Cancer incidence rate has been increasing drastically in recent years. One of the many cancer treatment methods is chemotherapy. Traditional medicine, in the form of complementary and alternative therapy, is actively used to treat cancer, and many herbs and active ingredients of such therapies are being intensely studied to integrate them into modern medicine. Ginseng is traditionally used as a nourishing tonic and for treating various diseases in Asian countries. The therapeutic potential of ginseng in modern medicine has been studied extensively; the main bioactive component of ginseng is ginsenosides, which have gathered attention, particularly for their prospects in the treatment of fatal diseases such as cancer. Ginsenosides displayed their anticancer and antimetastatic properties not only via restricting cancer cell proliferation, viability, invasion, and migration but also by promoting apoptosis, cell cycle arrest, and autophagy in several cancers, such as breast, brain, liver, gastric, and lung cancer. Additionally, ginsenosides can work synergistically with already existing cancer therapies. Thus, ginsenosides may be used alone or in combination with other pharmaceutical agents in new therapeutic strategies for cancer. To date however, there is little systematic summary available for the anticancer effects and therapeutic potential of ginsenosides. Therefore, we have reviewed and discussed all available literature in order to facilitate further research of ginsenosides in this manuscript.

A number of diverse studies have reported the anticancer properties of Cnidium officinale Makino (CO). However, the apoptotic effect of this traditional medicinal herb in human hepatocellular carcinoma cells (HepG2) remains to be elucidated. Therefore, the present study investigated the ability of CO to reduce cell viability through apoptotic pathways. Cell viability was determined using the 2,3‑bis [2-methyloxy-4-nitro-5-sulfophenyl]‑2H‑tetrazolium‑5‑carboxanilide assay. CO extract‑induced apoptosis in HepG2 cells was assessed by Hoechst 33258 staining. The cell cycle was monitored using fluorescence‑activated cell sorting analysis with propidium iodide staining. Furthermore, the present study explored whether various signaling molecules associated with HepG2 cell death were affected by CO treatment, including caspase‑3, B‑cell lymphoma 2 (Bcl-2), tumor protein p53 (p53), cyclin‑dependent kinase 4 (CDK4) and cyclin D. The expression levels of these genes were examined by reverse‑transcription polymerase chain reaction and western blotting. The expression levels of caspase‑3 and p53 were upregulated with CO extract treatment, whereas those of Bcl‑2, CDK4 and cyclin D were significantly downregulated. Cleaved caspase‑3 expression was upregulated following treatment with CO extract in a dose‑dependent manner. Collectively, the data suggest that CO extract has the potential to induce apoptosis of HepG2 cells and may act by suppressing the cell cycle, which leads to caspase‑3 cleavage and p53 signaling.

Microbiota in the digestive tract has become an interesting topic for researchers in recent years. The profile of chicken digestive tract microbiota and its relationship with health and production efficiency have become basic data for modulating the diversity and abundance of the digestive tract microbiota. This article reviews the techniques used to analyze the diversity, role, and function of the gastrointestinal microbiota and the mechanisms by which they are modulated. The gut microbiota plays an important role in animal production, especially during feed digestion and animal health, because it interacts with the host against pathogens. Feed modulation can be a strategy to modulate gut composition and diversity to increase production efficiency by improving growth conditions. Keywords: feed additive, metagenome, phytogenic, poultry production, prebiotic, probiotic.

Anti-metastatic Potential of Ethanol Extract of Saussurea involucrata against Hepatic Cancer in vitro Saussurea involucrata;liver cancer;metastasis;MMP-2;MMP-9;TIMP-1; The rates of morbidity and mortality of hepatocellular carcinoma (HCC) have not lessened because of difficulty in treating tumor metastasis. Mongolian Saussurea involucrata (SIE) possesses various anticancer activities, including apoptosis and cell cycle arrest. However, detailed effects and molecular mechanisms of SIE on metastasis are unclear. Thus, the present study was undertaken to investigate antimetastatic effects on HCC cells as well as possible mechanisms. Effects of SIE on the growth, adhesion, migration, aggregation and invasion of the SK-Hep1 human HCC cell line were investigated. SIE inhibited cell growth of metastatic cells in dose- and time-dependent manners. Incubation of SK-Hep1 cells with $200-400{\mu}g/mL$ of SIE significantly inhibited cell adhesion to gelatin-coated substrate. In the migration (wound healing) and aggregation assays, SIE treated cells showed lower levels than untreated cells. Invasion assays revealed that SIE treatment inhibited cell invasion capacity of HCC cells substantially. Quantitative real time PCR showed inhibitory effects of SIE on MMP-2/-9 and MT1-MMP mRNA levels, and stimulatory effects on TIMP-1, an inhibitor of MMPs. The present study not only demonstrated that invasion and motility of cancer cells were inhibited by SIE, but also indicated that such effects were likely associated with the decrease in MMP-2/-9 expression of SK-Hep1 cells. From these results, it was suggested that SIE could be used as potential anti-tumor agent.

Although various treatments have been used for weight loss to date, obese people rarely have safe and effective treatment options. Therefore, the antiobesity effects of several natural compounds are being actively investigated. This study was conducted to investigate the antiadipogenic effects of Monascus ruber-fermented Fagopyrum esculentum (red yeast buckwheat, RYB) in 3T3-L1 cells. We assessed the intracellular lipid content and adipocyte differentiation by oil red O staining and the expression of genes and proteins associated with adipocyte differentiation by reverse transcription–polymerase chain reaction and western blotting in 3T3-L1 cells. RYB dose dependently inhibited 3T3-L1 cell differentiation at concentrations of 50–800 μg/mL, without cytotoxic effects. It also suppressed the expression of adipogenic transcription factors, including peroxisome proliferator-activated receptor γ and CCAAT/enhancer-binding protein α, and adipocyte-specific genes, such as adipocyte fatty acid—binding protein (aP2), fatty acid synthase, and leptin, during preadipocyte differentiation into adipocytes. Furthermore, RYB reduced cyclin-dependent kinase 2 and cyclin expression and increased p21 and p27 expression, thus causing cell cycle arrest at the G1/S phase. Collectively, these results suggest that RYB may be an effective nutraceutical for weight loss as indicated by its ability to suppress adipogenesis-specific gene expression and cause cell cycle arrest at the G1/S interphase.

Adipose tissue development and function play a critical role in the regulation of energy balance, lipid metabolism, and the pathophysiology of metabolic syndromes. Although the effect of zinc ascorbate supplementation in diabetes or glycemic control is known in humans, the underlying mechanism is not well described. Here, we investigated the effect of a zinc-chelated vitamin C (ZnC) compound on the adipogenic differentiation of 3T3-L1 preadipocytes. Treatment with ZnC for 8 d significantly promoted adipogenesis, which was characterized by increased glycerol-3-phosphate dehydrogenase activity and intracellular lipid accumulation in 3T3-L1 cells. Meanwhile, ZnC induced a pronounced up-regulation of the expression of glucose transporter type 4 (GLUT4) and the adipocyte-specific gene adipocyte protein 2 (aP2). Analysis of mRNA and protein levels further showed that ZnC increased the sequential expression of peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα), the key transcription factors of adipogenesis. These results indicate that ZnC could promote adipogenesis through PPARγ and C/EBPα, which act synergistically for the expression of aP2 and GLUT4, leading to the generation of insulin-responsive adipocytes and can thereby be useful as a novel therapeutic agent for the management of diabetes and related metabolic disorders.