단삼 물 추출물의 LPS로 유도된 RAW 264.7 세포와 생쥐 염증모델에서의 항염증 효과 (Anti-inflammatory effects of Salvia miltiorrhiza Water extract in RAW 264.7 Cells and mouse induced by Lipopolysaccharide)

서지정보

· 발행기관 : 대한한방부인과학회
· 수록지 정보 : 대한한방부인과학회지 / 32권 / 2호 / 1 ~ 17페이지
· 저자명 : 김건희, 홍가경, 조한백, 최창민, 김송백

초록

Objectives: This study was performed to identify the anti-inflammatory effects of Salvia miltiorrhizae radix Water extract (SMW) on lipopolysaccharide (LPS) induced inflammation.




Methods: RAW 264.7 cells were treated with 500 ng/ml of LPS. SMW (0.1, 0.25, 0.5 mg/ml) was treated 1 h prior to LPS. Cell viability was measured by MTT assay. Levels of nitric oxide (NO) were measured with Griess reagent and pro-inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). We also examined molecular mechanisms such as mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB) activation by western blot. In addition, we observed mice survival rate after LPS and examined their cytokine levels of serum and liver tissue.




Results: SMW itself did not have cytotoxic effects in RAW 264.7 cells less than 0.5 mg/ml. SMW treatment inhibited the production of NO, and interleukin (IL)-1β which is pro-inflammatory cytokine. And SMW treatment inhibited the LPS-induced activation of MAPKs such as extracellular signal-regulated kinase1/2 (ERK1/2), p38 kinases (p38), c-Jun NH2-terminal kinase (JNK) and NF-κB. In addition, it also showed reducing the level of IL-1β on the serum and liver tissue of mice. Also, death of LPS-induced mice was inhibited by SMW.




Conclusions: The result suggests that treatment of SMW could reduce the LPS-induced inflammation. Thereby, SMW could be used as a protective agent against inflammation. Also, this study could give a clinical basis that SMW could be a drug or agent to prevent inflammatory diseases.

영어초록

Objectives: This study was performed to identify the anti-inflammatory effects of Salvia miltiorrhizae radix Water extract (SMW) on lipopolysaccharide (LPS) induced inflammation.




Methods: RAW 264.7 cells were treated with 500 ng/ml of LPS. SMW (0.1, 0.25, 0.5 mg/ml) was treated 1 h prior to LPS. Cell viability was measured by MTT assay. Levels of nitric oxide (NO) were measured with Griess reagent and pro-inflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). We also examined molecular mechanisms such as mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB) activation by western blot. In addition, we observed mice survival rate after LPS and examined their cytokine levels of serum and liver tissue.




Results: SMW itself did not have cytotoxic effects in RAW 264.7 cells less than 0.5 mg/ml. SMW treatment inhibited the production of NO, and interleukin (IL)-1β which is pro-inflammatory cytokine. And SMW treatment inhibited the LPS-induced activation of MAPKs such as extracellular signal-regulated kinase1/2 (ERK1/2), p38 kinases (p38), c-Jun NH2-terminal kinase (JNK) and NF-κB. In addition, it also showed reducing the level of IL-1β on the serum and liver tissue of mice. Also, death of LPS-induced mice was inhibited by SMW.




Conclusions: The result suggests that treatment of SMW could reduce the LPS-induced inflammation. Thereby, SMW could be used as a protective agent against inflammation. Also, this study could give a clinical basis that SMW could be a drug or agent to prevent inflammatory diseases.

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