The present study was conducted in order to investigate the inhibitory effects of ginsenoside Rg3 combined with chemotherapy on Eca-109 esophageal squamous cell carcinoma (ESCC) in mice. Tumor xenograft models were established in the right forelimb of 20 BALB/c nude mice by subcutaneous injection. The tumor-bearing mice were randomly assigned to 4 treatment groups (n=5 per group) as follows: the control group (saline), the ginsenoside Rg3 alone group (6 mg/kg/day, once a day for 3 weeks), the chemotherapy alone group (paclitaxel 10 mg/kg/day + cisplatin 5 mg/kg/day on days 1, 7, 14 and 21) and the chemotherapy + Rg3 group (combined treatment). The length and width of the tumor were directly measured with calipers at different time points and the tumor volume (cm) was calculated using the formula 0.52 × length × width every other day. The mice were sacrificed by cervical dislocation following completion of therapy, the tumors were removed and weighed and the expression levels of Ki-67 were determined by immunohistochemistry. The results indicated that the coadministration of ginsenoside Rg3 significantly enhanced the inhibitory effects of chemotherapy on tumor growth. In addition, the expression levels of Ki-67 in the chemotherapy + Rg3 group were significantly lower compared to those in the other 3 groups. The chemotherapy + Rg3 group also exhibited the lowest microvascular density among all four groups. These findings suggested that ginsenoside Rg3 may improve the antitumor efficacy of chemotherapy in Eca-109 ESCC in mice.
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http://dx.doi.org/10.3892/mco.2014.355 | DOI Listing |
This study investigates the synergistic inhibitory effects of combining the stimulator of interferon genes (STING) agonist cyclic diadenylate monophosphate (c-di-AMP) and ginsenoside RG3 on cisplatin (DDP)-resistant gastric cancer (GC) cells. The objective is to identify novel therapeutic targets and offers insights for the clinical management of DDP resistance. Various techniques were employed, including western blot, MTT assay, colony formation assay, scratch assay, transwell assay, tubule formation assay, flow cytometry, Hoechst 33342 fluorescence staining, and in vivo experiments, to investigate the potential mechanisms and effects of the combined application of the STING agonist and ginsenoside RG3 in reversing cisplatin resistance in gastric cancer.
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Department of Orthopedics, Shenzhen Third People's Hospital, Shenzhen, China.
Osteoporosis is mainly caused by an imbalance in osteoclast and osteoblast regulation, resulting in an imbalance in bone homeostasis. Ginsenoside Rg3 (Rg3) has been reported to have a therapeutic effect on alleviating osteoporosis. Nonetheless, the underlying mechanisms have not been completely elucidated.
View Article and Find Full Text PDFCurr Med Chem
January 2025
Department of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah, 21589, Saudi Arabia.
Cancer is one of the most devastating illnesses in the world, impacting millions of individuals every year. Despite various therapies, the final effect is unsatisfactory. Chemotherapy currently dominates as the primary option of treatment.
View Article and Find Full Text PDFMetabol Open
December 2024
Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 75 Mikras Asias, Goudi, 11527, Athens, Greece.
Pharm Dev Technol
January 2025
Department of Pharmacy, Changchun University of Chinese Medicine, Changchun, China.
The formation of inclusion complexes between Ginsenoside Rg3 and cyclodextrins represents a promising strategy to enhance the solubility of G-Rg3. Nevertheless, the molecular mechanisms underlying the interaction between G-Rg3 and cyclodextrins have yet to be fully elucidated. In this study, we employed a combination of molecular simulation and experimental methodologies to identify the most effective solubilizing carriers among G-Rg3, β-cyclodextrin (β-CD), 2-hydroxypropyl-β-cyclodextrin (HP-β-CD), and 2,6-dimethyl-β-cyclodextrin (DM-β-CD).
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