocardium. In doxorubicin (DOX)-induced H9c2 cells injury model, SGI reversed (Ca2+)i overload to protect cells. Conclusion: The results demonstrate SGI exerts cardioprotective effect by decreasing myocardial infarct size, restoring ST segment and reversing (Ca2+)i overload. It suggests that SGI may be a new clinical candidate to treat myocardial infarction.
KW - Calmodulin
KW - Calmodulin-dependent protein kinase II
KW - Intracellular Ca overload
KW - Ligustrazine
KW - Myocardial infarction
KW - Shenxiong glucose injection
KW - Tanshinol
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U2 - 10.4314/tjpr.v16i5.18
DO - 10.4314/tjpr.v16i5.18
M3 - Article
AN - SCOPUS:85020129175
SN - 1596-5996
VL - 16
SP - 1097
EP - 1104
JO - Tropical Journal of Pharmaceutical Research
JF - Tropical Journal of Pharmaceutical Research
IS - 5
ER -