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.

Cyclooxygenase(COX)-2 is an enzyme engaged in the synthesis of prostaglandin(PG) and is upregulated by inflammation. It is related with the expression of the vascular endothelial growth factor(VEGF) in the angiogenesis of granulation tissue. By using immunohistochemical stains, the expressions for COX-2 and VEGF were evaluated according to the degree of inflammation and the type of lesion, and the correlation between the expressions were investigated in the 39 periapical lesions (7 periapical granulomas, 7 periapical granulomas with epithelium, 25 periapical cysts) and 13 dentigerous cysts. The expression rate of COX-2 in histiocytes of periapical lesions(97.4%) was significantly higher than that of dentigerous cysts(69.2%)(p=0.0032). The expression rate of VEGF was highest in plasma cells in the periapical lesions(69.4%) and in dentigerous cysts(69.2%). COX-2 expression rate in endothelium and VEGF expression rate in epithelium were significantly higher in the periapical cysts than in the periapical granuloma and. VEGF expression rate in endothelium of the periapical lesions was increased in cases with resolving inflammation. For the periapical lesions, epithelial expression of COX-2 and VEGF showed a positive relationship(p=0.0301), and endothelial COX-2 expression revealed positive relationship with VEGF expressions in epithelium(p=0.0008), in histiocytes(p=0.0136), and in endothelium(p=0.0439). According to these findings, as the periapical lesion progressed from granuloma to cyst, the expressions of COX-2 and VEGF were increased. COX-2 expression was significantly correlated with VEGF expression, which suggests that COX-2 seems to be involved in the progression of periapical lesion by inducing the expression of VEGF.

Cyclooxygenase- 2 (COX-2) is an inducible enzyme that is not found in normal conditions,. but is induced by a varie ty of pathophysiologic conditions of tissues by growth factors. inflammatory stimuli. oncogenes and tumor promoters, COX-2 is upregulated in a number of epithelial cancers. including in oral premalignant and malignant lesions, The mode of action of COX-2 in carcinogenesis may include mutiple mechanisms that may be acting at different stages of malignant disease, In this study. the expression of COX- 2 protein was assessed quantitatively 없d qualitatively by immunohistochemistry during DMBA-induced hamster buccal pouch carcinogenesis, The immunoreactivity for COX-2 protein increased as the tissue passed from hyperplasia to dysplasia and SCC, The highest mean expression was SCC at 14 week, The differences between COX-2 expression in the normal and that the dysplastic and carcinomatous lesions was statistically significant, In addition. the mean values of COX -2 expression in the stromal cells increased gradually during malignant progression, The results suggest that increased COX-2 expression may be associated with the chemically induced carcinogenic progression of hamster buccal pouch model, The gradual increasing COX-2 expression de tected during the progressive manner toward more malignant lesions shows that the COX-2 protein can have an important role in both the early and the later stages of multistep oral carcinogenesis

Department of Oral Pathology, Dental Science Research Institute, College of Den디'suy， Chonnam National University It is well known that the expansion of radicular and dentigerous cyst is related to the change of osmotic pressure, while the prolifera디on ofthe 비피19 epithelium in odontogenic keratocyst. When the dentigerous cyst and odontogenic keratocyst has secondary infection, they present the loss of unique sπuctures and epithelial hyperplasia. There is a question whether inflammatory reaction affects cystic formation, expansion and their treatment. Present study is to evaluate the relationship between inflammation and epithelial hyperplasia using immunohistochemial study. Followings are result; 1. 까1e age of patients ranged from 10 to 73 years (mean age, 39 years) in radicular 이5t， 10 to 71 years (mean age, 35 years) in dentigerous cyst and 10 to 54 years (mean age, 23.4 years) in odontogenic keratocyst. The sex distribution of patient distributed 32 cases for male and 16 cases for female in radicular cyst, 13 and 10 in dentigerous cyst and equally 5 and 5 in odontogenic keratocyst. 2. Inflammatory cyst in the present study distributed 44/48 cases (9 1.7%) for radicular cyst, 15/ 23 cases for dentigerous cyst and 1/ 10 case for odontogenic keratocyst. 3. Evaluation of inflammatory reaction and antigen expression, ki-67 , cox-2 and glut-1 expression increase in the inflammatory radicular and dentigerous cyst. 4. In odontoge띠c keratocyst, expression of antigens increase regardless of inflammation. Above results showed that inflammation stimulate the proliferation of lining epithelium leading to cystic expansion.

The clinical importance of biologic markers remains elusive in gastric cancer. The aim of this study was to evaluate the prognostic value of p53, Ki-67, and COX-2 in gastric cancer. This retrospective study examined based on medical records of postoperative immunohistochemical test of 176 patients who demonstrated high expression of all three biological markers being tested (p53, Ki-67, and COX-2), among 357 gastric cancer patients who underwent surgical resection consecutively. This study demonstrates the correlation with biologic marker between clinical relationship and recurrence free survival (RFS). A positive correlation was observed between the expression of Ki-67 and p53, and a positive correlation was also observed between the expression of Ki-67 and COX-2 Expression of p53 did not correlate with any of the clinicopathological variables examined. Both Ki-67 and COX-2 expression significantly correlated with tumor depth, classified as early gastric cancer and advanced gastric cancer. The expression of COX-2 significantly correlated with tumor differentiation, with more tumors being of the undifferentiated type than of the differentiated type in the COX-2 positive group. A significant difference between p53 and RFS, also COX-2 expression and RFS was observed. This study showed that only p53 and COX-2 have significantly correlated with the RFS of gastric cancer.

본 연구에서는 마늘의 부산물로 발생하는 마늘대의 항산화 및 항염증 효과를 알아보기 위하여 LPS로 염증을 유도한 Raw 264.7 세포에 대한 열수추출물(ASSW)과 70% 에탄올 추출물(ASSE)의 효과를 살펴보았다. ASSW의 폴리페놀 함량은 37.08±1.51 mg(TAE)/g, ASSE의 폴리페놀 함량은 44.7±1.32 mg(TAE)/g 이 함유되어있음을 확인하였다. DPPH 실험과 ABTS+ 실험에서 ASSW, ASSE 모두 농도 의존적으로 증가하였으며, DPPH의 경우 1,000 μg/mL에서 대조군인 Vit.C의 50 μg/mL의 항산화능이 있다는 것이 확인되었고, ABTS+의 경우 500 μg/mL 이상부터 대조군인 Vit.C와 비슷한 효과를 나타냄으로서 ASSW, ASSE 모두 항산화능이 있다는 것을 확인하였다. MTT측정으로 인해 세포 독성을 가지지 않았던 농도대(5, 10, 25, 50, 100 μg/mL)에서 염증 억제 효과를 살펴보기 위해 NO를 측정한 결과 ASSW, ASSE 모두 25 μg/mL에서부터 유의적으로 분비량이 감소함을 확인하였으며 특히 100 μg/mL의 농도에서 약 18%, 23%의 억제 효과를 보였다. 또한 대식세포의 염증성 cytokine인 IL-6, TNF-α, IL-1β 및 PGE2의 분비량을 첨가 농도 의존적으로 억제함을 확인하였다. 특히 PGE2에 대해 ASSW, ASSE 100 μg/mL의 농도에서 약 55%, 60%의 감소효과를 보였다. ASSW의 iNOS, COX-2의 발현 저해효과는 나타내지 못하였지만, ASSE는 100 μg/mL의 농도에서 iNOS의 발현량이 현저하게 억제됨을 확인하였고, COX-2의 경우 농도 의존적으로 저하되어 특히 50 μg/mL, 100 μg/mL의 구간에서 단백질 발현 저해효과가 있음을 확인하였다. 이를 통해 ASSW, ASSE 모두 항산화 효과와 항염증 효과가 있음을 확인하였으며, ASSW 보다 ASSE에서 활성산소종(reactive oxygen species, ROS) 및 ROS에 의해 유발되는 염증을 억제시켜주는 소재가 될수있을 것이라 예상된다.

나비류 추출물은 전통적으로 다양한 활성을 보유하여 의약용으로 사용되어졌다. 5종의 나비(산제비나비[Papilio maackii], 호랑나비[Papilio xuthus], 배추흰나비[Pieris rapae], 남방호랑나비[Eurema hecabe], 왕오색나비[Sasakia charonda])를 이용하여 물, dimethly sulfoxide (DMSO), ehtanol 및 methanol로 추출한 추출물로 항산화 활성 및 Cox-2 promote

괴경 내부에 적색과 보라색 안토시아닌 색소가 풍부하게 함유되어 있고, 색상의 기호도 및 건강 기능성으로 인해 소비자로부터 기호도가 증대된 유색감자의 생리적 활성을 검토하기 위해 유색감자로서 괴경 내부가 적색인 홍영, 괴경 내부가 보라색인 자영의 추출물에 대하여 ORAC를 통한 정밀한 항산화력의 비교, NO 억제 및 iNOS, COX-2의 발현 억제 활성을 비교, 검토한 결과는 아래와 같다. 1. 유색감자 홍영 및 자영 추출물의 항산화 활성 검정 결과 추출물의 농도가 2ug/mL 이하 수준에서는 차이를 나타내지 않았으나, 10ug/mL 을 처리한 경우 시료 간 차이를 나타내었으며, 유색감자 중 괴경 내부의 색상이 적색인 홍영은 ORAC value 0.257, 자영은 ORAC value 0.402로 대조 표준액인 trolox 보다 낮은 수치를 보였지만, 각각의 추출물로부터 유색의 원인이 되는 안토시아닌을 순수 분리하여 활성을 평가할 경우 표준액인 trolox와 동등 혹은 그 이상의 항산화 효과를 기대할 수 있을 것이다. 2. 홍영 및 자영 추출물이 RAW 264.7 세포의 LPS에 의해 유도된 NO 생성을 억제함을 확인하였고, 또한 Western blot으로 분석한 결과 각 추출물에 의한 iNOS 발현 억제는 NO 형성 억제와 유사한 경향을 보였으므로, NO 형성 억제는 iNOS의 발현 저해 경로를 통하여 억제되는 것을 알 수 있고, 또한 홍영 및 자영 추출물이 LPS에 의해 형성되는 PGE2를 감소시킬 것으로 판단되는데, 이는 COX-2 단백질의 발현 저해를 통하여 확인할 수 있었다. 3. 유색감자 중 괴경 내부가 적색인 홍영품종은 자색인 자영품종에서 보다 상대적으로 우수한 COX-2 발현 단백질 저해효과가 확인되었으며, 괴경 내부가 보라색인 자영품종은 ORAC를 통한 항산화 활성, NO 및 iNOS 억제효과가 홍영 대비 30% 이상 증가된 양상을 나타내므로, 홍영과 자영 품종에 함유된 안토시아닌은 서로 다른 기능의 질환을 예방하거나 치료할 수 있을 것으로 판단되며, 향후 품종별 용도를 구분하여 활용하는 것이 바람직할 것으로 판단된다.