Anti-arrhythmic effect of diosgenin in reperfusion-induced myocardial injury in a rat model: activation of nitric oxide system and mitochondrial KATP channel

Badalzadeh, Reza; Yousefi, Bahman; Majidinia, Maryam; Ebrahimi, Hadi

doi:10.1007/s12576-014-0333-8

Cited by 27 publications

(29 citation statements)

References 39 publications

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“…preconditioning [18][19][20]. The mitoK ATP channel may also take part in the diosgenininduced anti-arrhythmic effect [21]. In our study, the nonspecific blocker of K ATP GLI, the mitochondria K ATP channel blocker 5-HD and the mitochondria K ATP opener DIAZ were applied to observe the effect of K ATP on the cardioprotection bestowed by CIHH.…”

Section: Discussionmentioning

confidence: 90%

KATP channels and MPTP are involved in the cardioprotection bestowed by chronic intermittent hypobaric hypoxia in the developing rat

Yang

Wang

et al. 2015

J Physiol Sci

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The aim of this study was to explore the mechanism underlying the cardioprotection bestowed by chronic intermittent hypobaric hypoxia (CIHH) against ischemia/reperfusion (I/R) injury in developing rats. Neonatal male rats were subjected to CIHH treatments that simulated an altitude of 3000 m a.s.l. for 28 days (CIHH28) and 42 days (CIHH42), respectively, or no treatment (control). The left ventricular function of isolated hearts was evaluated. The ultra-microstructure, superoxide dismutase (SOD) activity and total anti-oxidation capacity (TAC) of the myocardium were determined. The basic left ventricular function remained unchanged in CIHH rats, except for an increased coronary flow. The recovery of cardiac function from I/R, however, was much better in CIHH rats than in control rats. Compared to control rats, CIHH rats had much higher SOD levels and TAC, and the ultra-microstructure damage to mitochondria was considerably less. The cardiac protection of CIHH was canceled out by glibenclamide, an inhibitor of the ATP-sensitive potassium (K(ATP)) channel, 5-hydroxydecanoate, an inhibitor of mitochondrial K(ATP) (mitoKATP), and atractyloside, an opener of the mitochondrial permeability transition pore (MPTP). To the contrary, diazoxide, an opener of mitoKATP, and cyclosporin A, a blocker of MPTP opening, induced cardioprotection in control rats. These results suggest that CIHH protects the heart against I/R injury in developing rats through opening of the K(ATP) channel and inhibiting of opening of the MPTP.

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Section: Discussionmentioning

confidence: 90%

KATP channels and MPTP are involved in the cardioprotection bestowed by chronic intermittent hypobaric hypoxia in the developing rat

Yang

Wang

et al. 2015

J Physiol Sci

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“…Another important effect of the antioxidant diosgenin is its potential interest in the protection of cardiac cells from hypoxia-reoxygenation injury which can be mediated by ATP-sensitive potassium channels and through modulation of cell prodeath (Bax) and cell prosurvival (Bcl2, heme oxygenase 1, and Akt) molecules [74–78]. …”

Section: Pharmacology: Recent Datamentioning

confidence: 99%

Diosgenin: Recent Highlights on Pharmacology and Analytical Methodology

Jesus

Martins

Gallardo

et al. 2016

Journal of Analytical Methods in Chemistry

194

125

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Diosgenin, a steroidal sapogenin, occurs abundantly in plants such as Dioscorea alata, Smilax China, and Trigonella foenum graecum. This bioactive phytochemical not only is used as an important starting material for the preparation of several steroidal drugs in the pharmaceutical industry, but has revealed also high potential and interest in the treatment of various types of disorders such as cancer, hypercholesterolemia, inflammation, and several types of infections. Due to its pharmacological and industrial importance, several extraction and analytical procedures have been developed and applied over the years to isolate, detect, and quantify diosgenin, not only in its natural sources and pharmaceutical compositions, but also in animal matrices for pharmacodynamic, pharmacokinetic, and toxicological studies. Within these, HPLC technique coupled to different detectors is the most commonly analytical procedure described for this compound. However, other alternative methods were also published. Thus, the present review aims to provide collective information on the most recent pharmacological data on diosgenin and on the most relevant analytical techniques used to isolate, detect, and quantify this compound as well.

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“…Another important molecule is the K ATP channel due to its cardioprotection in various types of cardiovascular diseases (Badalzadeh et al 2014, 2015, Waza et al 2014. In addition, accumulating evidence has revealed that DM has been associated with dysfunction of the cardiovascular K ATP channels (Weintraub 2003).…”

Section: Introductionmentioning

confidence: 99%

Naringin protects cardiomyocytes against hyperglycemia-induced injuries in vitro and in vivo

Qin

et al. 2016

Journal of Endocrinology

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We previously reported that naringin (NRG) protects cardiomyocytes against high glucose (HG)-induced injuries by inhibiting the MAPK pathway. The aim of this study was to test the hypothesis that NRG prevents cardiomyocytes from hyperglycemia-induced insult through the inhibition of the nuclear factor kappa B (NF-κB) pathway and the upregulation of ATP-sensitive K + (K ATP ) channels. Our results showed that exposure of cardiomyocytes to HG for 24 h markedly induced injuries, as evidenced by a decrease in cell viability and oxidative stress, and increases in apoptotic cells as well as the dissipation of mitochondrial membrane potential (MMP). These injuries were markedly attenuated by the pretreatment of cells with either NRG or pyrrolidine dithiocarbamate (PDTC) before exposure to HG. Furthermore, in streptozotocin (STZ)-induced diabetic rats and in HG-induced cardiomyocytes, the expression levels of caspase-3, bax and phosphorylated (p)-NF-κB p65 were increased. The increased protein levels were ameliorated by pretreatment with both NRG and PDTC. However, the expression levels of bcl-2 and K ATP and superoxide dismutase (SOD) activity were decreased by hyperglycemia; the expression level of Nox4 and the ADP/ATP ratio were increased by hyperglycemia. These hyperglycemia-induced indexes were inhibited by the pretreatment of cardiomyocytes with NRG or PDTC. In addition, in STZ-induced diabetic rats, we also observed that NRG or PDTC contributed to protecting mitochondrial injury and myocardium damage. This study demonstrated that NRG protects cardiomyocytes against hyperglycemia-induced injury by upregulating K ATP channels in vitro and inhibiting the NF-κB pathway in vivo and in vitro.

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Anti-arrhythmic effect of diosgenin in reperfusion-induced myocardial injury in a rat model: activation of nitric oxide system and mitochondrial KATP channel

Cited by 27 publications

References 39 publications

KATP channels and MPTP are involved in the cardioprotection bestowed by chronic intermittent hypobaric hypoxia in the developing rat

KATP channels and MPTP are involved in the cardioprotection bestowed by chronic intermittent hypobaric hypoxia in the developing rat

Diosgenin: Recent Highlights on Pharmacology and Analytical Methodology

Naringin protects cardiomyocytes against hyperglycemia-induced injuries in vitro and in vivo

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