The protective effect of picroside II against hypoxia/reoxygenation injury in neonatal rat cardiomyocytes

Meng, Fanji; Hou, Zhiwen; Yang, Li; B, Yu

doi:10.3109/13880209.2012.664555

Cited by 19 publications

(15 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Normally, the generated ROS from metabolic processes can be scavenged by endogenous anti-oxidant enzymes such as SOD, 14 catalyzing the dismutation of the superoxide radical to hydrogen peroxide. However, in pathological conditions just like I/R injury, the overproduction of ROS can cause oxidation of lipids, proteins, and nucleic acids, resulting in cellular dysfunction.…”

Section: Discussionmentioning

confidence: 99%

The protective effect of ozone oxidative preconditioning against hypoxia/reoxygenation injury in rat kidney cells

et al. 2014

View full text Add to dashboard Cite

Ozone (O3) has been viewed as a novel treatment for different diseases in these years and oxidative stress and apoptosis play a key role in the pathogenesis of kidney diseases including renal ischemia and reperfusion (I/R). In the present study, we investigated the role of ozone oxidative preconditioning (OzoneOP) in attenuating oxidative stress and apoptosis in a hypoxia/reoxygenation (H/R) injury model using rat kidney cells. We induced H/R injury in kidney cells treated with or without OzoneOP. Oxidative stress parameters such as superoxide dismutase (SOD), malondialdehyde (MDA) and lactate dehydrogenase (LDH) were determined, as well as some apoptotic proteins. We observed that oxidative stress and apoptosis were increased in H/R group compared to OzoneOP group; however, these changes were significantly decreased by the treatment with OzoneOP. We concluded that OzoneOP can protect the kidney cells against H/R injury and its mechanism may be through the reduction of oxidative stress and apoptosis.

show abstract

Section: Discussionmentioning

confidence: 99%

The protective effect of ozone oxidative preconditioning against hypoxia/reoxygenation injury in rat kidney cells

et al. 2014

View full text Add to dashboard Cite

show abstract

“…On the contrary, endogenous antioxidases including SOD and GSH-Px can compromise the excessive ROS in vivo to regulate intracellular redox status. 25) Therefore, abrogating occurrence of lipid peroxidation and increasing levels of endogenous antioxidases may provide a repairing mechanism for ROS-mediated cell damage. The present study suggests that 100 µM salidroside significantly increased SOD and GSH-Px activities in endogenous H 2 O 2 treated EVC-304 cells, along with an attenuated MDA production.…”

Section: Discussionmentioning

confidence: 99%

Salidroside Inhibits Endogenous Hydrogen Peroxide Induced Cytotoxicity of Endothelial Cells

Zhao

Jin

Shen

et al. 2013

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Key words endothelial injury model; salidroside; oxidative stress; apoptosis; hydrogen peroxide Vascular endothelial cells serve as a barrier between tissue and blood stream, which plays an important role in maintaining vascular homeostasis. Oxidative stress has been implicated as a major cause of endothelial injuries in a variety of clinical abnormalities including artherosclerosis, 1) ischemia reperfusion injury, and diabetes. 2,3)Rhodiola rosea L. (Crassulaceae) has been used for a long time as folk medicine in Russia and China. 4) Its claimed benefits include anti-depress, anticancer, anti-stress, antioxidation and immune function improvement. 5) Salidroside (p-hydroxyphenethyl-β-D-glucoside, chemical structure shown in Fig. 1), a major active ingredient isolated from the plant R. rosea, has been used in the treatment of diabetes, hypertension, fatigue and hypoxia.6,7) Recent study showed that salidroside had been found to exhibit marked antioxidant effects and its activity in scavenging superoxide radicals is concentration-and time-dependent. 8) Salidroside was also reported to be capable of protecting SH-SY5Y cells against hydrogen peroxide-induced cell apoptosis in a dose-dependent manner 9) and protecting the PC12 cells against hypoglycemia/serum limitation-induced cytotoxicity. 10)Although salidroside has been known to have significant anti-oxidative and neuroprotective properties, there are no reports on its effects on the vascular endothelial cells.* To whom correspondence should be addressed. e-mail: jlmpcxlx@163.com; zhuyjw1971@nwu.edu.cn The authors declare no conflict of interest.

show abstract

“…Moreover, a recent study has also shown that picroside II could protect cardiomyocytes against oxidative stress and apoptosis induced by hypoxia/reoxygenation injury 15. However, the cardioprotection of picroside II has still not been demonstrated in animal models.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of picroside II on myocardial ischemia reperfusion injury in rats

Wu¹,

Li²,

Shu³

et al. 2014

DDDT

View full text Add to dashboard Cite

The aim of this study was to determine the effect of picroside II on myocardial ischemia reperfusion injury in rats and to explore its underlying mechanism. Isolated rat hearts underwent 30 minutes of global ischemia followed by 120 minutes of reperfusion. Different doses of picroside II (1 μM, 10 μM, and 100 μM) were given 20 minutes before ischemia. Phosphoinositide 3-kinase inhibitor (wortmannin) and nitric oxide synthase (NOS) inhibitor (L-NG-nitroarginine methyl ester) were given 10 minutes before picroside II treatment. The cardiac function, myocardial infarct size, apoptosis, myocardial nitric oxide content, the expressions of Bcl-2 and Bax, and the activation of the phosphoinositide 3-kinase/Akt/endothelial NOS pathway were evaluated. Treatment with 10 μM and 100 μM picroside II significantly improved postischemic myocardial function, reduced myocardial infarct size, inhibited apoptosis, increased myocardial NO content, upregulated Bcl-2, downregulated Bax, and increased the phosphorylation of Akt and endothelial NOS, but cardioprotection was not shown in the 1 μM picroside II treatment group and was abrogated by wortmannin and L-NG-nitroarginine methyl ester. Furthermore, cardioprotection in the 100 μM picroside II treatment group was superior to that in the 10 μM picroside II treatment group. In conclusion, the data reveals that picroside II has a significant protective effect on myocardial ischemia reperfusion injury in a dose-dependent manner, which was mediated by upregulating the phosphoinositide 3-kinase/Akt/endothelial NOS pathway to increase nitric oxide production and regulating the expressions of Bcl-2 and Bax to inhibit apoptosis.

show abstract

The protective effect of picroside II against hypoxia/reoxygenation injury in neonatal rat cardiomyocytes

Cited by 19 publications

References 33 publications

The protective effect of ozone oxidative preconditioning against hypoxia/reoxygenation injury in rat kidney cells

The protective effect of ozone oxidative preconditioning against hypoxia/reoxygenation injury in rat kidney cells

Salidroside Inhibits Endogenous Hydrogen Peroxide Induced Cytotoxicity of Endothelial Cells

Protective effect of picroside II on myocardial ischemia reperfusion injury in rats

Contact Info

Product

Resources

About