Ginseng is a natural product best known for its curative properties in diverse physiological processes such as cancer, neurodegenerative disorders, hypertension, and maintenance of hemostasis in the immune system. In previous decades, there have been some promising studies into the pharmacology and chemistry of ginseng components and the relationship between their structure and function. The emerging use of modified ginseng and development of new compounds from ginseng for clinical studies have been topics of study for many researchers. The present review deals with the anticancer, anti-inflammatory, antioxidant, and chemopreventive effects, and recent advances in microRNA technology related to red ginseng. The review also summarizes the current knowledge on the effect of ginsenosides in the treatment of cancer.

Gamma ray-induced in vitro mutagenesis and selection for salt (NaCl) tolerance were investigated in sugarcane (Saccharum officinarum L.). Embryogenic callus cultures were irradiated (10 to 80Gy) and subjected to in vitro selection by exposure of irradiated callus to NaCl (0, 50, 100, 150, 200, and 250mmolL−1). Increasing NaCl concentrations resulted in growth reduction and increased membrane damage. Salt-selected callus lines were characterized by the accumulation of proline, glycine betaine, and Na+ and K+ concentration. Higher accumulation of proline and glycine betaine was observed in NaCl stressed callus irradiated at 20Gy. Na+ concentration increased and K+ concentration decreased with increasing salt level. Irradiated callus showed 50–60% regeneration under NaCl stress, and in vitro-regenerated plants were acclimatized in the greenhouse, with 80–85% survival. A total of 138 irradiated and salt-selected selections were grown to maturity and their agronomic performance was evaluated under normal and saline conditions. Of these, 18 mutant clones were characterized for different agro-morphological characters and some of the mutant clones exhibited improved sugar yield with increased Brix%, number of millable canes, and yield. The result suggest that radiation-induced mutagenesis offers an effective way to enhance genetic variation in sugarcane

Toll-like receptor 4 (TLR4) signaling is an important therapeutic target to manage lipopolysaccharide (LPS)-induced inflammation. The transcription factor signal transducer and activator of transcription 3 (STAT3) has been identified as an important regulator of various immune-related diseases and has generated interest as a therapeutic target. Here, we investigated the time-dependent roles of STAT3 in LPS-stimulated RAW264.7 macrophages. STAT3 inhibition induced expression of the pro-inflammatory genes iNOS and COX-2 at early time points. STAT3 depletion resulted in regulation of nuclear translocation of nuclear factor (NF)-κB subunits p50 and p65 and IκBα/Akt/PI3K signaling. Moreover, we found that one Src family kinase, Lyn kinase, was phosphorylated in STAT3 knockout macrophages. In addition to using pharmacological inhibition of NF-κB, we found out that STAT3KO activation of NF-κB subunit p50 and p65 and expression of iNOS was significantly inhibited; furthermore, Akt tyrosine kinase inhibitors also inhibited iNOS and COX-2 gene expression during early time points of LPS stimulation, demonstrating an NF-κB- Akt-dependent mechanism. On the other hand, iNOS expression was downregulated after prolonged treatment with LPS. Activation of NF-κB signaling was also suppressed, and consequently, nitric oxide (NO) production and cell invasion were repressed. Overall, our data indicate that STAT3 differentially regulates early- and late-phase TLR4-mediated inflammatory responses.

Epigenetic regulation and modification govern the transcriptional mechanisms that promote disease initiation and progression, but can also control the oncogenic processes, cell signaling networks, immunogenicity, and immune cells involved in anti-inflammatory and anti-tumor responses. The study of epigenetic mechanisms could have important implications for the development of potential anti-inflammatory treatments and anti-cancer immunotherapies. In this review, we have described the key role of epigenetic progression: DNA methylation, histone methylation or modification, and protein methylation, with an emphasis on the activator protein-1 (AP-1) signaling pathway. Transcription factor AP-1 regulates multiple genes and is involved in diverse cellular processes, including survival, differentiation, apoptosis, and development. Here, the AP-1 regulatory mechanism by DNA, histone, or protein methylation was also reviewed. Various methyltransferases activate or suppress AP-1 activities in diverse ways. We summarize the current studies on epigenetic alterations, which regulate AP-1 signaling during inflammation, cancer, and autoimmune diseases, and discuss the epigenetic mechanisms involved in the regulation of AP-1 signaling.

Protium javanicum Burm. f. is a medicinal plant used in traditional medicine. Gum and oleoresins from this plant have been used as anti-inflammatory agents for treating ulcers, headaches, eyelid inflammation, and rheumatic pain. However, its anti-inflammatory mechanism of action is still unknown. To better understand the mechanism, we used lipopolysaccharide- (LPS-) treated RAW264.7 cells to measure inflammatory mediators with the Griess assay and to identify target signaling molecules by immunoblot analysis. In this study, we report that the Protium javanicum methanol extract (Pj-ME) plays an important role in suppressing nitric oxide (NO) levels without cytotoxicity. The effect of Pj-ME in LPS-induced expression leads to reduced inflammatory cytokine expression, specifically inducible nitric oxide synthase (iNOS), cyclooxygenase (COX-2), and tumor necrosis factor (TNF-α). Pj-ME significantly inhibited LPS-induced protein expression of the nuclear factor-kappa B (NF-κB) signaling pathway in a time-dependent manner. Syk and Src were identified as putative signaling molecules of Pj-ME-mediated anti-inflammatory activity, which were inhibited by Pj-ME. We demonstrated that Pj-ME controls the STAT3 signaling pathway by suppressing STAT3 and JAK phosphorylation and also downregulates the gene expression of IL-6. Therefore, these results elucidate Pj-ME as a novel anti-inflammatory naturally derived drug with anti-inflammatory and antioxidant properties which may be subject to therapeutic and prognostic relevance.