The Zoucheng Peoples Hospital

Jining, China

The Zoucheng Peoples Hospital

Jining, China
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Background: Although recent studies have found that heme oxygenase (HO)-1 plays an important role in myocardiac cell survival, the precise mechanisms occurring during hypoxia/reoxygenation (H/R) injury remain unclear. Therefore, the aim of this study was to investigate the cytoprotective mechanisms of HO-1 against H/R-induced myocardiac cell apoptosis and to explore whether the Akt signaling pathway contributed to the protection provided by HO-1. Methods: Cobalt protoporphyrin (CoPP, a pharmacologic inducer of HO-1) was employed to induce the over-expression of HO-1 before H/R in H9c2 cells. Hoechst staining and flow cytometry were used to examine the extent of apoptosis. Furthermore, the effect of HO-1 on Akt, JNK, and the expression of apoptosis-related proteins (c-JUN and Caspase-3) was determined by Western blotting. Results: The results showed that over-expressed HO-1 could significantly protect myocardiac cells against H/R-induced apoptosis in H9c2 cells. Furthermore, the protein expression of p‑Akt increased and of p‑JNK decreased in the H/R injury H9c2 cells when treated with CoPP. The apoptosis-related proteins c‑Jun and caspase-3 were both inhibited by over-expression of HO-1. At the same time, retreatment with zinc protoporphyrin (ZnPP, a specific inhibitor of HO-1 enzymatic activity) or LY294002 (an inhibitor of Akt1) reversed the HO-1-induced changes. Conclusion: In summary, our results suggest that HO-1 can decrease H/R-induced myocardiac cell apoptosis; the mechanism may be related to the activation of the Akt signaling pathway and, furthermore, to the inhibition of the JNK/c-Jun/caspase-3 signaling pathway. © 2016 Springer Medizin Verlag


Li C.,The Zoucheng Peoples Hospital | Wang T.,The Zoucheng Peoples Hospital | Zhang C.,The Zoucheng Peoples Hospital | Xuan J.,The Zoucheng Peoples Hospital | And 2 more authors.
Gene | Year: 2016

Quercetin (Que), a plant-derived flavonoid, possesses various biological functions. Moreover, Que exerts multiple beneficial actions in treatment of cardiovascular diseases and there are an inverse association between Que intakes and occurrence and development of various cardiovascular diseases. Some researchers have inferred that the mechanisms of Que to protect cardiomyocytes from ischemia/reperfusion (I/R) injury may be involved in modulation of intracellular signal pathways and regulation of proteins expression in vivo. The current study investigated whether Que has any protective effects on cardiomyocytes from hypoxia/reoxygenation (H/R) in vitro and its potential cardioprotective mechanisms. The cell viability of Que on H9c2 cardiomyoblast cells was assessed by MTT. Apoptosis was evaluated by both Hoechst33342 staining and Flow cytometric analysis (FACS). Furthermore, the effect of Que, SP600125 (JNK inhibitor) and SB203580 (p38 inhibitor) on mitogen-activated protein kinases (MAPKs) and the expression of apoptosis related proteins (Bcl-2, Bax and caspase-3) was determined by Western blotting. MTT assays showed that pretreatment with Que could increase the viability of H9c2 cardiomyocytes that suffered H/R. Both Hoechst33342 staining and FACS confirmed that Que could remarkably suppress the H/R-induced apoptotic cardiomyocytes. In addition, Que significantly alleviated H/R-induced the phosphorylation of JNK and p38, which further increased Bcl-2 expression and inhibited the activation of Bax and caspase-3 directly or indirectly. In summary, our results imply that Que can induce cardioprotection by inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways and modulate the expression of Bcl-2 and Bax proteins that provides a new experimental foundation for myocardial ischemia disease therapy. © 2015 Elsevier B.V.


Although recent studies have found that heme oxygenase (HO)-1 plays an important role in myocardiac cell survival, the precise mechanisms occurring during hypoxia/reoxygenation (H/R) injury remain unclear. Therefore, the aim of this study was to investigate the cytoprotective mechanisms of HO-1 against H/R-induced myocardiac cell apoptosis and to explore whether the Akt signaling pathway contributed to the protection provided by HO-1.Cobalt protoporphyrin (CoPP, apharmacologic inducer of HO-1) was employed to induce the over-expression of HO-1 before H/R in H9c2 cells. Hoechst staining and flow cytometry were used to examine the extent of apoptosis. Furthermore, the effect of HO-1 on Akt, JNK, and the expression of apoptosis-related proteins (c-JUN and Caspase-3) was determined by Western blotting.The results showed that over-expressed HO-1 could significantly protect myocardiac cells against H/R-induced apoptosis in H9c2 cells. Furthermore, the protein expression of pAkt increased and of pJNK decreased in the H/R injury H9c2 cells when treated with CoPP. The apoptosis-related proteins cJun and caspase-3 were both inhibited by over-expression of HO-1. At the same time, retreatment with zinc protoporphyrin (ZnPP, aspecific inhibitor of HO-1 enzymatic activity) or LY294002 (an inhibitor of Akt1) reversed the HO-1-induced changes.In summary, our results suggest that HO-1 can decrease H/R-induced myocardiac cell apoptosis; the mechanism may be related to the activation of the Akt signaling pathway and, furthermore, to the inhibition of the JNK/c-Jun/caspase-3 signaling pathway.

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