• Clinical and Experimental Reproductive Medicine
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• v.24 no.1
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• pp.35-42
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• 1997

The present study was designed to define the role of prostaglandin in the development and hatching of mouse embryo. The effects of indomethacin, an inhibitor of prostaglandin synthesis, on the development and hatching of morula and blastocyst were examined. In early morula stage, embryos were degenerated significantly at 100 ${\mu}M$ and 200 ${\mu}M$ indomethacin. However, the viability of embryos was not influenced by concentration in any other embryonic stages. In all embryonic stages, the hatching was suppressed with concentration dependent manner, but expansion was not suppressed. Particularly, in 84h embryos post hCG injection, the hatching was suppressed significantly compared with post hCG 72h or 96h embryos. When embryos were treated with 100 ${\mu}M$ indomethacin for a specific time (12h) in according to the development stage, the hatching was suppressed all groups. These suppressional effect was decreased as embryonic development stage was progressed. However, the expansion was not affected in all treatment group. This study suggests that hatching-related metabolic substances are synthesized from morula stage and intraembryonic signaling mediated prostaglandin was important for development and hatching of mouse embryo.

• The korean journal of orthodontics
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• v.20 no.1
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• pp.61-86
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• 1990

To study the effect of prostglandin $E_2$ and evening primrose oil on orthodontic tooth movement in rats, one hundred and sixty rats were divided into four groups of 40 rats each. One group, injected with saline on the palate subperiosteally, served as a control group. A second and third group were injected subperiosteally on the palate with $PGE_2$ $10{\mu}g$ and evening primrose oil 10mg respectively. The fourth group was given indomethacin $20{\mu}g/m{\ell}$ orally by water bottle. The maxillary first molar was moved mesially from the incisors using a 50gm force rubber band. In each group at the 1, 2, 3, 5, and 7th day, 4 rats were examined by light microscope, and 4 by electron microscope. The obtained results were as follows: 1. Osteoclastic activity was maximum at the 3rd day in the $PGE_2$ group on the interradicular alveolar bone of the first molar, followed by the evening primrose oil group, control group, and indomethacin group. 2. Root resorption and vacuolar changes were maximum in the $PGE_2$ group. 3. At the 3rd day of the $PGE_2$ group, the osteoclasts showed well developed ruffled borders and clear zones. At the same day, the evening primrose oil group also showed well developed ruffled borders and clear zones, but less than the $PGE_2$ group. 4. At the 3rd and 5th day of the $PGE_2$ group, fibroblasts showed phagocytized fragmented collagen fibers in the cytoplasm. At the 7th day of the $PGE_2$ group, fibroblasts showed collagen fibers forming at the cell membrane surface.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.3
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• pp.673-677
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• 2009

In order to verify the anti-inflammatory effects of Gelidium amansii, RAW264.7 macrophages were incubated with the extract of 70% ethanol solution (Ex), and activated with the endotoxin lipopolysaccharide (LPS). Ex inhibited the expression of the pro-inflammatory enzymes, including inducible nitric oxide (NO) synthase (iNOS) and cyclooxygenase-2 (COX-2), and the production of iNOS-mediated NO and COX-2-mediated prostglandin $E_2$ ($PGE_2$) production in a dose-dependent manner. Ex also reduced the release of the pro-inflammatory cytokines, including tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), interleukin-1${\beta}$ (IL-1${\beta}$) and IL-6 in LPS-activated macrophages, The observed anti-inflammatory effects of Ex was associated with inactivation of the nuclear factor ${\kappa}B$ (NF-${\kappa}B$) that mediates the induction of iNOS, COX-2, TNF-${\alpha}$, IL-1${\beta}$, and IL-6. Further studies showed that Ex inactivated NF-${\kappa}B$ through inhibition of phosphorylation of the inhibitory ${\kappa}B$ ($l{\kappa}B$), Taken together, these results suggest that Gelidium amansii exerts anti-inflammatory effects by inhibiting the expression of pro-inflammatory enzymes and the secretion of pro-inflammatory cytokines via inactivation of NF-${\kappa}B$ and/or $l{\kappa}B$.