ArticleBMC pharmacology & toxicology2017
The inhibitory effect of Isoliquiritigenin on the proliferation of human arterial smooth muscle cell.
Article in BMC pharmacology & toxicology, 2017. 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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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Dysregulation of Mitochondrial Homeostasis in Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Dynamin-related protein 1 mediates the therapeutic effect of isoliquiritigenin in diabetic intimal hyperplasia via regulation of mitochondrial fission.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- Therapeutic Intervention in Cancer by Isoliquiritigenin from Licorice: A Natural Antioxidant and Redox Regulator.Antioxidants (Basel, Switzerland) · 2022Review
- Comparative Pharmacokinetics of Seven Major Compounds in Normal and Atherosclerosis Mice after Oral Administration of Simiao Yong'an Decoction.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Nucleolin promotes Ang II‑induced phenotypic transformation of vascular smooth muscle cells via interaction with tropoelastin mRNA.International journal of molecular medicine · 2019Article
- The dietary flavonoid isoliquiritigenin is a potent cytotoxin for human neuroblastoma cells.Neuronal signaling · 2019Article
- Isoliquiritigenin Attenuates Monocrotaline-Induced Pulmonary Hypertension via Inhibition of the Inflammatory Response and PASMCs Proliferation.Evidence-based complementary and alternative medicine : eCAM · 2019Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIsoliquiritigenin (ISL) has various biological activities including as antioxidant and an inhibitor of PI3K/AKT signaling pathway. However, both oxidative stress and activated PI3K/AKT signaling contribute to the aberrant proliferation of vascular smooth muscle cells (VSMCs). This study is aimed to explore the effect of ISL on the proliferation of human arterial smooth muscle cells (HASMCs) and to investigate the underlying mechanisms.
methodsBrdU incorporation, cell cycle and reactive oxygen species (ROS) in normal or ISL treated HASMCs were analyzed by flow cytometry. Cell viablity was measured by CCK-8. Protein expression levels were examined by Western blot, and superoxide dismutase (SOD) activity was detected by using commercial kit.
resultsWe observed that ISL could inhibit the proliferation of HASMCs in a dose and time dependent manner. Cell cycle of ISL treated HASMCs arrested mainly in G1/S phase and accompanied with elevated expression of p27 and decreased expression of CyclinD1 and CyclinE. In addition, ISL could down-regulated the expression of p-PI3K and p-AKT, alleviated oxidative stress and enhanced the SOD activity in HASMCs. Furthermore, H
conclusionsTherefore, we concluded that ISL inhibited the proliferation of HASMCs via attenuating oxidative stress and suppressing PI3K/AKT signaling pathway. The inhibitory effect of ISL on PI3K/AKT signaling pathway, at least partly, was mediated by ROS.
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