ACI大鼠肝细胞癌模型在介入治疗实验中的初步应用

Initial application of a ACI-rat model of hepatocellular carcinoma in the experiments of interventional therapy

目的 评价在ACI大鼠肝细胞癌模型进行多种介入治疗方案的疗效及该模型在介入治疗实验中的应用价值。方法 在 5 8只雄性ACI大鼠肝包膜下植入MorrisHepatoma 3 92 4A肝癌瘤块( 1mm3) ,移植术后 13d行MR检查 ,测量肿瘤体积 (V1) ,第 14天时 ,经腹部切开术及胃十二指肠动脉逆行插管而采取以下介入治疗方案 :(A)丝裂霉素 4只 ;(B)降解淀粉 4只 ;(C)碘油 5只 ;(D)肝动脉结扎 4只 ;(E)丝裂霉素 +降解淀粉 4只 ;(F)丝裂霉素 +动脉结扎 5只 ;(G)丝裂霉素 +碘油 5只 ;(H)降解淀粉 +动脉结扎 4只 ;(I)碘油 +动脉结扎 4只 ;(J)丝裂霉素 +聚丙交酯复合乙交酯 (poly lactid co glycolid ,Plcg)微球 4只 ;(K)丝裂霉素 +碘油 +动脉结扎 4只 ;(L)丝裂霉素 +降解淀粉 +动脉结扎4只 ;(M) 0 9%生理盐水 (对照组 ,7只 )。 13d后再次行磁共振检查以确定肿瘤体积 (V2 )变化 ,并对各组间V2 /V1的比值进行比较。结果 肝癌移植率为 10 0 %。介入治疗后肿瘤体积与治疗前肿瘤体积之比 (V2 /V1)分别为A组 4 5 0 ,B组 12 73 ,C组 15 84,D组 10 17,E组 90 2 0 ,F组 7 16,G组 4 0 8,H组 3 45 ,I组 9 99,J组 2 86,K组 3 76,L组 7 71,M组 2 7 12。与对照组相比 ,采取A、G、H、J和K组方法能明显抑制肿瘤生长 ( χ2 值分别为 5

Objective To evaluate the therapeutic efficiency of various methods of interventional therapy in the ACI-rat model of hepatocellular carcinoma, and to assess the value of this model in the experiments of interventional therapy. Methods The subcapsular implantation of a solid Morris Hepatoma 3924A (1 mm 3) in the livers was carried out in 58 male ACI-rats. 13 days after the implantation, the tumor volume (V 1) was measured by using magnetic resonance tomography (MRT). After laparotomy and retrograde placement of catheter into the gastroduodenal artery (14 d), the following protocols of interventional therapy were performed: (A) Mitomycin C (n=4); (B) Degradable starch microspheres (DSM) (n=4); (C) Lipiodol (n=5); (D) Ligation (n=4); (E) Mitomycin C + DSM (n=4); (F) Mitomycin C + ligation (n=5); (G) Mitomycin C + Lipiodol (n=5); (H) DSM + ligation (n=4); (I) Lipiodol + ligation (n=4); (J) Mitomycin C + Poly-lactid-co-glycolid-microspheres (Plcg) (n=4); (K) Mitomycin C + Lipiodol + ligation (n=4); (L) Mitomycin C + DSM + ligation (n=4); (M) 0.9% NaCl (control group, n=7). 13 days after these therapies the change of the tumor volume (V 2) was determined by MRT again. Results The rate of implantation was 100%. V 2/V 1 was 4.50 in group A, 12.73 in group B, 15.84 in group C, 10.17 in group D, 90.20 in group E, 7.16 in group F, 4.08 in group G, 3.45 in group H, 9.99 in group I, 2.86 in group J, 3.76 in group K, 7.71 in group L, and 27.12 in group M, respectively. Compared to the control group, groups A, G, H, J and K showed significant reduced tumor growth (χ 2=5.238, 8.571, 5.238, 5.238, 5.238,P=0.045, 0.008, 0.045, 0.045, 0.045) in the period of observation, whereas the other groups showed no statistical significant differences by the tumor growth [χ 2=1.016(B), 3.086 (C), 1.016(D), 2.213(E), 3.086(F), 1.061(I), 1.061(L), P=0.348(B), 0.121(C), 0.348(D), 0.199(E), 0.121(F), 0.348(I), 0.348(L)]. Conclusion This model of hepatocellular carcinoma is suitable for the experimental studies of interventional therapy and it has wide useful value.