Effect of tongxinluo on vasoconstriction induced by the chronic injury of the adventitia in the rat carotid artery

Xie, Lian Na; Zeng, Ding Yin; Zhang, Hai‐Shan; Sun, Dan Meng; Pang, Xue Feng; Guan, Qi Gang

doi:10.1016/j.jep.2010.06.037

Cited by 8 publications

(4 citation statements)

References 28 publications

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“…Accumulating studies indicate that endothelium preservation is one of the mechanisms related to the cardiovascular protective effects of TXL. 21,25,47 Our previous studies have demonstrated that TXL counters myocardial reperfusion injury through the activation of the PKA/CREB/eNOS pathway 23 and protects endothelial connections through the promotion of VE-cadherin expression in the reflow area. 24 TXL was reported to protect HUVECs against ischemic injury by activating the PI3K/AKT/HIF-a signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Induction of Autophagy by Tongxinluo Through the MEK/ERK Pathway Protects Human Cardiac Microvascular Endothelial Cells From Hypoxia/Reoxygenation Injury

Cui

et al. 2014

Journal of Cardiovascular Pharmacology

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: In contrast to cardiomyocytes, autophagy in cardiac microvascular endothelial cells (CMECs) during ischemia/reperfusion (I/R) injury has not been fully investigated. Tongxinluo (TXL), a traditional Chinese medicine, was shown to be vascular protective. We aimed to elucidate the role of autophagy and its regulatory mechanisms by TXL in CMECs subjected to I/R injury. CMECs were exposed to different treatments for 30 minutes and subjected to hypoxia/reoxygenation each for 2 hours. The results indicated that hypoxia/reoxygenation significantly induced autophagy, as identified by an increased number of monodansylcadaverine-positive CMECs, increased autophagosome formation, and a higher type II/type I of light chain 3 ratio, but not Beclin-1 expression. Autophagy inhibition using 3-methyladenine was proapoptotic, but rapamycin-induced autophagy was antiapoptotic. TXL enhanced autophagy and decreased apoptosis in a dose-dependent manner, reaching its largest effect at 800 μg/mL. 3-methyladenine attenuated the TXL-promoted autophagy and antiapoptotic effects, whereas rapamycin had no additional effects compared with TXL alone. TXL upregulated mitogen-activated protein kinase and extracellular signal-regulated kinase (ERK) phosphorylation; however, PD98059 abrogated ERK phosphorylation and decreased autophagy and increased apoptosis compared with TXL alone. These results suggest that autophagy is a protective mechanism in CMECs subjected to I/R injury and that TXL can promote autophagy through activation of the mitogen-activated protein kinase/ERK pathway.

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Section: Discussionmentioning

confidence: 99%

Induction of Autophagy by Tongxinluo Through the MEK/ERK Pathway Protects Human Cardiac Microvascular Endothelial Cells From Hypoxia/Reoxygenation Injury

Cui

et al. 2014

Journal of Cardiovascular Pharmacology

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“…Accumulating studies suggest that TXL mediates endothelium preservation in a mechanism that improves cardiac functions [12, 32, 33]. In the previous studies, we have found that TXL protects ECs against MIRI through the PKA/CREB/eNOS pathway [13] and protects endothelial connections through regulating the expression of VE-cadherin [34].…”

Section: Discussionmentioning

confidence: 99%

Quantitative Proteomics Analysis of Ischemia/Reperfusion Injury-Modulated Proteins in Cardiac Microvascular Endothelial Cells and the Protective Role of Tongxinluo

Cui

Yuejin

et al. 2017

Cell Physiol Biochem

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Background: The protection of endothelial cells (ECs) against reperfusion injury has received little attention. In this study, we used Tandem Mass Tag (TMT) labeling proteomics to investigate the modulated proteins in an in vitro model of cardiac microvascular endothelial cells (CMECs) subjected to ischemia/reperfusion (I/R) injury and their alteration by traditional Chinese medicine Tongxinluo (TXL). Methods: Human CMECs were subjected to 2 h of hypoxia followed by 2 h of reoxygenation with different concentrations of TXL Protein expression profiles of CMECs were determined using tandem mass spectrometry. We evaluated several proteins with altered expression in I/R injury and summarized some reported proteins related to I/R injury. Results: TXL dose-dependently decreased CMEC apoptosis, and the optimal concentration was 800 µg/mL. I/R significantly altered proteins in CMECs, and 30 different proteins were detected between a normal group and a hypoxia and serum deprivation group. In I/R injury, TXL treatment up-regulated 6 types of proteins including acyl-coenzyme A synthetase ACSM2B mitochondrial (ACSM2B), cyclin-dependent kinase inhibitor 1B (CDKN1B), heme oxygenase 1 (HMOX1), transcription factor SOX-17 (SOX17), sequestosome-1 isoform 1 (SQSTM1), and TBC1 domain family member 10B (TBC1D10B). Also, TXL down-regulated 5 proteins including angiopoietin-2 isoform c precursor (ANGPT2), cytochrome c oxidase assembly factor 5 (COA5), connective tissue growth factor precursor (CTGF), cathepsin L1 isoform 2 (CTSL), and eukaryotic elongation factor 2 kinase (LOC101930123). These types of proteins mainly had vital functions, including cell proliferation, stress response, and regulation of metabolic process. Conclusions: The study presented differential proteins upon I/R injury through a proteomic analysis. TXL modulated the expression of proteins in CMECs and has a protective role in response to I/R.

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“…The tongxinluo capsule is an officially approved treatment in China for angina pectoris and ischemic stroke and the compound preparation was formulated on the basis of the meridian theory of traditional Chinese medicine [ 15 , 16 ]. The routine clinical dose range of tongxinluo capsule (3 capsules, 3 times per day) approximates to 60 mg·kg −1 ·day −1 of tongxinluo powder, which may correspond to the dose of 400 mg·kg −1 ·day −1 in rats by taking account of the ratio of 6.3 [ 25 ]. In published experimental studies in rats, the highest dose effective for cardiac dysfunction was 1.5 g·kg −1 ·day −1 [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

“…Sixteen (35.6%) of the 45 doxorubicin-administrated rats died from day 14 to 27. Animals that survived after DCM induction were randomly divided into three groups: (1) the high-dose tongxinluo group (TXL-H, n = 9): received tongxinluo superfine powder intragastrically at a dosage of 1.5 g·kg −1 ·day −1 for 4 weeks; (2) the low-dose tongxinluo group (TXL-L, n = 10): received tongxinluo superfine powder intragastrically at a dosage of 0.15 g·kg −1 ·day −1 for 4 weeks [ 24 , 25 ]; (3) the DCM control group (DCM-C, n = 10): received normal saline intragastrically at the same volume as the tongxinluo-treated groups for 4 weeks. Age-matched normal rats treated with normal saline intragastrically were used as normal controls (NOR-C, n = 9).…”

Section: Methodsmentioning

confidence: 99%

Traditional Chinese Medicine Tongxinluo Improves Cardiac Function of Rats with Dilated Cardiomyopathy

Shen

Jiang

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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The study aimed at testing the hypothesis that tongxinluo capsule might exert its cardioprotective effect by preventing ventricular remodeling and improving coronary microvascular function in a rat model of doxorubicin-induced dilated cardiomyopathy (DCM). Rats that survived DCM induction were randomly divided into three groups to be given 1.5 g·kg−1·day−1 (TXL-H, n = 9) or 0.15 g·kg−1·day−1 (TXL-L, n = 10) of tongxinluo, or normal saline at the same volume (DCM-C, n = 10) intragastrically. Age matched normal rats treated with normal saline were used as normal controls (NOR-C, n = 9). After four weeks of treatment, the DCM-C, TXL-H, and TXL-L groups exhibited significant cardiac dysfunction, left ventricular remodeling, and coronary microvascular dysfunction, compared with the NOR-C rats. However, myocardial functional parameters were significantly improved and microvascular density (MVD) increased in the TXL-H group compared with the DCM-C group (all P < 0.01). Left ventricular remodeling was prevented. There were close linear relationships between CVF and LVEF (r = −0.683, P < 0.05), MVD and LVEF (r = 0.895, P < 0.05), and MVD and CVF (r = −0.798, P < 0.05). It was indicated that high-dose tongxinluo effectively improved cardiac function in rat model of DCM.

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Effect of tongxinluo on vasoconstriction induced by the chronic injury of the adventitia in the rat carotid artery

Cited by 8 publications

References 28 publications

Induction of Autophagy by Tongxinluo Through the MEK/ERK Pathway Protects Human Cardiac Microvascular Endothelial Cells From Hypoxia/Reoxygenation Injury

Induction of Autophagy by Tongxinluo Through the MEK/ERK Pathway Protects Human Cardiac Microvascular Endothelial Cells From Hypoxia/Reoxygenation Injury

Quantitative Proteomics Analysis of Ischemia/Reperfusion Injury-Modulated Proteins in Cardiac Microvascular Endothelial Cells and the Protective Role of Tongxinluo

Traditional Chinese Medicine Tongxinluo Improves Cardiac Function of Rats with Dilated Cardiomyopathy

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