Network Pharmacologic Analysis of Dendrobium officinale Extract Inhibiting the Proliferation of Gastric Cancer Cells.

Globally, gastric cancer (GC) is one of the three most deadly cancers. Dendrobium officinale (D. officinale) is a traditional Chinese medicine (TCM), and its extract can significantly inhibit the proliferation of gastric cancer cells. However, there are no unified conclusions on its potential active components and possible mechanisms of action. This paper aims at exploring the potential active components, targets, and cell pathways of D. officinale extract in inhibiting the proliferation of gastric cancer cells by using network pharmacology and cytology experiments. In this paper, UPLC-MS/MS was used to identify the main chemical components in the extracts of D. officinale, and the an ADME model was used to screen the potential active components. Network pharmacology methods such as target prediction, pathway identification, and network construction were used to determine the mechanism through which the D. officinale extract inhibited gastric cancer cell proliferation. MTT assays, fluorescence confocal microscopy, clone formation, and flow cytometry were used to verify the inhibitory activity of the D. officinale extract on gastric cancer cell proliferation in vitro. The UPLC-MS/MS analysis identified 178 chemical components from the D. officinale extract. Network pharmacology analysis showed that 13 chemical components had the potential to inhibit the proliferation of gastric cancer cells, with the possible involvement of 119 targets and 20 potential signaling pathways. In vitro experiments confirmed that the D. officinale extract could significantly inhibit the proliferation of gastric cancer cells. Therefore, we believe that the D. officinale extract can inhibit the proliferation of gastric cancer cells through effects on multiple components, multiple targets, and multiple pathways.

Recombinant human growth hormone (rhGH) treatment of MKN-45 xenograft mice improves nutrition status and strengthens immune function without promoting tumor growth.

The aim of this study was to clarify the combined effects and dose-effect relationships of rhGH on tumor growth, nutrition status, and immune function in MKN-45 xenograft mice. In this study, animal models were induced in nude mice using the subcutaneous transplantation of MKN-45 cells, and rhGH was injected daily for 14 days. Three rhGH treatment dosages were set with reference to the equivalent dosage converted from human clinical dosage, including 2 IU (0.67 mg), 10 IU (3.35 mg) and 50 IU (16.75 mg) per kg body weight. The tumor volume, body weight and food intake were measured every two or three days. After 14 days of rhGH treatment, the tumors were isolated and weighed. The expression levels of Ki-67, vascular endothelial growth factor (VEGF) and CD31in tumor tissues were detected by immunohistochemistry (IHC). The protein expression levels of pJAK2, JAK2, pSTAT3, STAT3, pAKT, AKT, pERK and ERK were measured by western blotting. The percentage of active NK cells in peripheral blood mononuclear cells (PBMCs) was detected by fluorescence-activated cell sorting (FACS). The results showed that rhGH had improved the food intake, increased the body weight and strengthened the immune function of MKN-45 xenograft mice but had not promote tumor growth. MKN-45 xenograft mice treated with rhGH at a higher dosage gained more weight, while those treated with rhGH at a lower dosage showed stronger immune function and smaller tumor volume.