Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies have shown that the NRF-2 /HO-1 pathway participates in myocardial ischemic reperfusion injury (MI/R) and that Geniposide (GEN) could protect the myocardial against MI/R. This study aims to examine the protective effects of GEN on MI/R in diabetic rats and further explore the possible mechanism of action. During MI/R in rats, NRF-2 /HO-1signals changed significantly including NRF-2 and HO-1up-regulation, resulting in heart dysfuction, histological damage and increasing oxidative stress and cell apoptosis. Treatment with GEN can significantly improve the general condition and heart function in diabetic rats with decreasing the expression of cTnI, CK-MB, blood glucose, MDA, ROS, cell apoptosis and pathological damage in MI/R. In addition, GEN precondition can also significantly increase the weight of rats and the activity of SOD, CAT and GPx with up-regulating the expression of NRF-2 and HO-1 in MI/R. This study implied that Geniposide has a protective effect on myocardial ischemia reperfusion injury in diabetic rats, and its mechanism is associated with activating NRF2/HO-1 signaling pathway to suppress oxidative stress.
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PMID:Attenuation of Myocardial ischemia reperfusion injury by Geniposide preconditioning in diabetic rats. 3090 10

Geniposide (GP), extracted from a traditional Chinese herb Gardenia jasminoides, has extensive pharmacological effects. But the effects and the potential mechanisms of GP on myocardial ischemia/reperfusion (I/R) injury are poorly understood. In present study, we investigated the effect of GP on myocardial I/R injury in vivo and hypoxia/reoxygenation (H/R) in vitro respectively, and its mechanism. The results showed that GP reduced myocardial infarct size, alleviated acute myocardial injury, improved cardiac function, regulated apoptosis-related proteins and inhibited apoptosis. In vitro experiments revealed that GP enhanced the cell viability, regulated apoptosis-related proteins and prevented cell apoptosis during H/R in H9c2 cells. GP inhibited the expression of autophagy-related proteins and autophagosome accumulation both in vivo and in vitro. The effects of GP were blocked by rapamycin (RAPA) administration. In summary, our results showed that GP protected against myocardial I/R injury and involved inhibition of autophagy, which might be through activating AKT/mTOR signaling pathways.
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PMID:Inhibition of autophagy by geniposide protects against myocardial ischemia/reperfusion injury. 3244 99