ArticleMolecular and cellular biochemistry2021
Allicin can suppress the activity of vascular endothelial cells probably by regulating JAK2/STAT3 pathway.
Article in Molecular and cellular biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The trial behind it
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Allicin inhibits PD-L1 through the IL-6/JAK2/STAT3 pathway to suppress immune evasion in osteosarcoma.Frontiers in immunology · 2026Article
- Mini-review: The health benefits and applications of allicin.Frontiers in pharmacology · 2025Review
- Botulinum toxin type A inhibits the formation of hypertrophic scar through the JAK2/STAT3 pathway.Biomolecules & biomedicine · 2024Article
- Allicin and Cancer Hallmarks.Molecules (Basel, Switzerland) · 2024Review
- Quercetin inhibits fibroblasts proliferation and reduces surgery-induced epidural fibrosis via the autophagy-mediated PI3K/Akt/mTOR pathway.Bioengineered · 2022Article
- Allicin, an Antioxidant and Neuroprotective Agent, Ameliorates Cognitive Impairment.Antioxidants (Basel, Switzerland) · 2021Review
- Therapeutic candidates for keloid scars identified by qualitative review of scratch assay research for wound healing.PloS one · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Whether allicin can suppress the angiogenesis via inhibiting the activity of vascular endothelial cells (VECs) in preventing epidural hypertrophic scars remains unknown. VECs were treated by allicin at a gradient of concentrations. Cell activity was measured by CCK-8 assay, scratch assay and flow cytometry. Reverse-transcription PCR and Western Blot were used to measure the expression levels of relevant genes and proteins. After treated with allicin at concentrations of 0, 25, 50 and 100 mg/L, the viability of VECs significantly decreased at 24 h (p < 0.001*) and 48 h (p < 0.001*), and migration rate significantly decreased in scratch assay (p = 0.017*) and in Transwell assay (p = 0.021*). As the concentrations of allicin increased, the apoptosis rate of VECs rose up (p = 0.018*). There was no significant difference on cell numbers at S phase (p = 0.25), but cell numbers at G1 phase decreased (p = 0.039*) and at G2 phase increased (p = 0.047*). With the increase of allicin concentrations, the ability of tube formation for VECs significantly decreased (p < 0.001*). Comparing with control group, the expression of PCNA and BCL-2 decreased (p < 0.001*), while the expression of BAX increased significantly (p < 0.001*). Regarding to JAK2/STAT3 pathway, the expression levels of JAK3 and STAT3 decreased significantly with the increase of allicin concentrations (p < 0.001*). Allicin can suppress the activity of VECs probably by regulating JAK2/STAT3 pathway.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.