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目的了解氧化苦参碱对于对甲基硝基亚硝基胍(MNNG)诱导的大鼠消化道肿瘤的化学预防作用及其作用机制。方法 99只雄性 Wistar 大鼠分成4组分别服用不同的约物:阴性对照组(20只)、肿瘤模型组(36只)、氧化苦参碱干预组(23只)、氧化苦参碱对照组(20只)。给药28周后停药,正常饲料喂养至44周后观察各组大鼠的胃肠黏膜病变。并用免疫组化方法检测肿瘤模型组及氧化苦参碱干预组肿瘤组织中 Ki67的表达,用脱氧核糖核苷酸末端转移酶介导的原位缺口末端标记法(TUNEL)检测两组肿瘤组织细胞的凋亡。结果 92只(92.93%)大鼠完成实验。氧化苦参碱干预组肿瘤发生率为30.43%(7/23),明显低于肿瘤模型组[58.62%(17/29),P<0.05];阴性对照组肿瘤发生率为5%(1/20);氧化苦参碱对照组无肿瘤发生。肿瘤模型组发生肿瘤的中位体积为2.56(全距49.5)cm~3,大于氧化苦参碱干预组0.03(全距0.009)cm~3及对照组(0.5 cm~3,P<0.05)。肿瘤模型组大鼠消化道黏膜溃疡及异型增生的发生率也显著高于氧化苦参碱干预组(P<0.05)。肿瘤模型组肿瘤组织中 Ki67的表达阳性率(48±18)%显著高于氧化苦参碱干预组的肿瘤组织(25±24)%(P<0.05)。肿瘤模型组肿瘤组织细胞的凋亡率(11±7)%显著低于氧化苦参碱干预组的肿瘤组织[(30±16)%,P<0.05]。结论氧化苦参碱能通过抑制肿瘤细胞增殖,诱导其凋亡从而有效地抑制MNNG 诱导的大鼠消化道肿瘤发生。
Objective To investigate the chemopreventive effect of oxymatrine on p-methylnitroguanidine (MNNG)-induced gastrointestinal cancer in rats and its mechanism of action. Methods 99 male Wistar rats were divided into 4 groups to take different doses: negative control group (20), tumor model group (36), oxymatrine intervention group (23), oxymatrine control group (20 only). After 28 weeks of dosing, the drug was discontinued, and the gastrointestinal mucosal lesions of the rats in each group were observed after feeding for 44 weeks. Immunohistochemical method was used to detect the expression of Ki67 in the tumor model group and oxymatrine intervention group. Two groups of tumor tissue cells were detected by nick end labeling (TUNEL) mediated by deoxyribonucleotide terminal transferase. Apoptosis. Results 92 (92.93%) rats completed the experiment. The incidence of tumors in the oxymatrine intervention group was 30.43% (7/23), which was significantly lower than that in the tumor model group [58.62% (17/29), P<0.05]; the tumor incidence rate in the negative control group was 5% (1/ 20); Oxymatrine control group no tumor. The median tumor volume in the tumor model group was 2.56 (full distance 49.5) cm-3, which was greater than 0.03 in the oxymatrine intervention group (0.009) cm-3 in the whole group and 0.5 cm-3 in the control group (P<0.05). The incidence of digestive tract mucosal ulcers and dysplasia was also significantly higher in the tumor model group than in the oxymatrine intervention group (P<0.05). The positive expression rate of Ki67 in the tumor model group (48±18)% was significantly higher than that in the oxymatrine intervention group (25±24)% (P<0.05). The tumor cell apoptosis rate in the tumor model group was (11±7)%, which was significantly lower than that in the oxymatrine intervention group [(30±16)%, P<0.05]. Conclusion Oxymatrine can inhibit the proliferation of gastrointestinal cancer induced by MNNG effectively by inhibiting the proliferation of tumor cells and inducing apoptosis.