Essential oils are generally not only antibiotic and anticarcinogenic, 1,2) but also have a sedative effect on stress. It has been shown that these essential oils contain ketone, terpene, and phenolic ether for sedation.3) Although essential oils have been regarded as useful sedatives, 4) there is little information on the antimicrobial or antifungal activities of essential oils extracted from coniferous trees. Essential oils with antimicrobial properties from medicinal as well as other edible plants have been recognized since antiquity.2) In addition, essential oils are used as food flavoring agents, and have a broad spectrum of in vitro antimicrobial activities attributed to the high content of phenolic derivatives. 5) More recently, plant extracts have been developed and proposed for use in foods as natural antioxidants. 6) In the present study, we investigated the antimicrobial and antifungal activities of several essential oils extracted from the coniferous trees Pinus densiflora, Pinus koraiensis, and Chamaecyparis obtusa against bacteria and fungi that commonly cause foot rot and other diseases. The essential oils were quantified using gas chromatography (GC) and identified in gas chromatography-mass spectrometric (GC-MS) analysis. In addition, the antibacterial effects against grampositive and gram-negative bacteria and antifungal effects against fungi were assayed using essential oils distilled from the needles of coniferous trees. MATERIALS AND METHODS Essential Oil ExtractionThe needles of the Japanese red pine (P. densiflora), Korean pine (P. koraiensis), and Japanese cypress (C. obtusa) were collected at the Reforestation Experiment Site of Chungbu Forest Experiment Station, Gyeonggi province, Korea. The essential oil from freshly cut needles of each species was obtained by steam distillation using a manufactured apparatus with a condenser. Distillation continued for 2-3 h at 100°C, and the volatile compounds containing the water-soluble fraction were allowed to settle for 20 min. The essential oil layer was separated and finally purified through a microfiltering and dehydration process.Measurement of Refractive Index The refractive index of chemical compounds is considered important because it indicates characteristic physical properties. We determined the index of the oils using an Abbe refractometer equipped with a sodium lamp (Bausch & Lomb, GD8804, U.S.A.).Quantification and Identification Each essential oil compound was quantified using a gas chromatograph (GC, Shimadzu GC-14A, Japan) equipped with a Shimadzu CPB-20 capillary column (0.2 mm inner diameterϫ50 m length). First, the calibration curves for several standard essential oils were obtained, and the calibration equation of each compound was used for quantification. GC analysis was carried out using helium carrier gas with an FID detector, and the injection and detection temperatures were 150 and 200°C, respectively. The oven temperature was increased from 50 to 200°C at intervals of 2°C/min over 75 min. Some other essential oils were id...
To investigate the role of FSH in ovarian cancer development, the present study examined the expression of FSH receptor (FSH-R) and the effect of FSH on proliferation of normal, preneoplastic, and neoplastic ovarian surface epithelium (OSE) cells. Recently, immortalized OSE (IOSE) cell lines, including IOSE-29 (preneoplastic) and IOSE-29EC (neoplastic), were used. Our results indicated that FSH-R mRNA was expressed and that FSH exerted a growth stimulatory effect in normal, preneoplastic, and neoplastic OSE cells. To investigate the mechanism of the growth stimulatory effect, the activation of MAPKs by FSH was examined in preneoplastic and neoplastic OSE cells. Treatment with FSH resulted in MAPK activation of IOSE-29 and IOSE-29EC cells, whereas the stimulatory effect of FSH on cellular proliferation and MAPK activation was completely abolished in the presence of PD98059, a MAPK kinase inhibitor, suggesting that the growth stimulatory effect of FSH is mediated through MAPK activation in these OSE cells. In a time-dependent study, FSH significantly increased MAPK activity at 5-10 min in IOSE-29 cells. The activated MAPK declined to the control level after 20 min in these cells. Similarly, treatment with FSH significantly induced MAPK activation after 5 min and sustained it for 60 min in IOSE-29EC cells. In addition, treatment with FSH resulted in substantial phosphorylation of Elk-1, confirming that FSH action is mediated via activation of MAPK. In conclusion, we have demonstrated that FSH-R was expressed, and FSH induced growth stimulation in normal, preneoplastic, and neoplastic OSE cells. Furthermore, treatment with FSH stimulated activation of the MAPK cascade and phosphorylated Elk-1 in neoplastic OSE cells. These results suggest that the MAPK cascade may be involved in cellular functions such as growth stimulation in response to FSH in preneoplastic and neoplastic OSE cells.
Endometriosis is a disease in which tissue that normally grows inside the uterus grows outside the uterus and causes chronic pelvic pain and infertility. However, the exact mechanisms of the pathogenesis of endometriosis-associated infertility are unknown. Epigenetic dysregulation has recently been implicated in infertility. Here, we report a reduction of histone deacetylase 3 (HDAC3) protein amounts in eutopic endometrium of infertile women with endometriosis compared to a control group. To investigate the effect of HDAC3 loss in the uterus, we generated mice with conditional ablation of Hdac3 in progesterone receptor (PGR)-positive cells (Pgrcre/+Hdac3f/f; Hdac3d/d). Loss of Hdac3 in the uterus of mice results in infertility due to implantation failure and decidualization defect. Expression microarray and ChlP-seq analyses identified COL1A1 and COL1A2 as direct targets of HDAC3 in both mice and humans. Reduction of HDAC3 abrogated decidualization in a primary culture of human endometrial stromal cells (hESCs) similar to that observed in infertile patients with endometriosis. Whereas attenuation of HDAC3 resulted in p300 recruitment to Col1a1 and Col1a2 genes in the uterus of mice as well as hESCs, inhibition of p300 permitted hESCs to undergo decidualization. Collectively, we found attenuation of HDAC3 and overexpression of collagen type I in the eutopic endometrium of infertile patients with endometriosis. HDAC3 loss caused a defect of decidualization through the aberrant transcriptional activation of Col1a1 and Col1a2 genes in mice and COL1A1 and COL1A2 genes in humans. Our results suggest that HDAC3 is critical for endometrial receptivity and decidualization.
The inhibition of p53 activity by histone deacetylase 3 (HDAC3) has been reported, but the precise molecular mechanism is unknown. Here we show that programmed cell death 5 (PDCD5) selectively mediates HDAC3 dissociation from p53, which induces HDAC3 cleavage and ubiquitin-dependent proteasomal degradation. Casein kinase 2 alpha phosphorylates PDCD5 at Ser-119 to enhance its stability and importin 13-mediated nuclear translocation of PDCD5. Genetic deletion of PDCD5 abrogates etoposide (ET)-induced p53 stabilization and HDAC3 cleavage, indicating an essential role of PDCD5 in p53 activation. Restoration of PDCD5WT in PDCD5−/− MEFs restores ET-induced HDAC3 cleavage. Reduction of both PDCD5 and p53, but not reduction of either protein alone, significantly enhances in vivo tumorigenicity of AGS gastric cancer cells and correlates with poor prognosis in gastric cancer patients. Our results define a mechanism for p53 activation via PDCD5-dependent HDAC3 decay under genotoxic stress conditions.
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