Protective Effect of Qiliqiangxin Capsule on Energy Metabolism and Myocardial Mitochondria in Pressure Overload Heart Failure Rats

Zhang, Junfang; Wang, Cong; Wang, Hongtao; Tang, Siwen; Jia, Zhenhua; Wang, Lei; Xu, Dengfeng; Wu, Yiling

doi:10.1155/2013/378298

Cited by 46 publications

(51 citation statements)

References 17 publications

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“…18) CPT-1 is involved in fatty acid oxidation 19) and GLUT4 plays an important role in the oxidation of glucose. 20) To determine the potential mechanisms underlying the protective effects of ALLO, the mRNA expression of molecular markers (XO, PGC-1α, CPT-1, and GLUT4) was subjected to qRT-PCR analysis in the sham, AMI and ALLO groups. As depicted in Figure 4 (compared with the sham group, the mRNA expression of XO increased by 152.56% and 377.86% in the ALLO and AMI groups (P < 0.05); the mRNA expression of GLUT4 increased by 87.94% and 195.25% (P < 0.05); the mRNA expression of PGC-1α decreased by 50.31% and 84.42% (P < 0.05); and the mRNA expression of CPT-1 decreased by 24.76% and 54.45% (P < 0.05)).…”

Section: He Staining and Transmission Electron Microscopy (Tem)mentioning

confidence: 99%

“…Inside the cell, glucose is phosphorylated to glucose-6-phosphate, which subsequently enters glycolysis via phosphofructokinase I. Pyruvate, the end product of glycolysis, is taken up into the mitochondria and converted into acetyl-CoA by pyruvate dehydrogenase (PDH) to enter the Krebs cycle. GLUT4 is the key enzyme of glucose oxidation; 20) acetyl-CoA is the common product of glycolysis and FAO; the Krebs cycle produces NADH and FADH, which feed their electrons into the ETC and drive oxidative phosphorylation (as depicted in Figure 7). …”

Section: He Staining and Transmission Electron Microscopy (Tem)mentioning

confidence: 99%

“…19) GLUT4 is an important enzyme in the oxidation of glucose. 20) We examined the protein and mRNA expression of crucial signaling molecules (XO, PGC-1α, CPT-1 and GLUT4) to determine the molecular mechanism underlying the activity of ALLO in AMIinduced CHF. Although ALLO is often used for uremia in clinical practice, its role in cardiovascular disease has also been extensively studied.…”

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confidence: 99%

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Effect of Allopurinol on Myocardial Energy Metabolism in Chronic Heart Failure Rats After Myocardial Infarct

et al. 2016

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SummaryTo determine the effect of the xanthine oxidase (XO) inhibitor allopurinol on myocardial energy metabolism in a chronic heart failure rat model after myocardial infarct.An AMI model was established in 6-week-old rats via the ligation of the anterior descending coronary artery. Thirty-five rats were randomly divided into the following 3 groups: an ALLO group, an AMI group, and a Sham group. Heart failure was successfully diagnosed via echocardiography and blood tests. Xanthine oxidase (XO), malondialdehyde (MDA), PGC-1α, CPT-1, and GLUT4 were monitored in the myocardium.The TEM results demonstrated that myofilament lysis and mitochondrial swelling were alleviated in the ALLO group compared with the AMI group (without ALLO). The results also demonstrated that cardiac function was significantly improved in the ALLO group compared with the AMI group. Compared with the AMI group, the ALLO group exhibited increased respiratory-chain enzyme activity, as well as increased PGC-1α and CPT-1 mRNA and protein expression, decreased MDA content, and decreased XO and GLUT4 mRNA and protein expression.ALLO improves myocardial energy metabolism in rats with chronic heart failure, which may result from the regulation of PGC-1α in the setting of glycolipid metabolism, enhancing the production of ATP. (Int Heart J 2016; 57: 753-759) Key words: Reactive oxygen species (ROS), Mitochondria C hronic heart failure (CHF) is the terminal stage of heart disease and is the leading cause of death in affected patients. 1-4) The incidence of CHF in adults is nearly 1~2% in developed countries and is above 10% among patients older than 70 years of age.5) Synthetic treatments and assist devices have been introduced to improve myocardial remodeling, strengthen myocardial contraction, and alleviate cardiac overload. 6,7)Editorial p.661 Improving cardiomyocyte energy metabolism has attracted attention as a potential therapy for CHF. As early as 1934, Decherd, et al 8) observed that cardiomyocytes exist in a state of "energy starvation" in the setting of CHF. Recent studies have demonstrated that the activity of respiratory-chain enzymes decreases and changes in glycolipid metabolism in the setting of CHF, resulting in decreased myocardial ATP production. Additionally, the levels of reactive oxygen species (ROS) increase rapidly following myocardial infarction. An important source of reactive oxygen species ROS, 9,10) xanthine oxidase (XO), is over-expressed in CHF, 11,12) causes mitochondrial injury, and inhibits the activity of various respiratory-chain enzymes.13) Additionally, increased evidence indicates that cardiomyocyte glycolipid metabolism is disrupted in CHF. 14,15) Opie, et al 16) observed increased concentrations of high-energy phosphate among patients with CHF following the intravenous administration of ALLO, an XO inhibitor. However, the mechanisms underlying the activity of ALLO in the setting of CHF remain poorly understood. In this study, rat models of CHF introduced via the ligation of coronary arteries were constructe...

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Section: He Staining and Transmission Electron Microscopy (Tem)mentioning

confidence: 99%

Section: He Staining and Transmission Electron Microscopy (Tem)mentioning

confidence: 99%

mentioning

confidence: 99%

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Effect of Allopurinol on Myocardial Energy Metabolism in Chronic Heart Failure Rats After Myocardial Infarct

et al. 2016

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“…The other cardioprotective effects of qili-qiangxin were related to the regulation of the glycolipid substrate metabolism by activating AMPK (AMP-activated protein kinase)/PGC-1α (peroxisome proliferators-acti- vated receptor-γ coactivator-1α) axis. Also, it was suggested that qili-qiangxin reduced the accumulation of free fatty acids and lactic acid protecting cardiac myocytes and mitochondrial function [38].…”

Section: Qili-qiangxin Capsulesmentioning

confidence: 99%

Clinical Aspects of Aconitum Preparations

Tai

El-Shazly

et al. 2015

Planta Med

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Aconitum, also known as monkshood, wolfʼs bane, or devilʼs helmet, has been widely used in folk medicine in China, India, and certain parts of Europe [1-4]. The genus Aconitum (Ranunculaceae) comprises 300 species distributed all over the world [5]. The most common species are Aconitum carmichaelii Deb. and Aconitum kusnezoffii Rchb. in China, Aconitum japonicum Thunb. in Japan, Aconitum napellus L. in Europe, Aconitum ferox Wall. ex Ser. in India, and Aconitum noveboracense A. Gray ex Coville in the United States [5]. Several classes of secondary metabolites, especially alkaloids, have been isolated from different Aconitum sp. [6]. The type of the isolated major alkaloids may vary depending on the species such as aconitine, hypaconitine, and mesaconitine from A. carmichaelii, aconitine from A. napellus, hypaconitine from A. septentrionale Koelle, mesaconitine from A. kusnezoffii, bikhaconitine from A. ferox, talatisamine from A. kongboense Lauener, atisine from A. anthora L., and A. heterophyllum Wall. ex Royle, and lycaconitine from A. vulparia Rchb. [6]. Several isoquinoline alkaloids and phenethylamine derivatives have also been isolated, such as higenamine from A. japonicum, magnoflorine from A. vulparia and A. napellus, coryneine from A. carmichaelii, and N-methyl adrenaline from A. nasutum Fisch. ex Rchb. [6]. Lipo-alkaloids including lipoaconitines, lipomesaconitines, lipodeoxyaconitines, and lipohypaconitines were also isolated [7, 8]. The efficacy of Aconitum sp. in resolving critical clinical conditions has been proven by doctors practicing traditional Chinese medicine (TCM) and Ayurvedic medicine for centuries. However, the long history of Aconitum sp. misuse in homicide cases has shaken the faith in the potential safe application of this herb in therapy [9, 10]. The recent developments in analytical techniques which can identify and determine the concentrations of toxic compounds in herbal products with impressive accuracy and reliability have rekindled the interest in Aconitum preparations [1, 5, 6, 11, 12].

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“…Protective effects of QL were demonstrated by a multicenter randomized double‐blind clinical study including 512 heart failure patients 19. It was also reported that QL could improve cardiomyocyte metabolism and inhibit cardiomyocyte apoptosis 20, 21, 22, 23. Our previous work found that QL could promote cardiac angiogenesis and up‐regulate HIF‐1α expression in failing heart and hypoxic CMECs via NRG‐1/ErbB‐PI3K/Akt/mTOR pathway, thus promoting cardiac angiogenesis 24, 25.…”

Section: Introductionmentioning

confidence: 97%

Qiliqiangxin attenuates hypoxia‐induced injury in primary rat cardiac microvascular endothelial cells via promoting HIF‐1α‐dependent glycolysis

Wang

Han

et al. 2018

J Cellular Molecular Medi

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Protection of cardiac microvascular endothelial cells (CMECs) against hypoxia injury is an important therapeutic strategy for treating ischaemic cardiovascular disease. In this study, we investigated the effects of qiliqiangxin (QL) on primary rat CMECs exposed to hypoxia and the underlying mechanisms. Rat CMECs were successfully isolated and passaged to the second generation. CMECs that were pre‐treated with QL (0.5 mg/mL) and/or HIF‐1α siRNA were cultured in a three‐gas hypoxic incubator chamber (5% CO2, 1% O2, 94% N2) for 12 hours. Firstly, we demonstrated that compared with hypoxia group, QL effectively promoted the proliferation while attenuated the apoptosis, improved mitochondrial function and reduced ROS generation in hypoxic CMECs in a HIF‐1α‐dependent manner. Meanwhile, QL also promoted angiogenesis of CMECs via HIF‐1α/VEGF signalling pathway. Moreover, QL improved glucose utilization and metabolism and increased ATP production by up‐regulating HIF‐1α and a series of glycolysis‐relevant enzymes, including glucose transport 1 (GLUT1), hexokinase 2 (HK2), 6‐phosphofructokinase 1 (PFK1), pyruvate kinase M2 (PKM2) and lactate dehydrogenase A (LDHA). Our findings indicate that QL can protect CMECs against hypoxia injury via promoting glycolysis in a HIF‐1α‐dependent manner. Lastly, the results suggested that QL‐dependent enhancement of HIF‐1α protein expression in hypoxic CMECs was associated with the regulation of AMPK/mTOR/HIF‐1α pathway, and we speculated that QL also improved HIF‐1α stabilization through down‐regulating prolyl hydroxylases 3 (PHD3) expression.

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Protective Effect of Qiliqiangxin Capsule on Energy Metabolism and Myocardial Mitochondria in Pressure Overload Heart Failure Rats

Cited by 46 publications

References 17 publications

Effect of Allopurinol on Myocardial Energy Metabolism in Chronic Heart Failure Rats After Myocardial Infarct

Effect of Allopurinol on Myocardial Energy Metabolism in Chronic Heart Failure Rats After Myocardial Infarct

Clinical Aspects of Aconitum Preparations

Qiliqiangxin attenuates hypoxia‐induced injury in primary rat cardiac microvascular endothelial cells via promoting HIF‐1α‐dependent glycolysis

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