Aim: To study the effect of puerarin (Pue) on Na+ channel in rat ventricular myocytes.
Methods: Whole-cell patch-clamp technique was applied on isolated cardiomyocytes from rats.
Results: Pue inhibited cardiac INa in a positive rate-dependent and dose-dependent manner, with an IC(50) of 349 micromol/L. The kinetics of blockage of cardiac sodium channel by Pue resembled the ClassIa/Ic of antiarrhythmic agents. Pue 300 micromol/L did not alter the shape of the I-V curve of INa, but markedly shifted the steady-state inactivation curve of INa towards more negative potential by 15.9 mV, and postponed the recovery of INa inactivation state from (21.9+/-1.6) ms to (54.4+/-3.4) ms (P<0.01). It demonstrated that the steady state of inactivation was affected by Pue significantly.
Conclusion: Pue protected ventricular myocytes against cardiac damage and arrhythmias by inhibiting recovery from inactivation of cardiac Na+ channels.
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J Food Drug Anal
December 2024
Cardiovascular Research Group, Department of Pharmacy, COMSATS University Islamabad, Abbottabad Campus, University Road, Abbottabad-22060, KP, Pakistan.
Cinnamic acid (CA) possesses important cardiovascular effects such as cardioprotective, antiatherogenic, antihyperlipidemic and antioxidant, which predicts its potential role in the treatment of hypertension. The study was executed to investigate the antihypertensive potential of CA in Sprague Dawley (SD) rats followed by evaluation in diverse vascular preparations. Invasive blood pressure monitoring technique was used in normotensive and hypertensive rats, under anesthesia.
View Article and Find Full Text PDFFood Funct
January 2025
Department of Nutrition and Food Hygiene, School of Public Health, Cheeloo College of Medicine, Shandong University, Jinan, 250012, China.
Gut dysbiosis serves as an underlying risk factor for the development of hypertension. The resolution of this dysbiosis has emerged as a promising strategy in improving hypertension. Food-derived bioactive protein peptides have become increasingly more attractive in ameliorating hypertension, primarily due to their anti-inflammatory and anti-oxidant activities.
View Article and Find Full Text PDFShock
December 2024
Department of Emergency Medicine, Hubei Provincial Hospital of Traditional Chinese Medicine, Wuhan 430074, China.
Aims: Brain injury occupies the predominant cause of neurological dysfunction and mortality after successful cardiopulmonary resuscitation (CPR) from cardiac arrest (CA). This study investigates the role and mechanism of Sirtuin 6 (SIRT6) in post-cardiac arrest brain injury in rats.
Methods: All rats were subjected to asphyxial CA followed by CPR.
Cardiovasc Drugs Ther
January 2025
State Key Laboratory of Pathogenesis, Prevention and Treatment of High Incidence Diseases in Central Asia, First Affiliated Hospital of Xinjiang Medical University, Clinical Medical Research Institute, Xinjiang Medical University, No. 137 Liyushan South Road, Urumqi, 830054, China.
Purpose: To investigate the protective effect and mechanism of enhanced expression of endogenous macrophage migration inhibitory factor (MIF) on cardiac ischemia-reperfusion (I/R) injury.
Methods: A recombinant double-stranded adeno-associated virus serotype 9 with MIF or green fluorescent protein (GFP) genes (dsAAV9-MIF/GFP) was transduced into mice and neonatal rat ventricular myocytes (NRVMs). The models of cardiac 60 min ischemia and 24 h reperfusion and 12 h hypoxia/12 h reoxygenation (H/R) were established in mice and NRVMs, respectively.
Redox Biol
December 2024
Department of Emergency Medicine, Thomas Jefferson University, Philadelphia, PA, USA; Department of Biomedical Engineering, UAB, Birmingham, AL, USA. Electronic address:
Background: Diabetes increases ischemic heart injury via incompletely understood mechanisms. We recently reported that diabetic adipocytes-derived small extracellular vesicles (sEV) exacerbate myocardial reperfusion (MI/R) injury by promoting cardiomyocyte apoptosis. Combining in vitro mechanistic investigation and in vivo proof-concept demonstration, we determined the underlying molecular mechanism responsible for diabetic sEV-induced cardiomyocyte apoptosis after MI/R.
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