패혈증 쇼크에서 단삼 추출물의 억제 효과와 그 기전에 관한 연구 (Protective Effects and Mechanisms of Salvia Miltiorrhizae Radix Extract on Endotoxin Shock)

서지정보

· 발행기관 : 대한한방안이비인후피부과학회
· 수록지 정보 : 한방안이비인후피부과학회지 / 29권 / 3호 / 14 ~ 26페이지
· 저자명 : 신상호, 윤정민, 고우신, 윤화정

초록

Objectives : This study was performed to investigate the protective effects and mechanisms of Salvia miltiorrhizae Radix extract (SME) on endotoxin shock.
Methods : We used two models; LPS-induced sepsis model for in vivo model, and murine peritoneal macrophages responses for in vitro. SME was administrated orally to mice. After 1 hr, LPS was injected intraperitoneally. Survival rate was checked each time per 12 hr for 5 days. Mice were sacrificed 3 hr after LPS injection, then blood samples and organs were harvested. Cytokines secretion was measured by ELISA. Organs tissues were observed with microscope. Murine peritoneal macrophages were cultured for 1 hr either in a medium alone or in a medium that contained SME, as indicated. Then, the cells were treated with LPS for 24 hr. mRNA levels of cytokines were measured by real-time RT-PCR. Cytokine levels in the supernatants were measured by ELISA. The amount of nitrite was measured by using the Griess method to evaluate NO production. The cell lysates were analysed by Western blotting using antibodies for iNOS and β-actin was used as an internal control to monitor equal protein loading.
Results : SME improverd the survival rate of mice model. SME inhibited the secretion of inflammatory cytokines and organs damages on Endotoxin Shock model. SME suppressed cytokine expression, cytokine secretion,NO production, iNOS expression in LPS-induced murine peritoneal macrophages.
Conclusions : The results suggest that SME has protective effects on endotoxin shock through suppression of inflammatory cytokines, organ damages, NO production and so on.

영어초록

Objectives : This study was performed to investigate the protective effects and mechanisms of Salvia miltiorrhizae Radix extract (SME) on endotoxin shock.
Methods : We used two models; LPS-induced sepsis model for in vivo model, and murine peritoneal macrophages responses for in vitro. SME was administrated orally to mice. After 1 hr, LPS was injected intraperitoneally. Survival rate was checked each time per 12 hr for 5 days. Mice were sacrificed 3 hr after LPS injection, then blood samples and organs were harvested. Cytokines secretion was measured by ELISA. Organs tissues were observed with microscope. Murine peritoneal macrophages were cultured for 1 hr either in a medium alone or in a medium that contained SME, as indicated. Then, the cells were treated with LPS for 24 hr. mRNA levels of cytokines were measured by real-time RT-PCR. Cytokine levels in the supernatants were measured by ELISA. The amount of nitrite was measured by using the Griess method to evaluate NO production. The cell lysates were analysed by Western blotting using antibodies for iNOS and β-actin was used as an internal control to monitor equal protein loading.
Results : SME improverd the survival rate of mice model. SME inhibited the secretion of inflammatory cytokines and organs damages on Endotoxin Shock model. SME suppressed cytokine expression, cytokine secretion,NO production, iNOS expression in LPS-induced murine peritoneal macrophages.
Conclusions : The results suggest that SME has protective effects on endotoxin shock through suppression of inflammatory cytokines, organ damages, NO production and so on.

참고자료

· 없음