CopA3를 이용하여 피부 염증에 대하여 연구를 하였다. 산화질소와 cytokine의 생산은 면역세포의 대표적인 염증인자이다. 세포는 LPS 처리 후 한 시간 뒤에 CopA3를 처리하였다. 세포 독성이 나타나지 않는 농도인 5, 25, 50, 100 ${mu}g/ml$를 사용하였다. CopA3는 NO, TNF-${alpha}$, IL-$1{eta}$, IL-6, iNOS, COX-2의 생성을 저해 시켰다. iNOS와 COX-2 역시 100 ${mu}g/ml$의 농도에서 각각 54%, 65%가 저해가 되었다. 게다가 CopA3는 염증성 사이토 카인인 TNF-${alpha}$, IL-$1{eta}$, IL-6의 생성을 감소 시켰다. 이러한 결과로 CopA3는 염증 예방과 치료에 효과적임을 확인 할 수 있었다.
The objective of this study was to evaluate the effect of the synthetic CopA3 peptide of Copris tripartitus on skin inflammation. Regulatory mechanisms of cytokines and nitric oxide (NO) are involved in the immunological activity of RAW 264.7 cells. Tested cells were treated with different concentrations of CopA3 and further cultured for an appropriate time after lipopolyssacharide (LPS) addition. During the entire experimental period, 5, 25, 50, and 100 ${mu}g/ml$ of CopA3 had no cytotoxicity. At these concentrations, CopA3 inhibited tumor necrosis factor-${alpha}$ (TNF-${alpha}$), interleukin-$1{eta}$ (IL-$1{eta}$), and interleukin-6 (IL-6). CopA3 also inhibited the expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2). CopA3 inhibited the activity of iNOS and COX-2 by 41% and 59%, respectively, at 100 ${mu}g/ml$. In addition, CopA3 reduced the release of inflammatory cytokines including TNF-${alpha}$, IL-$1{eta}$, and IL-6. These results suggest that CopA3 may have significant effects on inflammatory factors and that it may be a potential anti-inflammatory therapeutic agent.
