ginsenoside-m1 and Carcinoma--Non-Small-Cell-Lung

Compound K [C-K; 20-

Topics: A549 Cells; AMP-Activated Protein Kinases; Antineoplastic Agents; Apoptosis; Autophagy; Carcinoma, Non-Small-Cell Lung; Cell Proliferation; Dose-Response Relationship, Drug; Drug Screening Assays, Antitumor; Ginsenosides; Humans; JNK Mitogen-Activated Protein Kinases; Lung Neoplasms; Molecular Conformation; Structure-Activity Relationship; TOR Serine-Threonine Kinases

This work aimed at preparing ginsenoside compound K (GCK)-loaded liposomes modified with TPGS (GCKT-liposomes) to enhance solubility and targeting capability of GCK, as well as inhibit the efflux of GCK from tumour cells.. GCKT-liposomes were prepared by the thin-film hydration method and characterized by particle size, polydispersity, zeta potential and drug encapsulation efficiency. A549 cells were used as antitumour cell model to access the cellular uptake of the GCK and perform its antitumour function. The enhancement of in vivo antitumour efficacy of GCKT-liposomes was evaluated by nude mice bearing tumour model.. The results showed that GCKT-liposomes achieved a comparatively high drug loading efficiency and reasonable particle size at the ratio of 7 : 3 (phospholipid: TPGS). The in vitro release demonstrated that the dissolution of GCK was remarkably improved by entrapping it into liposomes. In addition, GCKT-liposomes exhibited a great hypersensitizing effect on A549 cells, and the cellular uptake was enhanced. Compared with free GCK, the IC50 of GCKT-liposomes was significantly reduced (16.3 ± 0.8 vs 24.9 ± 1.0 μg/ml). In vivo antitumour assay also indicated that GCKT-liposomes achieved higher antitumour efficacy (67.5 ± 0.5 vs 40.8 ± 0.7%).. The novel GCKT-liposomes significantly improved the antitumour efficacy of GCK.

Topics: A549 Cells; Animals; Antineoplastic Agents, Phytogenic; Carcinoma, Non-Small-Cell Lung; Drug Carriers; Ginsenosides; Liposomes; Male; Mice, Nude; Panax; Phospholipids; Phytotherapy; Plant Extracts; Polyethylene Glycols; Vitamin E