HE ZHONG-LIN, CHEN PING, YAN HONG-TAO, et al. 125I stenting inhibits proliferation of smooth muscle cells in dogs after bile duct injury. [J]. Journal of army medical university, 2007, 29(3): 256-258.
HE ZHONG-LIN, CHEN PING, YAN HONG-TAO, et al. 125I stenting inhibits proliferation of smooth muscle cells in dogs after bile duct injury. [J]. Journal of army medical university, 2007, 29(3): 256-258.DOI:
I支架抑制犬胆管损伤后胆管平滑肌细胞增殖,预防胆管再狭窄的可行性。 方法 实验犬12 只(体质量15~18 kg)
随机分为普通支架组和
125
I支架组各6 只。用切断吻合法,造成胆总管损伤。术后30 d胆道狭窄形成后,分组将普通支架及
125
I支架从胆总管末端开口处释放到胆总管内。置入支架后60 d 分别行病理形态学检测
用免疫组织化学方法测定P53蛋白、增殖细胞核抗原(proliferating cell nuclear antigen) 及平滑肌肌动蛋白(smooth muscle actin),并测定外周血和支架周围放射性。 结果 支架置入后60 d
与普通支架组比较
125
I 支架组胆管最大内膜厚度显著减少(
P
<
0.05)
两组胆管狭窄面积百分比分别为(53.72±13.89) %和(17.34±9.28) %
差异有显著性(
P
<
0.05)
125
I 支架组胆管腔周长及胆管腔面积均较普通支架组明显增加(
P
<
0.05) ,
125
I支架组胆管平滑肌增殖细胞核抗原(PCNA) 及平滑肌肌动蛋白(SMA) 表达较弱
而P53蛋白表达增高
后者平滑肌PCNA 及SMA表达增高,而P53蛋白表达较弱。 结论
125
I 支架照射可抑制平滑肌细胞增殖
预防胆管再狭窄。
Abstract
Objective To explore the feasibility of preventing bile duct restenosis with the stent treated with
125
I and to elucidate the mechanisms of the inhibition of the smooth muscle cell proliferation and the increase of apoptosis after bile duct injury in dogs. Methods The experimental dogs were randomly divided into common stent
group and
125
I stent group
each of 6 animals. Duct was injured with cutting anastomosis. After formation of duct stenosis 90 d post operation
common stents and
125
I stents were inserted in the end of the bile common duct of the 2 groups respectively. Morphological study on the duct
immunohistochemistry for P53
proliferating cell nuclear antigen (PCNA) and smooth muscle actin (SMA)
the radiation of the peripheral blood and tissue around the stent were studied. Results The utmost intimal thickness of bile duct was found to be obviously less in the
125
I stent group compared to in common stent group after 90 d
and the percentages of the stenosis of the bile duct were (53.72±13.89) % and (17.34±9.28) %
respectively (
P
<
0.05). The circumference and area of bile duct lumen were obviously larger compared to that in the common stent group (
P
<
0.05). The expressions of PCNA and SMA in biliary smooth muscle cells were weaker in
125
I group than in the common group
and that of P53 was obviously up-regulated. Conclusion
125
I stent may inhibit the proliferation of smooth muscle cells and prevent the restenosis of bile duct.