CAJ | 학술논문

目的探讨大蒜素对慢性铁负荷大鼠抗氧化功能的影响及可能机制.方法36只SD大鼠按体重随机分为6组,即正常对照组(饲喂基础饲料)、慢性铁负荷模型组(饲喂高铁饲料)、正常+大蒜素40mg/kg组、慢性铁负荷+大蒜素30、40、60mg/kg组,每组6只.持续饲喂6周后,取血清、肝、结肠和肾组织测定铁含量、总铁结合力、丙二醛(MDA)含量及总超氧化物歧化酶(T-SOD)活性.结果与正常对照组比较,模型组血清铁、肝和结肠组织铁、MDA含量及肝组织T-SOD活性均显著升高(P<0.05,P<0.01),血清总铁结合力、结肠组织T-SOD活性均显著降低(P<0.01);与模型组比较,各剂量大蒜素组血清、结肠组织铁、肝组织MDA含量及中、高剂量大蒜素组肝组织铁含量均显著降低(P<0.05),血清总铁结合力、结肠和肾组织T-SOD活性均显著升高(P<0.05).结论大蒜素能增强大鼠机体的抗氧化能力,对铁过负荷所致的氧化应激具有一定的保护作用.
목적탐토대산소대만성철부하대서항양화공능적영향급가능궤제.방법36지SD대서안체중수궤분위6조,즉정상대조조(사위기출사료)、만성철부하모형조(사위고철사료)、정상+대산소40mg/kg조、만성철부하+대산소30、40、60mg/kg조,매조6지.지속사위6주후,취혈청、간、결장화신조직측정철함량、총철결합력、병이철(MDA)함량급총초양화물기화매(T-SOD)활성.결과여정상대조조비교,모형조혈청철、간화결장조직철、MDA함량급간조직T-SOD활성균현저승고(P<0.05,P<0.01),혈청총철결합력、결장조직T-SOD활성균현저강저(P<0.01);여모형조비교,각제량대산소조혈청、결장조직철、간조직MDA함량급중、고제량대산소조간조직철함량균현저강저(P<0.05),혈청총철결합력、결장화신조직T-SOD활성균현저승고(P<0.05).결론대산소능증강대서궤체적항양화능력,대철과부하소치적양화응격구유일정적보호작용.
Objective To explore the protective effects of allicin on oxidative stress and its possible mechanism. Methods 36 SD rats were randomly divided into 6 groups:control group (basal diet, 50 mg·kg-1 Fe), iron group (high iron diet, 1000 mg·kg-1 Fe), allicin group (basal diet, ig given allicin 40 mg·kg-1), iron+low, medium and high allicin groups (high iron diet, ig given allicin 30, 40 and 60 mg·kg-1), once daily for 6 weeks. Levels of serum and tissues iron status, total iron-binding capacity (TIBC), MDA and T-SOD were determined. Results Compared with control group, the contents of serum iron status, liver and colon tissues iron status, MDA, and liver tissues T-SOD in model group were all increased significantly (P<0.05, P<0.01), while serum TIBC, colon tissues T-SOD were all decreased significantly (P<0.01);Compared with model group, the contents of serum and colon tissues iron status, liver tissues MDA in each dose group, and liver tissues iron status in medium and high allicin groups were all decreased significantly (P<0.05), while serum TIBC, colon and renal tissues T-SOD were all increased significantly (P<0.05). Conclusion Allicin can increase antioxidative effect and protect against oxidative stress in rats induced by iron overload.