Poria cocos is a well-known traditional Chinese traditional medicine (TCM) that grows around roots of pine trees in China, Korea, Japan, and North America. Poria cocos has been used in Asian countries to treat insomnia as either a single herb or part of an herbal formula. In a previous experiment, pachymic acid (PA), an active constituent of Poria cocos ethanol extract (PCE), increased pentobarbital-induced sleeping behaviors. The aim of this experiment was to evaluate whether or not PCE and PA modulate sleep architectures in rats as well as whether or not their effects are mediated through GABAA-ergic transmission. PCE and PA were orally administered to individual rats 7 days after surgical implantation of a transmitter, and sleep architectures were recorded by Telemetric Cortical encephalogram (EEG) upon oral administration of test drugs. PCE and PA increased total sleep time and non-rapid eye movement (NREM) sleep as well as reduced numbers of sleep/wake cycles recorded by EEG. Furthermore, PCE increased intracellular chloride levels, GAD65/67 protein levels, and α-, β-, and γ-subunits of GABAA receptors in primary cultured hypothalamic neuronal cells. These data suggest that PCE modulates sleep architectures via activation of GABAA-ergic systems. Further, as PA is an active component of PCE, they may have the same pharmacological effects.

This study was conducted in order to investigate the reduction activity of red ginseng extract (RGE; Panax ginseng, C. A. Meyer) on hydroxyl radical (·OH) using an electron spin resonance (ESR) spectrometer and spin-trapping techniques. ·OH generated by a Fenton Reaction System was trapped by 5, 5-dimethyl-l-pyrroline-N oxide (DMPO). The decay rate showed approximately pseudo-firs order kinetics over the period of measurement (by 10 min), and the half lifetime of the DMPO/·OH signal was estimated as approximately 8.15 min. However, the half lifetime of RGE/·OH was estimated as approximately 7.5 min, and the half lifetime of RGE was higher than that of DMPO/·OH adduct only. The order of reduction activities was ascorbic acid > N, Nʹ-dimethylthiourea (DMTU) > RGE > trolox > mannitol in the Fenton Reaction System. Thus, these observations indicate that RGE reaction with ·OH has relative reduction activity. The second-order rate constant of RGE/·OH may be 3.5~4.5 × 109 M-¹ ∙ S-¹.

The anti-inflammatory effect of PHBV/Collagen (PHCP) was examined in a mouse model of lipopolysaccharide (LPS)-induced skin inflammation. Vascular permeability on the back skin was measured by the local accumulation of Evan’s blue dye after subcutaneous injection of LPS (30 µg site^-1 ). Dye leakage in the skin showed a significant increase at 2 h after injection of LPS. This LPS-induced dye leakage was also completely inhibited by HO-1 inhibitor, ZnPP, and antioxidants, including methyl gallate, trolox, and mannitol. To study the possible mechanisms underlying the in vivo anti-inflammatory effect of PHCP against LPS-induced inflammation, we also examined the effects of PHCP on malondialdehyde (MDA) and glutathione levels in skin tissues and found that pretreatment with PHCP resulted in inhibited MDA elevation and a remarkable reduction of glutathione level. In addition, similar results were obtained after pretreatment with antioxidants, including trolox and mannitol, and HO-1 inhibitor, ZnPP. Histopathologically, an influx of neutrophils into the skin dermis was detected between 24 h and 72 h after LPS injection (30, 100 µg site^-1), compared to control animals after injection of saline. This increase was greater in mice treated with 100 µg of LPS than in those treated with 30 µg of LPS and was significantly suppressed by pretreatment with PHCP, antioxidants, and HO-1 inhibitor. These results collectively suggest that PHCP has an anti-inflammatory effect against LPS-induced inflammation model in vivo and may be a good candidate for the skin tissue engineering biomedical application primarily through manipulation of the redox state.

The objective of this study was to determine the effect of macrophages on growth of human colon cancer cells. The results showed that co-culture of colon cancer cells with macrophages inhibited the growth of colon cancer cells (HCT116 and SW620) depending on the number of macrophages, RAW 264.7 cells, and activated THP-1 cells accompanied by down regulation of pSTAT3 in cancer cells. We also found that expression and release of cancer cell growth inhibitory cytokines, IL-1 receptor antagonist (IL-1ra) and IL-10, was increased in macrophages. Blocking of the STAT3 pathway with specific inhibitor and siRNA of STAT3 abolished the growth of colon cancer cells and expression of IL-1ra and IL-10. In addition, neutralization of IL-1ra and IL-10 with antibodies resulted in reversal of macrophage-induced inhibition of cancer cell growth. These data showed that IL-1ra and IL-10 released from macrophages inhibit growth of colon cancer cells through inhibition of the STAT3 pathway.

In this study, a nanofibrous scaffold was obtained by co-electrospinning poly (3-hydroxybutyrate- co-3-hydroxyvalerate) (PHBV) and collagen in 2,2,2-trifluoroethanol at a ratio of 3/7. The fiber diameters were in the range of 250-600 nm. It was found that PHBV/Collagen (PHCP) nanofibrous scaffold showed greater proliferation than the PHBV nanofibrous scaffold induced by oxidant in NIH3T3 cells. Otherwise, in the early-stage wound-healing mouse model, wound closure was evaluated according to wound size reduction and histology of regenerated skin on the backs of mice. Each of the tissues removed on day 0, 3, 6, 9, 12, 15, and 18 was used for analysis of biochemical and pathological changes. None of the nanofiber-attached mice showed significant difference on the third day, however, from the third day until the ninth day, significantly faster healing was observed in PHCP-attached mice, compared to control wounds in epithelialization, wound contraction, and histopathological examinations. These results strongly support the beneficial effects of biomedical application of PHCP nanofiber in acceleration of the initial phase of wound healing through α-SM actin contraction.

In vivo redox reaction is involved in the processes of oxidative diseases. Thus, direct and non-invasive measurement of in vivo free radical reactions in living animals should be essential to understanding the roles of free radicals in pathophysiological phenomena. Electron spin resonance (ESR) technique has been utilized in analysis of free radicals, which are generated through imbalance of in vivo redox status. In vivo ESR/spin probe technique using nitroxide radicals as spin probes was developed for estimation of in vivo free radical reactions in whole living animals. This technique using a probe may become a powerful tool for use in clarifying mechanisms of disease and in monitoring pharmaceutical therapy. The application of ESR was introduced and discussed in this article.

Chronic inflammatory diseases such as Crohn′s disease and ulcerative colitis are associated with increased risk of colon adenocarcinoma. Apoptic induction of colon cancer cells by cytokines and death receptors is an important anti-cancer therapy. We observed that co-administration of TNFα and IFNγ in human colon cancer cell line, HCT116, resulted in cell death and expression of IL-32. Cleavage forms of caspase-3, caspase-9, and PARP were increased in TNFα / IFNγ-treated HCT116. mRNA expression of death receptors, including TNFR1 and Fas were not changed and NO generation was not induced by combination of TNFα and IFNγ. However, mRNA expression of IL-32α, β, and γ was increased in TNFα / IFNγ-treated HCT116. To determine the effect of IL-32 in HCT116 cell apoptosis by TNFα / IFNγ stimulation, IL-32 siRNA-transfected HCT116 cells were cultured with TNFα / IFNγ and cell proliferation was measured. IL-32 siRNA induced slight recovery of cell viability of TNFα / IFNγ-stimulated HCT116. These results suggest that IL-32 is not directly related to apoptosis of HCT116 by TNFα / IFNγ stimulation. However, IL-32 expression by TNFα or TNFα / IFNγ in a colon cancer cell line is very interesting because of the unknown effect of IL-32 in colon cancer. Our study will contribute to development of studies for IL-32 function in human colon cancer and anti-cancer therapies using cytokines.

Flavonoids are a large family of polyphenolic compounds synthesized by plants that have a common chemical structure. Flavonoids may be further divided into subclasses, Anthocyanidins, Flavan-3- ols, Flavanones, Flavonols, Flavones, Isoflavones. Flavonoids have antioxidant and antiradical activities. The antiradical efficacy of flavonoids have established structure-activity relationships (SAR) of the antioxidant activity. Reactivity of flavonoids is highly dependent on the configuration of OH groups on the flavonoid B and C rings, there being little contribution from A ring to antioxidant effectiveness. This short article presents the current knowledge on structural aspects on their free radical reactions of flavonoids.

We tested the effects of roasted and non-roasted Zizyphi Spinosi Semen (ZSS) hot water extracts on pentobarbital-induced sleeping behavior, pentylentetrazole-induced convulsions, and locomotor activity in mice. Both ZSS extracts decreased locomotor activity and pentylentetrazole-induced convulsions. Both extracts alos dose-dependently shortened the sleep onset and prolonged the sleep time induced by pentobarbital, with roasted extract being more potent. In addition, chemical constituents in HPLC also were different. Thus, both roasted and non-roasted ZSS extracts potentiate the sleep onset and the sleeping time induced by pentobarbital, decrease locomotor activity, and reduce pentylentetrazole-induced convulsions, with roasting improving extract potency.