Neurohumoral Modulation During Waon Therapy in Chronic Heart Failure　― Subanalysis of Waon-CHF Study ―

Ichiki, Tomoko; Burnett, John C.; Scott, Christopher G.; Heublein, Denise M.; Miyata, Masaaki; Kinugawa, Koichiro; Inoue, Teruo; Investigators, Waon-Chf Study

doi:10.1253/circj.cj-16-1117

Cited by 13 publications

(5 citation statements)

References 30 publications

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“…NO is a classic vasodilator agent. It maintains an effective balance with the vasoconstrictive agents in physiological conditions; thus, the blood vessels over contract when NO secretion suppresses [43]. This explanation indicates another theory about COQ10's effect on the kidneys, which leads to increased impairment in kidney function.…”

Section: Discussionmentioning

confidence: 85%

Coenzyme Q10 coadministration with diclofenac augmented impaired renal function in broiler chickens (Gallus gallus domesticus)

Albadrany

Naser

2020

Vet World

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Aim: This study aimed to investigate the effects of coenzyme Q10 (COQ10) and diclofenac coadministration on the hepatorenal function in broiler chickens (Gallus gallus domesticus). Materials and Methods: Birds (21 days old) were divided into six groups of eight birds each. The 1st group was the control, the 2nd group was treated orally with COQ10 (30 mg/kg b.wt), the 3rd and 4th groups were treated intraperitoneally with diclofenac sodium at doses 1 and 2 mg/kg b.wt, respectively, and the 5th and 6th groups were treated with COQ10 (dose 30 mg/kg b.wt, P.O.) and diclofenac sodium (dose 1 mg/kg b.wt, I.P.) and COQ10 (dose 30 mg/kg b.wt, P.O.) and diclofenac sodium (dose 2 mg/kg b.wt, I.P.), respectively. The experiment lasted 5 days. Twenty-four hours after the last administration, all the birds were sacrificed through cervical dislocation; blood samples were collected for serum biochemical analysis. Results: COQ10 induced a significant increase in aspartate aminotransferase (AST), urea, creatinine, sodium, potassium, and chloride, while diclofenac induced a significant increase in alanine aminotransferase (ALT), AST, total cholesterol, triglyceride, high-density lipoprotein, urea, creatinine, sodium, potassium, and chloride. However, when COQ10 and diclofenac were coadministered, we observed that COQ10 decreased the liver injury caused by diclofenac. However, COQ10 could not relieve the kidney injury caused by diclofenac, but worsened the impaired renal function. Conclusion: COQ10 protects the liver against diclofenac-induced liver injury while augmenting diclofenac-induced kidney injury.

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Section: Discussionmentioning

confidence: 85%

Coenzyme Q10 coadministration with diclofenac augmented impaired renal function in broiler chickens (Gallus gallus domesticus)

Albadrany

Naser

2020

Vet World

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“…The results showed that compared with the DOX group, SAL could significantly improve heart function, reducing levels of myocardial injury markers and relieving cardiomyocyte apoptosis. Recent researches (Francesco et al, 2017; Ichiki et al, 2017; Vecchis and Ariano, 2018) have shown that RAAS plays a key role in CHF treatment. Therefore, serum levels of renin, Ang-II, and ALD were measured in this study.…”

Section: Discussionmentioning

confidence: 99%

Salsolinol Attenuates Doxorubicin-Induced Chronic Heart Failure in Rats and Improves Mitochondrial Function in H9c2 Cardiomyocytes

et al. 2019

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Backgrounds: Salsolinol (SAL), a plant-based isoquinoline alkaloid, was initially isolated from Aconiti Lateralis Radix Praeparata (ALRP) and identified as the active cardiotonic component of ALRP. This study was aimed to explore the therapeutic effect and mechanism by which SAL attenuates doxorubicin (DOX)-induced chronic heart failure (CHF) in rats and improves mitochondrial function in H9c2 cardiomyocytes. Methods: Rats were intraperitoneally injected with DOX to establish CHF model. Therapeutic effects of SAL on hemodynamic parameters, serum indices, and the histopathology of the heart were analyzed in vivo. Moreover, H9c2 cardiomyocytes were pretreated with SAL for 2 h before DOX treatment in all procedures in vitro. Cell viability, cardiomyocyte morphology, proliferation, and mitochondrial function were detected by a high-content screening (HCS) assay. In addition, a Seahorse Extracellular Flux (XFp) analyzer was used to evaluate the cell energy respiratory and energy metabolism function. To further investigate the potential mechanism of SAL, relative mRNA and protein expression of key enzymes in the tricarboxylic acid cycle in vivo and mitochondrial calcium uniporter (MCU) signaling pathway-related molecules in vitro were detected. Results: The present data demonstrated the pharmacological effect of SAL on DOX-induced CHF, which was through ameliorating heart function, downregulating serum levels of myocardial injury markers, alleviating histological injury to the heart, increasing the relative mRNA expression levels of key enzymes downstream of the tricarboxylic acid cycle in vivo, and thus enhancing myocardial energy metabolism. In addition, SAL had effects on increasing cell viability, ameliorating DOX-induced mitochondrial dysfunction, and increasing mitochondrial oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) in H9c2 cardiomyocyte. Moreover, we found that SAL might have an effect on improving mitochondrial respiratory function and energy metabolism via inhibiting excessive activation of MCU pathway in H9c2 cells. However, the protective effect could be ameliorated by ruthenium red (an MCU inhibitor) and abrogated by spermine (an MCU activator) in vitro. Conclusion: The therapeutic effects of SAL on CHF are possibly related to ameliorating cardiomyocyte function resulting in promotion of mitochondrial respiratory and energy metabolism. Furthermore, the potential mechanism might be related to downregulating MCU pathway. These findings may provide a potential therapy for CHF.

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“…14 Notably, Ichiki et al show that CNP levels were significantly inhibited by Waon therapy in HF patients with renal impairment, suggesting that worsening renal function associated with HF (cardiorenal syndrome) could be a potential target for Waon therapy. 11 On the basis of these findings, it would appear that Waon therapy ameliorates activation of the RAAS and NP systems, particularly in the advanced clinical stages of HF with optimal RAAS inhibitors or comorbidities such as hypertension, diabetes, or renal failure. Furthermore, it is also anticipated that Waon therapyinduced neurohumoral modulation may reverse cardiac remodeling, leading to improved adverse outcomes in those specific HF subtypes, as shown by a retrospective study that Waon therapy reduced cardiac death and rehospitalization in chronic HF patients.…”

Section: Article P 709mentioning

confidence: 99%

Renin-Angiotensin-Aldosterone System and Natriuretic Peptides as Possible Targets of Waon Therapy in Heart Failure

Fukushima

Kinugawa

2017

Circ J

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Neurohumoral Modulation During Waon Therapy in Chronic Heart Failure　― Subanalysis of Waon-CHF Study ―

Cited by 13 publications

References 30 publications

Coenzyme Q10 coadministration with diclofenac augmented impaired renal function in broiler chickens (Gallus gallus domesticus)

Coenzyme Q10 coadministration with diclofenac augmented impaired renal function in broiler chickens (Gallus gallus domesticus)

Salsolinol Attenuates Doxorubicin-Induced Chronic Heart Failure in Rats and Improves Mitochondrial Function in H9c2 Cardiomyocytes

Renin-Angiotensin-Aldosterone System and Natriuretic Peptides as Possible Targets of Waon Therapy in Heart Failure

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Neurohumoral Modulation During Waon Therapy in Chronic Heart Failure ― Subanalysis of Waon-CHF Study ―

Cited by 13 publications

References 30 publications

Coenzyme Q10 coadministration with diclofenac augmented impaired renal function in broiler chickens (Gallus gallus domesticus)

Coenzyme Q10 coadministration with diclofenac augmented impaired renal function in broiler chickens (Gallus gallus domesticus)

Salsolinol Attenuates Doxorubicin-Induced Chronic Heart Failure in Rats and Improves Mitochondrial Function in H9c2 Cardiomyocytes

Renin-Angiotensin-Aldosterone System and Natriuretic Peptides as Possible Targets of Waon Therapy in Heart Failure

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Neurohumoral Modulation During Waon Therapy in Chronic Heart Failure　― Subanalysis of Waon-CHF Study ―