Celecoxib, a cyclooxygenase (COX)-2 selective inhibitor, was approved as a non-steroidal anti-inflammatory drug (NSAID), and this therapeutic application has been expanded to several other diseases, including colon cancer. Notably, a treatment strategy combining the use of celecoxib and radiation therapy has been employed for improving the control of local cancers. In this study, we examined the effect of celecoxib on irradiation-induced intestinal damage. The twenty four mice (BALB/c) were divided into four groups; 1) sham-irradiated control group, 2) celecoxib-treated group, 3) irradiated group, and 4) celecoxib-treated irradiation group. Mice were orally administered celecoxib at a dose of 25 mg/kg in a 0.1 mL volume, daily for 4 days after irradiation exposure (10 Gy). Then, histological examinations of the jejunal villous height, crypt survival, and crypt size were performed. The expression of COX-2 after administration of celecoxib in irradiated mice was examined by employing immunohistochemistry, Western blotting, and qPCR analysis. The jejunal villi height and the crypt survival were reduced in the irradiation group compared with the sham-irradiated group. Celecoxib treatment in irradiation mice even more decreased those indicators. Crypt size was increased in the radiation group compared to the sham-irradiated control group, whereas the size was decreased in the celecoxibtreated irradiation group compared with the group exposed to the radiation injury. COX-2 expression was detected in the crypt of the small intestine, and COX-2 expression was increased in the crypt lesion following radiation exposure. However, COX-2 expression was reduced in the celecoxib-treated irradiation group. Therefore, in the present study, we confirmed that celecoxib treatment after irradiation aggravated the irradiation-induced intestinal damage. These results suggest that a caution need to be administered when celecoxib treatment is performed in combination with radiation therapy for cancer treatment.

The purpose of the present study was to investigate the effect of IFN- on prostaglandin synthesis, cyclooxygenase-2 (COX-2) gene expression in vitro and concentration of progesterone (P4) in endometrial cells. Epithelial and stromal cells cultured in vitro were isolated from bovine endometrium and stimulated with increasing doses of IFN- (0, 0.02, 0.2 and 2 ug/ml). Human chorionic gonadotropin (hCG, 1.5 IU/ml) was used as a positive control. Prostaglandin and levels in the culture media were analyzed by enzyme immunoassays and total RNA was extracted from the cells for RT-PCR. P4 concentrations of blood samples were assayed by chemiluminescent immuno assays system. In epithelial cells, COX-2 gene expression was increased in the presence of IFN- (p<0.05), but it was not significantly different in all groups of stromal cells except for 2 ug/ml IFN- group (p<0.05). Although IFN- did not affect and production in epithelial cells, it decreased and production significantly in stromal cells (p<0.05). In vivo experiment, blood concentration of P4 was significantly increased after addition of IFN- (1 ug/ml). The results indicate that PG production was mediated by COX-2 expression in stromal cells but it was not affected in epithelial cells and this suggest that treatment of IFN- could improve the implantation environment of uterine by maintenance of high P4 concentration.

In ruminants, Interferon-τ (IFN-τ) has the role of recognizing pregnancy signals produced by the embryo and it may have an important role during the luteolysis. Therefore, the purpose of the present study was to investigate the effect of IFN-τ on prostaglandin synthesis, cyclooxygenase-2 (COX-2) gene expression in vitro and secretion of progesterone (P4) in vivo. The epithelial and stromal cells isolated from bovine endometrium were cultured with different doses of IFN-τ (0, 0.02, 0.2 and 2 μg/ml). Human chorionic gonadotropin (hCG, 1.5 IU/ml) was used as a positive control. Prostaglandin E2 and F2α levels in the culture media were analyzed by enzyme immunoassays, and total RNA was extracted from the cells for RT-PCR. P4 concentrations in blood samples were assayed by chemiluminescent immunoassay system. In epithelial cells, COX-2 gene expression was increased in the presence of IFN-τ (p<0.05), but it was not significantly different in all groups of stromal cells except 2 μg/ml IFN-τ group (p<0.05). Although IFN-τ did not affect PGE2 and PGF2α production in epithelial cells, it decreased PGE2 and PGF2α production significantly in stromal cells (p<0.05). In vivo experiment, the P4 concentrations in blood sample was significantly increased after injection of 1 μg/ml IFN-τ. These results indicate that PG production was mediated by COX-2 expression in the stromal cells but it did not affect in the epithelial cells, and suggest that treatment of IFN-τ was to improve the implantation environment of uterine by maintenance of high P4 concentration. * This work was carried out with the support of “Cooperative Research Program for Agriculture Science & Technology Development (Project No. PJ907008)” Rural Development Administration, Republic of Korea.

The human embryonic-lethal abnormal vision-like protein, HuR, stabilizes mRNA containing adenine- and uridine- rich elements in their 3’untranslated region. Because cyclooxygenase-2 (COX-2) mRNA is a cellular transcript that contains an adenine- and uridine-rich element, it can be regulated by the HuR protein. In this study, we examined the relationship between COX-2, HuR, MVD, and the clinicopathological parameters. Nineteen out of 43 cases of HNSCC showed high level of COX-2expression, and 68% of these patients showed high COX-2 immuno-reactivity indicating the strong expression of the cytoplasmic HuR protein. Also, MVD expression in the cases with high COX-2 expression was higher than in the cases with low COX-2 expression. These results suggest a strong correlation between the overexpression of cytoplasmic HuR and COX-2 expression in HNSCC, and that COX-2 is associated with MVD in HNSCC. In conclusion, COX-2 regulated by cytoplasmic HuR may be a good tumor angiogenic factor in HNSCC.

Periodontopathogens including Porphyromonas gingivalis interact with host periodontal cells and the excessive subsequent host responses contribute a major part to the development of periodontal diseases. Cyclooxygenase(COX)-2-synthesized has detrimental activities in terms of periodontal pathogenesis. The present study investigated induction of COX-2 expression by P. gingivalis in human monocytic THP-1 cells. Live P. gingivalis increased expression of COX-2, but not that of COX-1, which was demonstrated at both mRNA and protein levels. Elevated levels of were released from P. gingivalis-infected THP-1 cells. Pharma-cological inhibition of p38 mitogen-activated protein kinase(MAPK) and extracellular signal-regulated kinase(ERK) substantially attenuated P. gingivalis-induced COX-2 mRNA expression. Indeed, activation of p38 MAPK and ERK was observed in P. gingivalis-infected THP-1 cells. Also, P. gingivalis induced activation of nuclear factor-κB (NF-κB)which is an important transcription factor for COX-2. These results suggest that COX-2 expression is up regulated in P. gingivalis-infected monocytic cells, at least in part, via p38 MAPK, ERK, and NF-κB.

Paeoniae Radix has been used as a traditional medicine for various diseases including hepatic disease. However, the inhibitory effect of Paeoniae Radix on intestinal inflammation has not been fully understood yet. The aim of this study was to evaluate the effect of Paeoniae Radix on colitis induced by dextran sulfate sodium in mice. To investigate the protective effects of Paeoniae Radix, the colitis mice were induced by drinking water containing 5% dextran sulfate sodium for 7 days. Mice were randomized into groups receiving Paeoniae Radix (100 ㎎/㎏), sulfasalazine (150 ㎎/㎏) as a positive control, or water as a negative control. We evaluated the effects of Paeoniae Radix on clinical signs induced by dextran sulfate sodium, measuring weight loss, colon length, and disease activity index. Additionally, to find a possible explanation for the anti-inflammatory effects of Paeoniae Radix, we evaluated the effects of Paeoniae Radix on the interleukin-6 and cyclooxygenase-2 levels in colitis tissue. The results indicated that mice treated with dextran sulfate sodium showed measurable clinical signs, including weight loss and reduced colon length. However, Paeoniae Radix treatment significantly improved the weight loss and disease activity index as clinical symptoms. Moreover, Paeoniae Radix inhibited the interleukin-6 and cyclooxygenase-2 expression levels in colon tissues treated with dextran sulfate sodium. Taken together, the findings of this study suggest that Paeoniae Radix may be useful for treating intestinal inflammation, including ulcerative colitis.

To search for immunoactive natural products exerting anti-inflammatory activity, we have evaluated the effects on the water extracts of Artemisia princeps Pampanini (APP) on lipopolysaccharide-induced nitric oxide (NO), tumor necrosis factor-α (TNF-α), and prostaglandin E2 (PGE2) production by RAW 264.7 macrophage cell line. Our data indicate that this extract is a potent inhibitor of NO production and it also significantly decreased PGE2 and TNF-α production. Consistent with these results, the protein and mRNA expression level of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) was inhibited by water extracts of APP in a dose-dependent manner. These results suggest that APP may exert anti-inflammatory and analgesic effects possibly by suppressing the inducible NO synthase and COX-2 expressions.

최근 곤충자원은 약용 및 식용으로 활용하려고 많은 연구가 되고 있으며 미래의 자원으로 발전할 수 있는 가능성은 충분하다. 본 연구는 곤충자원 중 칠성무당벌레와 무당벌레를 이용하여 생물학적 활성과 함께 약용 및 식용으로의 활용가능성을 알아보고자 하였다. 생물학적 활성을 알아보기 위하여 이들 추출물을 이용하여 항산화관련 실험인 DPPH, FRAP, linoleic acid 산화 억제실험을 하였으며, 분자 염증에 관련된 유전자인 Cyclooxygena