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Centella asiatica Linn. (C. asiatica) extract has been shown to possess high antioxidant activity due to its phenols and flavonoids. This study tested the efficacy of 70%-ethanol (EtOH) crude extracts of C. asiatica and its fractions (H 2 O, EtOAc, CH 2 Cl 2 , and hexane) to modulate human follicle dermal papilla cells. In addition, we analyzed the extracts for major phytochemicals as well as free radical scavenging activity. Our results from ABTS and DPPH assays showed that the amounts of phenolic and flavonoid compounds in the extracts were both related to its free radical scavenging activity. While the EtOAc fraction of C. asiatica demonstrated the highest free radical scavenging activity, it was toxic to human follicle dermal papilla cells. The cell viability test was positive when cells were treated with EtOH crude extract and H 2 O fraction. VEGF gene expression, quantified by real-time PCR analysis of the EtOH crude extract, showed a significant level of induction, indicating that the growth promotion effect in human follicle dermal papilla cells was related to VEGF gene expression, which has a positive hair growth stimulating effect. The EtOH crude extract of C. asiatica may offer potential in hair growth promoting products.

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Conventional chemotherapeutic agents for colorectal cancer (CRC) cause systemic side effects and eventually become less efficacious owing to the development of drug resistance in cancer cells. Therefore, new therapeutic regimens have focused on the use of natural products. The anticancer activity of several parts of Calotropis gigantea has been reported; however, the effects of its stem bark extract on inhibition of cancer cell proliferation have not yet been examined. In this study, the anticancer activity of C. gigantea stem bark extract, both alone and in combination with 5-fluorouracil (5-FU), was evaluated. A crude ethanolic extract was prepared from dry, powdered C. gigantea barks using 95% ethanol. This was then partitioned to obtain dichloromethane (CGDCM), ethyl acetate, and water fractions. Quantitative analysis of the constituent secondary metabolites and calotropin was performed. These fractions exhibited cytotoxicity in HCT116 and HT-29 cells, with CGDCM showing the highest potency in both the cell lines. A combination of CGDCM and 5-FU significantly enhanced the cytotoxic effect. Moreover, the resistance of normal fibroblast, HFF-1, cells to this combination demonstrated its safety in normal cells. The combination significantly enhanced apoptosis through the mitochondria-dependent pathway. Additionally, the combination reduced adenosine triphosphate production and increased the production of reactive oxygen species, demonstrating the mechanisms involved in the induction of apoptosis. Our results suggest that CGDCM is a promising anti-cancer agent and may enhance apoptosis induction by 5-FU in the treatment of CRC, while minimizing toxicity toward healthy cells.

The de novo lipogenesis (DNL) pathway has been identified as a regulator of cancer progression and aggressiveness. Downregulation of key lipogenesis enzymes has been shown to activate apoptosis in cancerous cells. Epigallocatechin gallate (EGCG) inhibits cancer cell proliferation without causing cytotoxicity in healthy cells. The present study aimed to investigate the effects of EGCG on the promotion of apoptosis associated with the DNL pathway inhibition in cancer cells, both in vitro and in vivo. We observed that two colorectal cancer cell lines (HCT116 and HT‐29) had a higher cytotoxic response to EGCG treatment than hepatocellular carcinoma cells, including HepG2 and HuH‐7. EGCG treatment decreased cell viability and increased mitochondrial damage‐triggered apoptosis in both HCT116 and HT‐29 cancer cells. Additionally, we treated mice transplanted with HCT116 cells with 30 or 50 mg·kg−1 EGCG for 7 days to evaluate the apoptotic effects of EGCG treatment in a xenograft mouse model of cancer. We observed a decrease in intracellular fatty acid levels, which suggested that EGCG‐induced apoptosis was associated with a decrease in fatty acid levels in cancer. Suppression of ATP synthesis by EGCG indicated that cell death induction in cancer cells could be mediated by shared components of the DNL and energy metabolism pathways. In addition, EGCG‐induced apoptosis suppressed the expression of the phosphorylation protein kinase B and extracellular signal‐regulated kinase 1/2 signaling proteins in tumors from xenografted mice. Cytotoxic effects in unaffected organs and tissues of the mouse xenograft model were absent upon EGCG treatment.

The non-structural protein 1 (NS1) of avian influenza virus was defined as one of the virulent factors. To understand the effect of NS1 protein of influenza virus H5N1 isolated in Thailand on type I (α/β) interferon (IFN) synthesis, five reverse genetic viruses were constructed and used as models. The viruses were generated using NS genomic segment from A/Peurto Rico/8/1934 (H1N1) and four avian influenza viruses isolated from the first outbreak in Thailand. All the viruses have the rest of the genome from A/Peurto Rico/8/1934 (H1N1). The constructed viruses were named (1) NS1 PR8/34, (2) NS1 wild type, (3) NS1 L15FD53G, (4) NS1 N171I and (5) NS1 E71K, respectively. The type I (α/β) IFN gene expression in control and infected primary chicken embryonic fibroblast cells were analyzed by quantitative polymerase chain reaction. The results show that the inhibition of IFN-β gene expression by NS1 wild type infected cells is stronger than NS1 N171I, NS1 E71K, NS1 PR8/34 and NS1 L15FD53G, respectively. The data suggest that the difference of amino acid sequence of NS1 protein contributes to the IFN-β antagonist. In contrast, the difference of the NS1 protein does not influence in the IFN-α antagonistic activity.

Background: Resistance to chemotherapeutic agents is usually found in cancer stem cells (CSCs) and cancer stem-like cells that are often regarded as the target for cancer monitoring. However, the different patterns of their transcriptomic profiling is still unclear. Objective: This study aims to illustrate the transcriptomic profile of CSCs and butyrate-resistant colorectal carcinoma cells (BR-CRCs), by comparing them with parental colorectal cancer (CRC) cells in order to identify distinguishing transcription patterns of the CSCs and BR-CRCs. Methods: Parental CRC cells HCT116 (HCT116-PT) were cultured and induced to establish the butyrate resistant cell model (HCT116-BR). Commercial enriching of the HCT116-CSCs were grown in a tumorsphere suspension culture, which was followed firstly by the assessment of butyrate tolerance using MTT and PrestoBlue. Then their gene expression profiling was analyzed by microarray. Results: The results showed that both butyrate-resistant HCT116 cells (HCT116-BR) and HCT116-CSCs were more tolerant a butyrate effects than HCT116-PT cells. Differentially expressed gene profiles exhibited that IFI27 , FOXQ1 , PRF1 , and SLC2A3 genes were increasingly expressed in CSCs, and were dramatically overexpressed in HCT116-BR cells when compared with HCT116-PT cells. Moreover, PKIB and LOC399959 were downregulated both in HCT116-CSCs and HCT116-BR cells. Conclusion: Our findings shed light on the transcriptomic profiles of chemoresistant CRC cells. This data should be useful for further study to provide guidelines for clinical prognosis to determine the guidelines for CRC treatment, especially in patients with chemoresistance and designing novel anti-neoplastic agents.