Lingguizhugan decoction attenuates doxorubicin-induced heart failure in rats by improving TT-SR microstructural remodeling

Li, Xueping; Xu, Guangmin; Wei, Shujun; Zhang, Baocheng; Yao, Huan; Chen, Yuchi; Liu, Weiwei; Wang, Baojia; Zhao, Juan; Gao, Yongxiang

doi:10.1186/s12906-019-2771-6

Cited by 23 publications

(21 citation statements)

References 53 publications

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“…When the left ventricle is dysfunctional, it is rapidly synthesized and released into the blood due to myocardial dilation. As a sensitive marker of heart failure, BNP reflects not only left ventricular systolic and diastolic dysfunction, but also valvular dysfunction and right ventricular dysfunction (Li et al, 2019). In accordance with previous results, EF and FS decreased significantly, while LVIDs, LVIDd and BNP increased abnormally in the doxorubicin-induced heart failure animal model group, (Hang et al, 2017;Wen et al, 2019) indicating that there was serious cardiac damage and left ventricular dilatation, that is, the cardiac pumping function decreased.…”

Section: Discussionsupporting

confidence: 89%

“…Heart failure refers to the circulatory dysfunction characterized by the decrease of cardiac output and cannot meet the metabolic needs of the body due to the decrease of myocardial diastolic and systolic function or the limitation of ventricular filling caused by various causes. Heart failure is a social and public health problem that seriously threatens life and health in the process of aging in developed and developing countries all over the world ( Li et al, 2019 ). At present, these drugs for the treatment of heart failure are widely used in the clinic, such as cardiotonic glycosides, diuretics, B–receptor blockers, calcium channel blockers, angiotensin-Ⅱconverting enzyme inhibitors.…”

Section: Introductionmentioning

confidence: 99%

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aFGF Targeted Mediated by Novel Nanoparticles-Microbubble Complex Combined With Ultrasound-Targeted Microbubble Destruction attenuates Doxorubicin-Induced Heart Failure via Anti-Apoptosis and Promoting Cardiac Angiogenesis

et al. 2021

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The purpose of this study was to evaluate the protective effect of acidic fibroblast growth factor targeted mediated by novel nanoparticles–cationic lipid microbubbles complex (aFGF–NP + CPMBs) combined with ultrasound targeted microbubble destruction (UTMD)on doxorubicin–induced heart failure (HF)and its mechanism. Heart failure rats induced by intraperitoneal injection with doxorubicin (DOX) to achieve cummulative dose of 15mg/kg for continuous 6 weeks showed left ventricular dysfunction, seriously oxidative stress, cardiomyocyte apoptosis, and decrease of myocardial vascular density. In contrast, aFGF–NP + CPMBs combined with UTMD therapy (3ug/kg, caudal vein injection, twice a week, 6weeks)prominently ameliorated left ventricular dysfunction by increased ejection fraction (EF) and fractional shortening (FS), decreased brain natriuretic peptide (BNP); strengthened the ability of antioxidant stress confirmed by increasing the activity of SOD and reducing the production of MDA; exerted the effect of anti–cardiomyocyte apoptosis and promotion angiogenesis by inhibited Bax expression and increased Bcl–2 expression and platelet endothelial cell adhesion molecule (CD31) expression. Taken together, the research suggested that aFGF targeted mediated by novel nanoparticles–cationic lipid microbubbles complex combined with UTMD should be a promising targeted treatment for heart failure.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

aFGF Targeted Mediated by Novel Nanoparticles-Microbubble Complex Combined With Ultrasound-Targeted Microbubble Destruction attenuates Doxorubicin-Induced Heart Failure via Anti-Apoptosis and Promoting Cardiac Angiogenesis

et al. 2021

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“…Digoxin, as a digitalis glycoside, improves the hemodynamic and neurohormonal perturbations which plays a crucial role in Heart Failure (HF) induced renal dysfunction. Abnormal energy metabolism increased production of reactive oxygen species (ROS), and defects in excitation-contraction are the hallmarks of Heart Failure due to impaired ventricular fi lling or blood ejection [19,20]. Digoxin increases intracellular calcium in myocardial cells and inhibits the sodium-potassium pump, besides, induces an increase in intracellular Na+ and Ca2+ [21].…”

Section: Discussionmentioning

confidence: 99%

Evaluating plasma Digoxin concentration after an intravenous loading dose in patients with renal failure

Eslami¹,

Mortezapour²,

Samavat³

et al. 2021

Arch Clin Nephrol

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Background: Digoxin is a medication of Glycoside family which is commonly prescribed for patients with atrial fi brillation, atrial fl utter, and heart failure. With a narrow therapeuticlevel(0.5-2 ng/mL), careful monitoring of digoxin blood level is necessary. Symptoms of digoxin toxicity include nausea, vomiting, visual changes, altered mental status, hyperkalemia, and cardiovascular collapse. As renal failure decreases the clearance of digoxin, and impaired renal function is common in heart failure, this population is at higher risk of toxicity. Methods & materials:In this prospective study, patients with chronic kidney disease-nondialysis (CKD-ND) who were admitted with heart failure or atrial fi brillation at university hospital, were enrolled. Digoxin-naive patients were treated with a 10 mcg/kg intravenous digoxin loading dose. Serum digoxin level was measured 6 to 12 hours after the last loading dose. Patients were followed for 48 hours for signs of toxicity. Correlation between therapeutic digoxin level and degree of renal failure was evaluated. The effect of serum electrolyte (magnesium, calcium, and potassium) concentration on digoxin level was determined. Pregnant women were excluded from study.Results: From 2018 to 2020, 87 CKD patients, (60 (69%) men and 27 (31%) women) aged from 31 to 92 years old, with a mean age of 70.51 ± 14.06 years were admitted to the cardiac unit. Near 80% of the cohort were CKD stage 3 and 4 patients. About half of patients had digoxin levels in therapeutic range (45 cases = 51.7%), followed by 24.1% with supra therapeutic and the other 24.1% with toxic levels. There was signifi cant relationship between GFR and serum digoxin concentration (p-value = 0.038); the lower the GFR was, the higher was the digoxin level and also between serum creatinine and digoxin level (p value: .04). Serum digoxin concentration had signifi cant correlation with serum magnesium level (p-value = 0.006). Conclusion:this study demonstrated that monitoring plasma Digoxin concentration after an intravenous loading dose in patients with renal failure can be very helpful to prevent digoxin toxicity. The lower the GFR was, the higher the digoxin level and the risk for toxicity if the bolus and even maintenance do not monitor meticulously.

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“…In acute injury, miR-24 was suppressed, where its upregulation promoted cell survival and possessed antiapoptotic and antifibrotic effects [12,13]. On the contrary, chronic injuries upregulated miR24 in the heart [8,14,15]. Moreover, serum and cardiac expression of miR-24 was found to be upregulated in atrial fibrillation [16] and heart failure patients [8,17].…”

Section: Introductionmentioning

confidence: 99%

Pachymic Acid Attenuated Doxorubicin-Induced Heart Failure by Suppressing miR-24 and Preserving Cardiac Junctophilin-2 in Rats

Younis

Salama

Shaheen

et al. 2021

IJMS

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Defects in cardiac contractility and heart failure (HF) are common following doxorubicin (DOX) administration. Different miRs play a role in HF, and their targeting was suggested as a promising therapy. We aimed to target miR-24, a suppressor upstream of junctophilin-2 (JP-2), which is required to affix the sarcoplasmic reticulum to T-tubules, and hence the release of Ca2+ in excitation–contraction coupling using pachymic acid (PA) and/or losartan (LN). HF was induced with DOX (3.5 mg/kg, i.p six doses, twice weekly) in 24 rats. PA and LN (10 mg/kg, daily) were administered orally for four weeks starting the next day of the last DOX dose. Echocardiography, left ventricle (LV) biochemical and histological assessment and electron microscopy were conducted. DOX increased serum BNP, HW/TL, HW/BW, mitochondrial number/size and LV expression of miR-24 but decreased EF, cardiomyocyte fiber diameter, LV content of JP-2 and ryanodine receptors-2 (RyR2). Treatment with either PA or LN reversed these changes. Combined PA + LN attained better results than monotherapies. In conclusion, HF progression following DOX administration can be prevented or even delayed by targeting miR-24 and its downstream JP-2. Our results, therefore, suggest the possibility of using PA alone or as an adjuvant therapy with LN to attain better management of HF patients, especially those who developed tolerance toward LN.

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Lingguizhugan decoction attenuates doxorubicin-induced heart failure in rats by improving TT-SR microstructural remodeling

Cited by 23 publications

References 53 publications

aFGF Targeted Mediated by Novel Nanoparticles-Microbubble Complex Combined With Ultrasound-Targeted Microbubble Destruction attenuates Doxorubicin-Induced Heart Failure via Anti-Apoptosis and Promoting Cardiac Angiogenesis

aFGF Targeted Mediated by Novel Nanoparticles-Microbubble Complex Combined With Ultrasound-Targeted Microbubble Destruction attenuates Doxorubicin-Induced Heart Failure via Anti-Apoptosis and Promoting Cardiac Angiogenesis

Evaluating plasma Digoxin concentration after an intravenous loading dose in patients with renal failure

Pachymic Acid Attenuated Doxorubicin-Induced Heart Failure by Suppressing miR-24 and Preserving Cardiac Junctophilin-2 in Rats

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