- 결명자 추출물이 D-Galactosamine 유발 간 손상에 미치는 영향
- ㆍ 저자명
- 홍경희,엄민영,안지윤,하태열,Hong. Kyung-Hee,Um. Min-Young,Ahn. Ji-Yun,Ha. Tae-Youl
- ㆍ 간행물명
- 한국식품영양학회지
- ㆍ 권/호정보
- 2012년|25권 3호|pp.546-553 (8 pages)
- ㆍ 발행정보
- 한국식품영양학회
- ㆍ 파일정보
- 정기간행물| PDF텍스트
- ㆍ 주제분야
- 기타
This study was performed to evaluate the biological activity and protective effect of Cassia tora ethanol extracts against D-galactosamine induced hepatotoxicity in rats. Male Sprague-Dawley rats were grouped into normal group, D-galactosamine treated group(control), D-galactosamine plus 0.25% Cassia tora extracts treated group and D-galactosamine plus 0.5% Cassia tora extracts treated group. Normal and control group were fed control diet and Cassia tora extracts treated groups were fed experimental diets containing 0.25% or 0.5% Cassia tora ethanol extracts for 5 weeks. Body weight gain and liver weight of rats were not significantly different between groups. Cholesterol and triglyceride concentrations in serum and liver were significantly lower in rats treated only with D-galactosamine compared to normal group, and improved in Cassia tora extracts supplemented rats. D-galactosamine treatment significantly increased serum aspartate transaminase, alanine transaminase, gamma glutamyl transferase and alkaline phosphatase, however, the activities of aspartate transaminase and alanine transaminase were significantly decreased in Cassia tora extracts supplemented rats when compared with D-galactosamine treated control group. Cassia tora extracts significantly suppressed the D-galactosamine-induced elevation of liver thiobarbituric acid reactive substances(TBARS) contents. Superoxide dismutase activity was decreased by D-galactosamine treatment, however by the supplementation of Cassia tora ethanol extracts, significantly increased in dose-dependent manner. Glutathione peroxidase activity in rats fed diets containing Cassia tora extracts was decreased compared to control. Based on these results, we concluded that Cassia tora ethanol extracts may prevents the D-galactosamine-induced hepatotoxicity probably via an antioxidant mechanism.