Fabrication of Biogenic Silica Nanostructures from Sorghum bicolor Leaves for Food Industry Applications

Silicon - Due to the large production of sorghum, the generation of associated agricultural residues, which contain high contents of silica, is inevitable. Also, these agricultural residues are not...     

Ononitol Monohydrate—A Glycoside Potentially Inhibit HT-115 Human Colorectal Cancer Cell Proliferation through COX-2/PGE-2 Inflammatory Axis Regulations

We aimed to inhibit HT-115 human colorectal cancer cell proliferation using ononitol monohydrate (OMH), a bioactive principle isolated from Cassia tora (L.). The cytotoxicity of OMH has been assayed using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide), cell and nuclear morphology, and apoptosis mechanisms have been analyzed using real-time PCR. Higher doses of OMH potentially inhibit 84% of HT-115 cell viability; we observed that the IC₅₀ level was 3.2 µM in 24 h and 1.5 µM in 48 h. The treatment with 3.2 µM of OMH for 48 h characteristically showed 64% apoptotic cells and 3% necrotic cells, confirmed by propidium iodide and acridine orange/ethidium bromide (AO/ErBr) staining. We found the overexpression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE-2) in the control HT-115 cells, which was directly associated with colorectal tumorigenesis. However, 3.2 µM of OMH treatment to HT-115 cells for 48 h significantly reduced inflammatory genes, such as TNF-α/IL-1β and COX-2/PGE-2. The downregulation of COX-2 and PGE-2 was more significant with the 3.2 µM dose when compared to the 1.5 µM dose of OMH. Additionally, the protein levels of COX-2 and PGE-2 were decreased in the 3.2 µM OMH-treated cells compared to the control. We found significantly (p ≤ 0.01) increased mRNA expression levels of tumor-suppressor genes, such as pRb2, Cdkn1a, p53, and caspase-3, and decreased Bcl-2, mdm2, and PCNA after 48 h was confirmed with apoptotic stimulation. In conclusion, the antiproliferative effect of OMH via the early suppression of protumorigenic inflammatory agents TNF-α/IL-1β, COX-2/PGE-2 expression, and the increased expression levels of tumor-suppressor genes Cdkn1a and pRb2, which enhanced the activation of Bax and p53.