Cai, H.

Astragalus polysaccharide regulates proliferation, migration and invasion of lung cancer cells via janus kinase/signal transducer and activator of transcription signaling pathway - Vol.83(6), Nov-Dec - Mumbai Indian Journal of Pharmaceutical Science 2021 - 1215-1220p.

To evaluate the regulatory effects of Astragalus polysaccharide on the proliferation, migration and invasion
of lung cancer cells via the Janus kinase/signal transducer and activator of transcription signaling pathway.
The inhibitory effects of treatment with Astragalus polysaccharide at different concentrations (0, 0.5, 1.0, 2.0,
4.0, 8.0 and 16.0 mg/ml) for different time (24, 48 and 72 h) on the proliferation of adenocarcinomic human
alveolar basal epithelial cells in the logarithmic growth phase were detected by methyl thiazolyl tetrazolium
assay and its inhibitory effects on the migration and invasion of adenocarcinomic human alveolar basal
epithelial cells were determined by wound healing assay and Transwell migration and invasion assays
respectively. In contrast with control group, the proliferation of adenocarcinomic human alveolar basal
epithelial cells treated with different concentrations of Astragalus polysaccharide for 24, 48 and 72 h was
remarkably inhibited in a dose and time dependent manner under the same drug concentration, longer
the action time, higher the proliferation inhibition rate of adenocarcinomic human alveolar basal epithelial
cells; under the same action time, higher the drug concentration, higher the proliferation inhibition
rate of adenocarcinomic human alveolar basal epithelial cells. The number of migrating cells dropped
significantly in Astragalus polysaccharide groups (p<0.05), which was more obvious with the increase of
Astragalus polysaccharide concentration (p<0.05). Astragalus polysaccharide can dramatically inhibit the
proliferation of lung cancer adenocarcinomic human alveolar basal epithelial cells in a concentration and
time-dependent manner and also effectively suppress their migration and invasion. The mechanism may
be related to its ability to up-regulate the protein expressions of Src homology region 2 containing protein
tyrosine phosphatase 2 and suppressor of cytokine signaling 3 and inhibit the over-activation of the Janus
kinase/signal transducer and activator of transcription signaling pathway in lung cancer adenocarcinomic
human alveolar basal epithelial cells.


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