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Cited by 28Pulmonary Hypertension Research and TreatmentsNitric Oxide and Endothelin EffectsVascular Anomalies and Treatments

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Effect of asiaticoside on endothelial cells in hypoxia‑induced pulmonary hypertension

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Wang, Xiaobing, Cai, Xueli, Wang, Wu, Jin, Yi, Chen, Mayun, Huang, Xiaoying, Zhu, Xiaochun, Wang, Liangxing·2017·Molecular Medicine Reports
DOI 10.3892/mmr.2017.8254PMC PMC5783505
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Abstract

Pulmonary hypertension (PH) is a chronic progre-ssive disease with limited treatment options. The exact etiology and pathogenesis of PH remain to be elucidated, however there is novel evidence that implicates abnormal endothelial cells (ECs) apoptosis and dysfunction of ECs to be involved in the initiation of PH. Asiaticoside (AS) is a saponin monomer extracted from a medicinal plant called Centella asiatica, which had a preventing effect of hypoxia‑induced pulmonary hypertension (hypoxic PH) by blocking transforming growth factor‑β1/SMAD family member 2/3 signaling in our previous study. The present study demonstrated that AS can prevent the development of hypoxic PH and reverse the established hypoxic PH. AS may activate the nitric oxide (NO)‑mediated signals by enhancing the phosphorylation of serine/threonine‑specific protein kinase/eNOS, thus promoting NO production, and prevent ECs from hypoxia‑induced apoptosis. All these findings imply that AS may be a potential therapeutic option for hypoxic PH patients due to its effect on the vitality and function of endothelial cells.

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  • Asiaticoside regulates PI3K/Akt signalling pathway both in vivo and in vitro to promote cell survival and viability.

    “In addition, asiaticoside was confirmed to regulate the PI3K/Akt signalling pathway both in vivo and in vitro to promote cell survival and viability.”

    From Therapeutic Properties and Pharmacological Activities of Asiaticoside and Madecassoside: A Review (2023) · cites this paper as [111]

    The Discussion (page unavailable) states that asiaticoside upregulated PI3K/Akt/eNOS signalling in vivo and in vitro. It also reports improved viability and reduced apoptosis in cultured endothelial cells under hypoxia. The paper does not show that the pathway promoted cell survival or viability in vivo, so that part of the claim extends beyond the reported findings. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • Asiaticoside activates NO production by enhancing phosphorylation of serine/threonine-specific protein kinase/eNOS, thus preventing ECs from hypoxic PH-induced apoptosis.

    “asiaticoside can activate nitric oxide (NO) production by enhancing the phosphorylation of serine/threonine‐specific protein kinase/eNOS, thus preventing ECs from hypoxic PH‐induced apoptosis.”

    From Therapeutic Properties and Pharmacological Activities of Asiaticoside and Madecassoside: A Review (2023) · cites this paper as [111]

    The Discussion (page unavailable) reports increased NO production, Akt/eNOS phosphorylation, and reduced hypoxia-induced apoptosis with asiaticoside treatment. It also says the precise mechanism and cause-and-effect relationship remain unresolved, so the claim overstates the proposed pathway as an established causal chain. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • Asiaticoside restores misadjusted levels of vascular mediators, preserves EC morphology and function, and protects against EC cell injury.

    “Asiaticoside was also found to restore misadjusted levels of vascular mediators, preserve EC morphology and function, and protect against EC cell injury.”

    From Therapeutic Properties and Pharmacological Activities of Asiaticoside and Madecassoside: A Review (2023) · cites this paper as [111]

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Research works printed but not linked: 25

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Metadata

Authors
Wang, X., Cai, X., Wang, W., Jin, Y., Chen, M., Huang, X., Zhu, X., & Wang, L.
Affiliations
  • First Affiliated Hospital of Wenzhou Medical University (CN)
  • Wenzhou Medical University (CN)
Corresponding author
  • Zhu, Xiaochun
  • Wang, Liangxing
ORCID
Venue
Molecular Medicine Reports
Publisher
Spandidos Publications
Published
2017-12-12
Volume
17
Issue
2
Pages
2893-2900
ISSN
  • 1791-2997 (ISSN-L)
  • 1791-3004
DOI
10.3892/mmr.2017.8254
PMC
PMC5783505
OpenAlex
W2772480581
Cited by
28
References
1
Citations by year
2026: 3 · 2025: 1 · 2024: 6 · 2023: 3 · 2022: 2 · 2021: 5 · 2020: 4 · 2019: 3 · 2018: 1
FWCI
1.76
Type
journal article
Language
en
Open access
Licence
cc-by-nc-nd
Locations
  • Molecular Medicine Reports (publishedVersion, cc-by-nc-nd)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Funders
National Natural Science Foundation of China (81700062, 81473406, 81470250)
Topics
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Pulmonary Hypertension Research and Treatments
  • Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Genetics (clinical) › Vascular Anomalies and Treatments
Keywords
asiaticoside, hypoxic pulmonary hypertension, endothelial cells, endothelial cell apoptosis, Centella asiatica, saponins, nitric oxide, eNOS phosphorylation, TGF-β1/Smad signaling, endothelial dysfunction
MeSH terms
Animals, Hypoxia, Anti-Infective Agents, Antioxidants, Hypertension, Pulmonary, Male, Nitric Oxide, Phosphorylation, Triterpenes, Signal Transduction, Rats, Sprague-Dawley, Centella, Endothelial Cells

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