The Metabolic Effects of Traditional Chinese Medication Qiliqiangxin on H9C2 Cardiomyocytes

Lin, Shenghui; Wu, Xiaoting; Tao, Ling; Bei, Yihua; Zhang, Haifeng; Zhou, Yanliz; Shen, Shutong; Xiao, Junjie; Li, Xinli

doi:10.1159/000438580

Cited by 27 publications

(31 citation statements)

References 26 publications

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“…The PPAR family consists of PPAR-α, PPAR-δ, and PPAR-γ. It has been reported that activation of PPAR-γ prevented lipopolysaccharide-mediated cardiac dysfunction and that PGC-1α was required for QLQX-associated enhancement in cardiomyocyte mitochondrial energy metabolism 26, 27. In our previous study, we also demonstrated that QLQX could improve cardiac function and attenuate cardiac remodeling after AMI by activating PPAR-γ 7.…”

Section: Discussionmentioning

confidence: 55%

Traditional Chinese Medication Qiliqiangxin Protects Against Cardiac Remodeling and Dysfunction in Spontaneously Hypertensive Rats

Wang¹,

Zhang²,

Yu³

et al. 2017

Int. J. Med. Sci.

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Qiliqiangxin (QLQX), a traditional Chinese herbs medication, exerted protective effect in chronic heart failure patients in a multicenter randomized double-blind study. QLQX has also been found to improve cardiac function and reduce cardiac fibrosis in spontaneously hypertension animal model. However, the effect of longterm treatment with QLQX in such a condition and the related molecular mechanisms remain largely unknown. In the present study, thirteen-week-old spontaneously hypertensive rats (SHRs) were treated by daily intragastric administration of QLQX or saline for one year. Echocardiography, electron microscopy, and Masson's trichrome staining were used to determine cardiac function, mitochondria ultrastructure, and cardiac fibrosis, respectively. Quantitative reverse transcription polymerase chain reactions (qRT-PCRs) and Western blotting were used to determine gene expressions. We found that QLQX significantly improved cardiac function and reduced gene markers of pathological hypertrophy including ANP, BNP, and Myh7. QLQX also attenuated cardiac fibrosis and apoptosis in SHRs as evidenced by downregulation of α-SMA, collagen I, collagen III, and TGF-β expressions and reduction of Bax to Bcl-2 ratio. Moreover, the damage of mitochondrial ultrastructure was greatly improved and the reduction of PPAR-α, PPAR-γ, and PGC-1α expression levels was significantly restored in SHRs by treatment with QLQX. In conclusion, longterm treatment with QLQX protects against cardiac remodeling and dysfunction in hypertension by increasing PPARs and PGC-1α.

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Section: Discussionmentioning

confidence: 55%

Traditional Chinese Medication Qiliqiangxin Protects Against Cardiac Remodeling and Dysfunction in Spontaneously Hypertensive Rats

Wang¹,

Zhang²,

Yu³

et al. 2017

Int. J. Med. Sci.

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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: 96%

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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“…Recent work has presented that QL is an effective agent in the cardiovascular diseases treatment [9,10]. QL showed the protective effects in the cardiovascular system via reducing myocardial apoptosis and cardiac fibrosis, thus protecting cardiac function.…”

Section: Introductionmentioning

confidence: 99%

Qiliqiangxin improves oxidized low-density lipoprotein-induced human coronary artery endothelial cells injury

Du¹,

Lv²,

Meng³

et al. 2018

biomedicalresearch

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Qiliqiangxin (QL) has protective effect for the cardiovascular diseases treatment. This study aim to evaluate the effect of QL on the cell viability, cell apoptosis and caspase-3 activity in oxidized LDL (oxLDL)-induced Human Coronary Artery Endothelial Cells (HCAECs). HCAECs were treated with QL (0-1µg/ml) and oxLDL (150 μg/ml). The HCAECs viability was detected by cell proliferation assay and Lactate Dehydrogenase (LDH) release assay. The HCAECs apoptosis was evaluated by the annexin V-FITC assay. The activity of caspase-3 of HCAECs was measured by colorimetric caspase-3 assay. Cell migration assay and capillary-like tube formation assay on Matrigel were performed. Treatment of HCAECs to ox-LDL (150 μg/ml) decreased cell viability, stimulated apoptosis and enhanced caspase-3 activity. In addition, treatment with QL (0.5 µg/ml) alone did not affect cell viability and LDH release. Furthermore, the treatment with QL (0.5 µg/ml) significantly increased ox-LDL (150 μg/ml) decreased cell viability. Treatment with QL (0.5 µg/ml) reduced ox-LDL-stimulated apoptosis and caspase-3 activity in HCAECs in a dose-dependent manner. QL (0.5 µg/ml) attenuated ox-LDL (150 μg/ml) abolished cell migration and tube formation. Our study demonstrated that QL prevents ox-LDLinduced HCAECs injury by decreasing the apoptosis via caspase-3 activity.

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The Metabolic Effects of Traditional Chinese Medication Qiliqiangxin on H9C2 Cardiomyocytes

Cited by 27 publications

References 26 publications

Traditional Chinese Medication Qiliqiangxin Protects Against Cardiac Remodeling and Dysfunction in Spontaneously Hypertensive Rats

Traditional Chinese Medication Qiliqiangxin Protects Against Cardiac Remodeling and Dysfunction in Spontaneously Hypertensive Rats

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

Qiliqiangxin improves oxidized low-density lipoprotein-induced human coronary artery endothelial cells injury

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