Anti-proliferative activity of Ensete superbum Roxb. Cheesman extract and its active principles on human colorectal cancer cell lines.

Ensete superbum Roxb. Cheesman (wild banana) is a plant traditionally used for the treatment of fever and diarrhea. On a preliminary screening, the ripe peel aqueous extract (PA) exhibited higher cytotoxicity (cell viability of 49% against HCT-15 at 75 µg/ml; and 46% against Caco2 at 50 µg/ml), superior anti-inflammatory (IC50 of 0.49 µg/ml), and greater anti-mutagenic activity at 500 µg/plate compared to the aqueous extracts of seed (SA), flower (FA) and bract (BA). Therefore, we further evaluated the anti-proliferative activity of PA and its fractions. The ability to inhibit the growth of cell lines (HCT-15 and Caco2) was used for the bio-guided fractionation and isolation of active compounds in PA using chromatographic techniques. Multiple extractions of the PA yielded the peel dioxane fraction (PD), and column fractionation of PD yielded eight compounds, of which three (Compound D-PDD, Compound E-PDE, and Compound G-PDG) possessed higher cytotoxic activity. At 10 µg/ml, the cell viability of HCT-15 was 50.1%, 46.5%, and 61.9%, respectively; Caco2 was 98.2%, 62.9%, and 64.7%, respectively, for PDD, PDE, and PDG. These compounds also showed apoptotic effect as evidenced by measuring the mitochondrial membrane potential, dual staining (acridine orange/ethidium bromide), DNA fragmentation, and the ROS status in colorectal cell lines. The UPLC-HRMS/MS, FTIR, and NMR data revealed the active compounds as quercetin-3-O-rutinoside, 3,5-dimethoxy-4-hydroxybenzoic acid, and 4',5,7-trihydroxyflavone. These findings indicate the anti-proliferative potential of PA, and warrant further investigation of its active principles in the amelioration of colorectal cancer in in vivo models. PRACTICAL APPLICATION: The potential of an underutilized crop as a source of therapeutic agents for colon cancer was established, as the study showed a high cytotoxic activity of wild bananas against HCT-15 and Caco2 cell lines. Bioactivity guided fractionation of peel fraction identified the active compounds present in wild banana, and their anticancer activity was attributed to the induction of cell death. The study indicated that wild banana has the potential to inhibit the growth of colon cancer cells.

Overview of oral cavity squamous cell carcinoma: Risk factors, mechanisms, and diagnostics.

Oral cavity squamous cell carcinoma (OCSCC) is the most common malignancy of the oral cavity. The substantial risk factors for OCSCC are the consumption of tobacco products, alcohol, betel quid, areca nut, and genetic alteration. However, technological advancements have occurred in treatment, but the survival decreases with late diagnosis; therefore, new methods are continuously being investigated for treatment. In addition, the rate of secondary tumor formation is 3-7% yearly, which is incomparable to other malignancies and can lead to the disease reoccurrence. Oral cavity cancer (OCC) arises from genetic alterations, and a complete understanding of the molecular mechanism involved in OCC is essential to develop targeted treatments. This review aims to update the researcher on oral cavity cancer, risk factors, genetic alterations, molecular mechanism, classification, diagnostic approaches, and treatment.

Protective effects of phenolics rich extract of ginger against Aflatoxin B1-induced oxidative stress and hepatotoxicity.

Aflatoxin B1 (AFB1) is one of the predominant mycotoxin contaminant in food and feed, causing oxidative stress and hepatotoxicity. Ginger phenolics have been reported for its antioxidant potential and hepatoprotective activity. The present study investigated the protective effects of phenolics rich ginger extract (GE) against AFB1 induced oxidative stress and hepatotoxicity, in vitro and in vivo. The phenolic acid profiles of GE showed 6-gingerol and 6-shogaol as predominant components. Pretreatment of HepG2 cells with GE significantly inhibited the production of intracellular reactive oxygen species (ROS), DNA strand break, and cytotoxicity induced by AFB1. A comparable effect was observed in in vivo. Male Wistar rats were orally treated with GE (100 and 250mg/kg) daily, with the administration of AFB 1 (200µg/kg) every alternative day for 28days. Treatment with GE significantly reduced AFB1 induced toxicity on the serum markers of liver damage. In addition, GE also showed significant hepatoprotective effect by reducing the lipid peroxidation and by enhancing the antioxidant enzymes activities. These results combined with liver histopathological observations indicated that GE has potential protective effect against AFB1 induced hepatotoxicity. Additionally, administration of GE up-regulated Nrf2/HO-1 pathway, which further proved the efficiency of GE to inhibit AFB1 induced hepatotoxicity.