Baicalein Protects Cardiomyocytes Against Mitochondrial Oxidant Injury Associated with JNK Inhibition and Mitochondrial Akt Activation

Huang, Her Hsiung; Shao, Zuoyi; Li, Chang Qing; Hoek, Terry L. Vanden; Li, Jing

doi:10.1142/s0192415x14500050

Cited by 19 publications

(10 citation statements)

References 48 publications

(54 reference statements)

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“…Neurotoxin 6-hydroxydopamine (6-OHDA) induces initiation of mitochondria-regulated apoptotic cascade events in SH-SY5Y cells, which can be ameliorated by the administration of sulfuretin through inhibition of GSK-3β signaling and inactivation of NF-κB signaling [89]. Baicalein, isolated from Scutellaria baicalensis Georgi , increases mitochondrial phosphorylation of Akt-Thr308 and GSK-3β-Ser9, resulting in prevention of cytochrome c release in primary cultured chick cardiomyocytes [90]. …”

Section: Natural Compounds Regulate Mitochondrial Activity Through Gsmentioning

confidence: 99%

The Key Roles of GSK-3β in Regulating Mitochondrial Activity

Yang

Chen

Gao

et al. 2017

Cell Physiol Biochem

176

119

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Glycogen synthase kinase-3β (GSK-3β), a serine/threonine protein kinase, has been reported to show essential roles in molecular pathophysiology of many diseases. Mitochondrion is a dynamic organelle for producing cellular energy and determining cell fates. Stress-induced translocated GSK-3β may interact with mitochondrial proteins, including PI3K-Akt, PGC-1α, HK II, PKCε, components of respiratory chain, and subunits of mPTP. Mitochondrial pool of GSK-3β has been implicated in mediation of mitochondrial functions. GSK-3β exhibits the regulatory effects on mitochondrial biogenesis, mitochondrial bioenergetics, mitochondrial permeability, mitochondrial motility, and mitochondrial apoptosis. The versatile functions of GSK-3β might be associated with its wide range of substrates. Accumulative evidence demonstrates that GSK-3β inactivation may be potentially developed as the promising strategy in management of many diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). Intensive efforts have been made for exploring GSK-3β inhibitors. Natural products provide us a great source for screening new lead compounds in inactivation of GSK-3β. The key roles of GSK-3β in mediation of mitochondrial functions are discussed in this review.

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Section: Natural Compounds Regulate Mitochondrial Activity Through Gsmentioning

confidence: 99%

The Key Roles of GSK-3β in Regulating Mitochondrial Activity

Yang

Chen

Gao

et al. 2017

Cell Physiol Biochem

176

119

View full text Add to dashboard Cite

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“…Likewise, there was attenuation of markers of organ injury in EPO treated pigs in the HS-65 BV +VP series. The protective effects at the cell level reported by us [20] and others [32] in rats involve at the very least Akt activation (phosphorylation); a kinase that plays a key role in cell survival and other adaptive responses including mitochondrial bioenergetic function and enhanced myocardial contractility [33], [34]. In addition, plasma IL-10 was higher in pigs that received EPO at the end of blood reinfusion.…”

Section: Discussionmentioning

confidence: 89%

Effects of Intraosseous Erythropoietin during Hemorrhagic Shock in Swine

et al. 2014

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ObjectiveTo determine whether erythropoietin given during hemorrhagic shock (HS) ameliorates organ injury while improving resuscitation and survival.MethodsThree series of 24 pigs each were studied. In an initial series, 50% of the blood volume (BV) was removed in 30 minutes and normal saline (threefold the blood removed) started at minute 90 infusing each third in 30, 60, and 150 minutes with shed blood reinfused at minute 330 (HS-50BV). In a second series, the same HS-50BV protocol was used but removing an additional 15% of BV from minute 30 to 60 (HS-65BV). In a final series, blood was removed as in HS-65BV and intraosseous vasopressin given from minute 30 (0.04 U/kg min−1) until start of shed blood reinfusion at minute 150 (HS-65BV+VP). Normal saline was reduced to half the blood removed and given from minute 90 to 120 in half of the animals. In each series, animals were randomized 1∶1 to receive erythropoietin (1,200 U/kg) or control solution intraosseously after removing 10% of the BV.ResultsIn HS-50BV, O2 consumption remained near baseline yielding minimal lactate increases, 88% resuscitability, and 60% survival at 72 hours. In HS-65BV, O2 consumption was reduced and lactate increased yielding 25% resuscitability. In HS-65BV+VP, vasopressin promoted hemodynamic stability yielding 92% resuscitability and 83% survival at 72 hours. Erythropoietin did not affect resuscitability or subsequent survival in any of the series but increased interleukin-10, attenuated lactate increases, and ameliorated organ injury based on lesser troponin I, AST, and ALT increases and lesser neurological deficits in the HS-65BV+VP series.ConclusionsErythropoietin given during HS in swine failed to alter resuscitability and 72 hour survival regardless of HS severity and concomitant treatment with fluids and vasopressin but attenuated acute organ injury. The studies also showed the efficacy of vasopressin and restrictive fluid resuscitation for hemodynamic stabilization and survival.

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“…Phosphorylation of Akt and ERK1/2 was significantly increased. Our findings suggested that the underlying mechanisms of the protection of baicalein against AKI might be related to the inhibition of apoptosis, DNA laddering was also attenuated [14]. AKI is a severe complication of acute MI and cardiac surgery, and a treatment for preventing AKI might significantly improve clinical outcomes.…”

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confidence: 73%