간섬유증 동물모델에서 인진호 열수 추출물의 간 보호 효과 (Hepatoprotective Effect of Artemisia capillaris Thunb Water Extract in an Animal Model of Liver Fibrosis)

서지정보

· 발행기관 : 한국식품영양과학회
· 수록지 정보 : 한국식품영양과학회지 / 51권 / 4호 / 302 ~ 310페이지
· 저자명 : 김민주, 최정원, 이세희, 신유옥, 노성수

초록

본 실험에서는 8주간 thioacetamide(TAA)로 간섬유증 유발과 동시에 인진호 열수 추출물을 경구 투여하여 간섬유증에 미치는 영향에 대하여 실험을 진행하였으며 다음과 같은 결과를 얻었다. 인진호 열수 추출물은 TAA 주입으로 인해 증가한 혈청 내 암모니아 수치와 myeloperoxidase 활성을 유의하게 감소시켰다. 그리고 간 조직 내 항산화 관련 인자인 Nrf2, HO-1, catalase, GPx-1/2의 발현을 증가시켜 산화적 스트레스 관련 인자인 NOX2와 p22phox의 발현을 유의하게 감소시켰으며, 이로 인해 섬유화와 관련된 인자인 α- SMA와 collagen Ⅰ의 발현을 유의하게 감소시켜 간섬유증을 약화했다.

영어초록

This study investigated the hepatoprotective effect of Artemisia capillaris Thunb water extract (AE) in a thioacetamide (TAA)-induced liver fibrosis model using mice. The animal experiment was conducted with a normal group, a control group, a positive control group (silymarin 50 mg/kg), and an AE group (AE 200 mg/kg). Except for the normal group, hepatic fibrosis was induced by intraperitoneal administration of TAA 3 times a week for 8 weeks in the remaining groups (100 mg/kg for 1 week, 200 mg/kg for 2∼3 weeks, and 400 mg/kg for 4∼8 weeks). Moreover, the AE or silymarin was administered orally daily for 8 weeks. At the end of 8 weeks, ammonia levels and the myeloperoxidase (MPO) activity in the serum were measured. The expression of antioxidant, oxidative stress, inflammation, and fibrosis-related proteins in the liver tissue was measured by western blot test. Serum analysis revealed that the ammonia levels and MPO activity that were increased by the TAA were significantly decreased by the AE treatment. Also, treatment with AE significantly reduced the oxidative stress, increased by TAA by increasing the expression of antioxidant-related proteins in the liver tissue. Our study confirmed that the expression of inflammation and fibrosis-related proteins was significantly reduced due to the reduction of oxidative stress. In conclusion, these results suggest that AE treatment alleviates hepatic fibrosis by reducing oxidative stress through the activation of the NF-E2-related factor 2 (Nrf2) pathway.

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