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首页> 外文期刊>World Journal of Gastroenterology >Anti-hepatoma effect of arsenic trioxide on experimental liver cancer induced by 2-acetamidofluorene in rats.
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Anti-hepatoma effect of arsenic trioxide on experimental liver cancer induced by 2-acetamidofluorene in rats.

机译：三氧化二砷对2-乙酰氨基芴诱导的实验性肝癌的抗肝癌作用。

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AIM: To study the anti-hepatoma efficiency of arsenic trioxide (As(2)O(3)) in the treatment of experimental rat hepatocellular carcinoma (HCC) induced by 2-acetamidofluorene (2-FAA) and to elucidate the possible mechanisms. METHODS: SD rats (2 mo old) had been fed with 2-FAA for 8 wk to induce HCC, and then they were treated with As(2)O(3) or matrine. On d 29, the rats were killed and the liver was weighed and liver tumors were counted. The histological changes of liver tissue were observed under microscope, and the cellular dynamic parameters were studied by flow cytometry. Immunohistochemistry (two-step method) was used to observe the expression of vascular endothelial growth factor (VEGF) and micro-vessel density (MVD) on consecutive sections. The pathological parameters were also analyzed, the levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bilirubin (TBi), and direct bilirubin (DBi). RESULTS: The number of liver tumors decreased significantly in groups treated with As(2)O(3), especially in medium-dose (1 mg/kg) group (t = 2.80, P<0.01). As(2)O(3) caused HCC cell death via apoptosis; necrosis was seen and apoptosis was common when the dose was 1 mg/kg. Proliferation index decreased sharply in medium-dose (1 mg/kg) group (7.87+/-4.11 vs 24.46+/-6.49, t = 2087, P<0.01), but not in 0.2 mg/kg group. However, S-phase fraction decreased dramatically in both groups, it reached the bottom level only when the dose was 1 mg/kg compared with control (0.40+/-0.13 vs 3.01+/-0.51, t = 2.97, P<0.01), and it was obviously accompanied with accumulation of cells in G(0)/G(1) (G(0)/G(1) restriction). The expressions of VEGF and MVD in medium-dose (1 mg/kg) group were significantly lower than normal saline group (0.63+/-0.74 vs 2.44+/-0.88, P<0.05; 15.75+/-3.99 vs 47.44+/-13.41, t = 2.80, P<0.01). Compared with normal saline group, medium- and low-dose groups As(2)O(3) and matrine lowered the levels of ALT in serum (61.46+/-9.46, 63.75+/-20.40, 61.18+/-13.00 vs 108.98+/-29.86, t = 2.14, P<0.05), but had no effect on the level of serum AST, TBi, and DBi. CONCLUSION: As(2)O(3) had inhibitory effect on growth of experimental HCC in rats induced by 2-FAA, but had no obvious effect on normal hepatic cells. The mechanisms may involve decrease of cell division, accumulation of cells in G(0)/G(1) phase, apoptosis of tumor cells, and inhibitory effect on angiogenesis through blocking VEGF.
机译：目的：研究三氧化二砷（As（2）O（3））在2-乙酰氨基芴（2-FAA）诱导的实验性大鼠肝细胞癌（HCC）的治疗中的抗肝癌作用，并阐明可能的机制。方法：SD大鼠（2月龄）用2-FAA喂食8周诱导肝癌，然后用As（2）O（3）或苦参碱治疗。在第29天，处死大鼠并称重肝脏并计数肝肿瘤。在显微镜下观察肝组织的组织学变化，并通过流式细胞术研究细胞动力学参数。免疫组织化学（两步法）用于观察连续切片上血管内皮生长因子（VEGF）和微血管密度（MVD）的表达。还分析了病理参数​​，血清天冬氨酸转氨酶（AST），丙氨酸转氨酶（ALT），总胆红素（TBi）和直接胆红素（DBi）的水平。结果：As（2）O（3）治疗组的肝肿瘤数量明显减少，尤其是中剂量（1 mg / kg）组（t = 2.80，P <0.01）。 As（2）O（3）通过凋亡导致HCC细胞死亡；当剂量为1 mg / kg时，可见坏死并常见凋亡。中等剂量（1 mg / kg）组的增殖指数急剧下降（7.87 +/- 4.11 vs 24.46 +/- 6.49，t = 2087，P <0.01），而在0.2 mg / kg组则没有。然而，两组的S期分数均显着下降，仅在剂量为1 mg / kg时才达到最低水平（0.40 +/- 0.13对3.01 +/- 0.51，t = 2.97，P <0.01） ，并且显然伴随有细胞在G（0）/ G（1）中的积累（G（0）/ G（1）限制）。中剂量（1 mg / kg）组的VEGF和MVD表达明显低于生理盐水组（0.63 +/- 0.74 vs 2.44 +/- 0.88，P <0.05; 15.75 +/- 3.99 vs 47.44 + / -13.41，t​​ ＝ 2.80，P ＜0.01）。与生理盐水组相比，中，低剂量组As（2）O（3）和苦参碱降低了血清中的ALT水平（61.46 +/- 9.46、63.75 +/- 20.40、61.18 +/- 13.00与108.98 +/- 29.86，t = 2.14，P <0.05），但对血清AST，TBi和DBi的水平没有影响。结论：As（2）O（3）对2-FAA诱导的大鼠实验性HCC的生长具有抑制作用，但对正常肝细胞无明显作用。该机制可能涉及细胞分裂的减少，G（0）/ G（1）相中细胞的积累，肿瘤细胞的凋亡以及通过阻断VEGF对血管生成的抑制作用。

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