Danshenol A inhibits TNF-α-induced expression of intercellular adhesion molecule-1 (ICAM-1) mediated by NOX4 in endothelial cells

Zhao, Wenwen; Feng, Haitao; Guo, Shuhui; Han, Yantao; Chen, Xiuping

doi:10.1038/s41598-017-13072-1

Cited by 39 publications

(31 citation statements)

References 46 publications

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“…Additionally, MME is downregulated by NF-κB pathway via microRNA miR155 in B-lymphoma cells [31]. The pro-inflammatory cytokine TNFα activates NF-κB pathway [22], which subsequently upregulates ICAM-1 (intercellular adhesion molecule 1) expression [32]. TNFα is increased in cord blood when mothers are overweight [27], and fpEC also respond to TNFα with an induction of ICAM-1 expression [33].…”

Section: Discussionmentioning

confidence: 99%

Maternal Overweight Downregulates MME (Neprilysin) in Feto-Placental Endothelial Cells and in Cord Blood

Weiss

Berger

Brandl

et al. 2020

IJMS

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Maternal overweight in pregnancy alters the metabolic environment and generates chronic low-grade inflammation. This affects fetal development and programs the offspring’s health for developing cardiovascular and metabolic disease later in life. MME (membrane-metalloendopeptidase, neprilysin) cleaves various peptides regulating vascular tone. Endothelial cells express membrane-bound and soluble MME. In adults, the metabolic environment of overweight and obesity upregulates endothelial and circulating MME. We here hypothesized that maternal overweight increases MME in the feto-placental endothelium. We used primary feto-placental endothelial cells (fpEC) isolated from placentas after normal vs. overweight pregnancies and determined MME mRNA, protein, and release. Additionally, soluble cord blood MME was analyzed. The effect of oxygen and tumor necrosis factor α (TNFα) on MME protein in fpEC was investigated in vitro. Maternal overweight reduced MME mRNA (−39.9%, p < 0.05), protein (−42.5%, p = 0.02), and MME release from fpEC (−64.7%, p = 0.02). Both cellular and released MME protein negatively correlated with maternal pre-pregnancy BMI. Similarly, cord blood MME was negatively associated with pre-pregnancy BMI (r = −0.42, p = 0.02). However, hypoxia and TNFα, potential negative regulators of MME expression, did not affect MME protein. Reduction of MME protein in fpEC and in cord blood may alter the balance of vasoactive peptides. Our study highlights the fetal susceptibility to maternal metabolism and inflammatory state.

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Section: Discussionmentioning

confidence: 99%

Maternal Overweight Downregulates MME (Neprilysin) in Feto-Placental Endothelial Cells and in Cord Blood

Weiss

Berger

Brandl

et al. 2020

IJMS

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“…Therefore, Danshen represents a traditional Chinese medicine (TCM) that has a relatively high safety profile. To date, the chemical constituents of Danshen have been well identified, including more than 30 lipophilic compounds that have a diterpene chinone structure (tanshinone I-VI, cryptotanshinone, isotanshinone I-II, Danshenol A etc) and more than 50 hydrophilic compounds that mainly have a phenolic acid structure (Danshensu, salvianolic acid A, salvianolic acid B, protocatechuic aldehyde, etc) [1,[5][6][7] . More recently, Tasly Pharmaceuticals, Inc has completed a Phase III clinical trial to evaluate the safety and efficacy of Dantonic® (T89, also known as Compound Danshen Dripping Pills) in patients with chronic stable angina pectoris (ClinicalTrials.gov Identifier: NCT01659580).…”

Section: Introductionmentioning

confidence: 99%

Salvia miltiorrhizaBurge (Danshen): a golden herbal medicine in cardiovascular therapeutics

2018

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Salvia miltiorrhiza Burge (Danshen) is an eminent medicinal herb that possesses broad cardiovascular and cerebrovascular protective actions and has been used in Asian countries for many centuries. Accumulating evidence suggests that Danshen and its components prevent vascular diseases, in particular, atherosclerosis and cardiac diseases, including myocardial infarction, myocardial ischemia/reperfusion injury, arrhythmia, cardiac hypertrophy and cardiac fibrosis. The published literature indicates that lipophilic constituents (tanshinone I, tanshinone IIa, tanshinone IIb, cryptotanshinone, dihydrotanshinone, etc) as well as hydrophilic constituents (danshensu, salvianolic acid A and B, protocatechuic aldehyde, etc) contribute to the cardiovascular protective actions of Danshen, suggesting a potential synergism among these constituents. Herein, we provide a systematic up-to-date review on the cardiovascular actions and therapeutic potential of major pharmacologically active constituents of Danshen. These bioactive compounds will serve as excellent drug candidates in small-molecule cardiovascular drug discovery. This article also provides a scientific rationale for understanding the traditional use of Danshen in cardiovascular therapeutics.

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“…In the endothelial cells, TNFα has been shown to inhibit endothelial nitric oxide synthase (eNOS) expression via the destabilization of eNOS mRNA [9] and increase the expression of the adhesion molecules via the activation of the NFκB pathway [10]. In the endothelial and vascular smooth muscle cells, TNFα activates NADPH oxidase to induce oxidative stress [11].…”

Section: Introductionmentioning

confidence: 99%

Tumor Necrosis Factor Alpha Deficiency Improves Endothelial Function and Cardiovascular Injury in Deoxycorticosterone Acetate/Salt-Hypertensive Mice

Cai

Huang

Liu

et al. 2020

BioMed Research International

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It has been shown that the inflammatory cytokine tumor necrosis factor α (TNFα) plays a role in the development of hypertension and end-stage renal diseases. We hypothesize that TNFα contributes to endothelial dysfunction and cardiac and vascular injury in deoxycorticosterone acetate (DOCA)/salt-hypertensive mice. The wild-type or TNFα-deficient mice were uninephrectomized and implanted with DOCA pellet treatment for 5 weeks; the mice were given either tap water or 1% NaCl drinking water. DOCA mice developed hypertension (systolic blood pressure (SBP): 167±5 vs. 110±4 mmHg in control group, p<0.05), cardiac and vascular hypertrophy, and the impairment of endothelium-dependent relaxation to acetylcholine (EDR). TNFα deficiency improved EDR and lowered cardiac and vascular hypertrophy with a mild reduction in SBP (152±4 vs. 167±5 mmHg in DOCA group, p<0.05) in DOCA mice. The mRNA expressions of the inflammatory cytokines, including TNFα, interleukin 1β (IL1β), monocyte chemotactic protein 1 (MCP1), and monocyte/macrophage marker F4/80 were significantly increased in the aorta of DOCA-hypertensive mice; TNFα deficiency reduced these inflammatory gene expressions. DOCA-hypertensive mice also exhibited an increase in the vascular oxidative fluorescence intensities, the protein expressions of gp91phox and p22phox, and the fibrotic factors transforming growth factor β and fibronectin. TNFα deficiency reduced oxidative stress and fibrotic protein expressions. The DOCA mice also showed a decrease in the protein expression of eNOS associated with increased miR155 expression; TNFα deficiency prevented a decrease in eNOS expression and an increase in miR155 expression in DOCA mice. These results support the idea that TNFα significantly contributes to vascular inflammation, vascular dysfunction, and injury in hypertension.

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Danshenol A inhibits TNF-α-induced expression of intercellular adhesion molecule-1 (ICAM-1) mediated by NOX4 in endothelial cells

Cited by 39 publications

References 46 publications

Maternal Overweight Downregulates MME (Neprilysin) in Feto-Placental Endothelial Cells and in Cord Blood

Maternal Overweight Downregulates MME (Neprilysin) in Feto-Placental Endothelial Cells and in Cord Blood

Salvia miltiorrhizaBurge (Danshen): a golden herbal medicine in cardiovascular therapeutics

Tumor Necrosis Factor Alpha Deficiency Improves Endothelial Function and Cardiovascular Injury in Deoxycorticosterone Acetate/Salt-Hypertensive Mice

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