CAJ | 학술논문

目的:通过观察小鼠体内自由基水平和抗氧化酶活性的影响,探讨芥菜籽对氧化偶氮甲烷(azoxymethane,AOM)诱导的小鼠大肠肿瘤的预防作用机制.方法:60只昆明品系小鼠随机分为AOM 模型组、AOM+5%MS、AOM+10%MS干预组和正常对照组.观察记录各组小鼠肿瘤发生率;检测小鼠血清中抗氧化酶(SOD、CAT、GSH-PX)的活力和脂质过氧化产物丙二醛(MDA)的水平.结果:正常对照组小鼠无肿瘤发生.AOM模型组、5%MS和10%MS干预组三组间肿瘤发生率有差异(χ2=6.607,P=0.048);AOM模型组小鼠平均肿瘤数为(2.20±1.21)个,而5%MS和10%MS干预组小鼠平均肿瘤数分别为(1.07±1.10)个和(0.67±0.89)个,与模型组相比有显著性差异(P<0.05).小鼠血清抗氧化酶SOD、CAT、GSH-PX的活力:AOM模型组明显低于正常对照组(P<0.05);MS干预组与AOM模型组相比均有所提高(P<0.05);其中10%MS干预组提高小鼠血清抗氧化酶活力的作用最明显,与5%MS干预组相比有显著性差异(P<0.05).小鼠血清脂质过氧化产物(MDA)含量:AOM 模型组明显高于正常对照组(P<0.05);MS 干预组与AOM模型组相比均有所下降(P<0.05);其中10%MS干预组降低小鼠血清MDA的效果最明显,与5%MS干预组相比有显著性差异(P<0.05).结论:芥菜籽能明显降低AOM 诱导的小鼠大肠癌发生率并减少小鼠的平均肿瘤数,且随芥菜籽浓度的增加,其预防作用增强.芥菜籽能明显增强体内抗氧化的能力,提高体内自由基清除酶的活性,其预防机制可能与其抗氧化作用有关,通过减少自由基对细胞的损伤,预防基因突变和肿瘤发生.
목적:통과관찰소서체내자유기수평화항양화매활성적영향,탐토개채자대양화우담갑완(azoxymethane,AOM)유도적소서대장종류적예방작용궤제.방법:60지곤명품계소서수궤분위AOM 모형조、AOM+5%MS、AOM+10%MS간예조화정상대조조.관찰기록각조소서종류발생솔;검측소서혈청중항양화매(SOD、CAT、GSH-PX)적활력화지질과양화산물병이철(MDA)적수평.결과:정상대조조소서무종류발생.AOM모형조、5%MS화10%MS간예조삼조간종류발생솔유차이(χ2=6.607,P=0.048);AOM모형조소서평균종류수위(2.20±1.21)개,이5%MS화10%MS간예조소서평균종류수분별위(1.07±1.10)개화(0.67±0.89)개,여모형조상비유현저성차이(P<0.05).소서혈청항양화매SOD、CAT、GSH-PX적활력:AOM모형조명현저우정상대조조(P<0.05);MS간예조여AOM모형조상비균유소제고(P<0.05);기중10%MS간예조제고소서혈청항양화매활력적작용최명현,여5%MS간예조상비유현저성차이(P<0.05).소서혈청지질과양화산물(MDA)함량:AOM 모형조명현고우정상대조조(P<0.05);MS 간예조여AOM모형조상비균유소하강(P<0.05);기중10%MS간예조강저소서혈청MDA적효과최명현,여5%MS간예조상비유현저성차이(P<0.05).결론:개채자능명현강저AOM 유도적소서대장암발생솔병감소소서적평균종류수,차수개채자농도적증가,기예방작용증강.개채자능명현증강체내항양화적능력,제고체내자유기청제매적활성,기예방궤제가능여기항양화작용유관,통과감소자유기대세포적손상,예방기인돌변화종류발생.
@@@@Objective: To investigate the chemopreventive effects of mustard seed (MS) on azoxymethane (AOM)-induced colorectal tumor in mice, and explore the anticancer mechanisms of MS based on free radical reactions during tumorigenesis. Methods: A total of 60 Kunming mice were randomly divided into four groups: AOM alone, AOM+5%MS, AOM+10%MS, and untreated control. The incidence of colorectal tumor in each group was determined. A colorimetric assay was used to detect the activity of antioxidant enzymes (SOD, CAT, and GSH-PX) and levels of the lipid peroxidation product malondialdehyde (MDA) in the serum of all mice. Results: No tumorous lesion was found in the untreated control group. However, the tumor incidences in the other three groups were statistically significant (χ2=6.607, P=0.048, P<0.05). The tumor burdens (number of tumors per mouse) were 2.20 ± 1.21 in the AOM alone group, 1.07 ± 1.10 (P<0.05) in the AOM+5%MS group, and 0.67 ± 0.89 (P<0.05) in the AOM+10%MS group. The activities of the serum anti-oxidases SOD, CAT, and GSH-PX were significantly lower in the AOM alone group than in the control, and the difference was significant (P<0.05). The activities of serum SOD, CAT, and GSH-PX were significantly higher in the AOM+10%MS group than in the AOM alone and AOM+5%MS groups (P<0.05). The serum MDA content was significantly higher in the AOM alone group than in the control group (P<0.05). The serum MDA content was significantly lower in the AOM+10%MS group than in the AOM alone and AOM+5%MS groups (P<0.05). Conclusion: MSs exert chemo-preventive activities against AOM-induced colorectal cancer in mice, and can reduce the tumor incidence and average number of tumors. With increased MS concentration, the preventive effect on colorectal cancer strengthens. Thus, MSs can enhance the in vivo antioxidant ability and free radical-scavenging enzyme activity. The preventive mechanism of MSs on colorectal cancer may be related to its antioxidant activity, which can prevent genetic mutations and tumor incidence by reducing free radical damage to cells.