Antiarrhythmic efficacy of ethmozine in patients with ventricular tachycardia as determined by programmed electrical stimulation

Miura, Dennis S.; Wynn, Jonathan; Torres, Vilma; Laux, Barbara; Keefe, Deborah L.; Somberg, John C.

doi:10.1016/0002-8703(86)90095-5

Cited by 21 publications

(4 citation statements)

References 17 publications

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“…The ability of moricizine to prevent induction of VT with PES was also evaluated in patients with a history of VT or cardiac arrest (25). Noninducible patients continued on long-term therapy with moricizine.…”

Section: A Programmed Electrical Stimulation (Pes) Study Was Conductementioning

confidence: 99%

See 1 more Smart Citation

Moricizine Hydrochloride: Pharmacology, Pharmacokinetics, and Clinical Studies

Weber¹,

DeGaetano²,

Korobow³

et al. 1993

Cardiovascular Drug Reviews

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Section: A Programmed Electrical Stimulation (Pes) Study Was Conductementioning

confidence: 99%

“…Patients were also tested with intravenous procainamide and PES (25). Of the 18 patients tested, 4 were not inducible and 2 patients induced while on moricizine were not induced by procainamide.…”

Section: Electrophysiological Studiesmentioning

confidence: 99%

Moricizine Hydrochloride: Pharmacology, Pharmacokinetics, and Clinical Studies

Weber¹,

DeGaetano²,

Korobow³

et al. 1993

Cardiovascular Drug Reviews

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“…Neferine is a bisbenzylisoquinoline alkaloid isolated from lotus seed embryos that has various therapeutic properties including anticancer, antiarrhythmic, antithrombotic, and antithrombotic effects [17][18][19][20]. In addition, neferine protects against hypoxia-induced stress-mediated inflammation.…”

Section: Introductionmentioning

confidence: 99%

Neferine Protects against Hypoxic‐Ischemic Brain Damage in Neonatal Rats by Suppressing NLRP3‐Mediated Inflammasome Activation

Zhu

Huang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Hypoxic-ischemic encephalopathy (HIE) is recognized as the main cause of neonatal death, and efficient treatment strategies remain limited. Given the prevalence of HIE and the associated fatality, further studies on its pathogenesis are warranted. Oxidative stress and neuroinflammatory injury are two important factors leading to brain tissue injury and nerve cell loss in HIE. Neferine, an alkaloid extracted from lotus seed embryo, exerts considerable effects against several diseases such as cancers and myocardial injury. In this study, we demonstrated the neuroprotective effect of neferine on HIE and hypothesized that it involves the inhibition of neuronal pyroptosis, thereby ameliorating neurological inflammation and oxidative stress. We demonstrated that the mRNA levels of proteins associated with pyroptosis including caspase-1, the caspase adaptor ASC, gasdermin D, interleukin- (IL-) 18, IL-1β, and some inflammatory factors were significantly increased in neonatal HIBD model rats compared to those in the control group. The increase in these factors was significantly suppressed by treatment with neferine. We stimulated PC12 cells with CoCl2 to induce neuronal HIBD in vitro and investigated the relationship between neferine and pyroptosis by altering the expression of the NLRP3 inflammasome. The overexpression of NLRP3 partially reversed the neuroprotective effect of neferine on HIBD, whereas NLRP3 knockdown further inhibited caspase-1 activation and IL-1β and IL18 expression. In addition, simultaneous alteration of NLRP3 expression induced changes in intracellular oxidative stress levels after HIBD. These findings indicate that neferine ameliorates neuroinflammation and oxidative stress injury by inhibiting pyroptosis after HIBD. Our study provides valuable information for future studies on neferine with respect to neuroinflammation and pyroptosis.

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“…Previous studies have demonstrated its antioxidation, anti-inflammation, and anticancer properties [ 13 , 14 , 15 ]. Neferine can be potentially useful to treat cardiovascular diseases such as arrhythmia, thrombosis, and platelet aggregation [ 17 , 18 ]. Further, it is known to exert protective effects against Alzheimer’s disease, amnesia, and depression [ 15 , 19 , 20 ], which is suggestive of the plausible application of this phytochemical for curative purposes [ 18 ].…”

Section: Introductionmentioning

confidence: 99%

Anti-Adipogenic Effect of Neferine in 3T3-L1 Cells and Primary White Adipocytes

2020

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Neferine, an alkaloid component extracted from lotus seed embryos, is known for its anti-inflammatory, anticancer, and antioxidant properties. However, the anti-adipogenic activity of neferine has not been thoroughly investigated. In this study, neferine was found to inhibit lipid accumulation in a dose-dependent manner during the differentiation of 3T3-L1 cells without inducing cytotoxicity. Real-time polymerase chain reaction and immunoblot analysis revealed the downregulation in the expression of peroxisome proliferator activated receptor gamma (PPARγ), CCAAT/enhancer-binding protein alpha (C/EBPα), sterol regulatory element-binding protein-1c (SREBP-1c), and fatty acid synthase (FAS) and the upregulation in carnitine palmitoyltransferase-1 (CPT-1) and sirtuin 1 (SIRT1) levels following neferine treatment. Furthermore, neferine increased the phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC), which is an important regulator of fatty acid oxidation. Our result indicates that neferine attenuates adipogenesis and promotes lipid metabolism by activating AMPK-mediated signaling. Therefore, neferine may serve as a therapeutic candidate for obesity treatment.

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Antiarrhythmic efficacy of ethmozine in patients with ventricular tachycardia as determined by programmed electrical stimulation

Cited by 21 publications

References 17 publications

Moricizine Hydrochloride: Pharmacology, Pharmacokinetics, and Clinical Studies

Moricizine Hydrochloride: Pharmacology, Pharmacokinetics, and Clinical Studies

Neferine Protects against Hypoxic‐Ischemic Brain Damage in Neonatal Rats by Suppressing NLRP3‐Mediated Inflammasome Activation

Anti-Adipogenic Effect of Neferine in 3T3-L1 Cells and Primary White Adipocytes

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