Zhai Zhen-guo, Jiang Han-dong, Qin Xiao-mei, Wang Chen
Beijing Institute of Respiratory Medicine-Beijing Chaoyang Hospital, Capital University of Medical Sciences, Beijing 100020, China.
Zhonghua Jie He He Hu Xi Za Zhi. 2004 Feb;27(2):97-100.
To study the effect of sulfate polysaccharide of algae (SPA) on lung carcinoma and it's mechanism.
(1) C57BL/6 mice implanted with Lewis lung carcinoma were used as experimental animal model. The mice were randomly divided into a control group, SPA groups (3 groups) and a FT-207 group. After inoculation with Lewis lung carcinoma, the control group was treated with NS, the 3 SPA groups were treated with SPA 20 mg, 40 mg, and 80 mg/kg respectively, and the FT-207 group with FT-207 150 mg/kg for 10 days. The inhibiting activity of SPA on Lewis lung carcinoma was assayed, and proliferation of A549 tumor cells treated with SPA was detected by MTT assay. (2) New Zealand rabbits were randomly divided into a control group, a SPA 500 mg/kg group and a CTX 100 mg/kg group. Serum pharmacological method, and both in vivo and in vitro anti-tumor experiments were used in the study. After incubating A549 with SPA containing serum at different concentrations, the growth and apoptosis of cells, cell cycle, apoptosis rate and expression of apoptosis associated genes such as p53 and bcl-2 were detected by flow-cytometric assay.
(1) SPA significantly inhibited the growth of implanted Lewis lung carcinoma in vivo and the effect had a dose dependent manner. The inhibitory rates of SPA on C57BL mice implanted Lewis lung carcinoma were 35.27% (P < 0.01), 48.29% (P < 0.01), and 65.41% (P < 0.01) respectively, which showed dose-dependent effects. SPA directly added to the culture medium neither induced A549 lung cancer cell apoptosis nor inhibited its proliferation in vitro. (2) SPA containing serum significantly induced A549 lung cancer cell apoptosis and inhibited its proliferation, with an increased expression of p53 and decreased expression of bcl-2 positive proteins, showing time and dose-dependent relationship.
SPA possessed remarkable inhibitory activity against lung neoplasia in animal models and lung cancer cell strain. The anti tumor activity of SPA was considered to be derived from apoptosis induction, which might be associated with the increased expression of p53 and decreased expression of bcl-2 positive proteins.
研究藻类硫酸多糖（SPA）对肺癌的作用及其机制。
（1）将接种Lewis肺癌的C57BL/6小鼠作为实验动物模型。小鼠随机分为对照组、SPA组（3组）和FT-207组。接种Lewis肺癌后，对照组给予生理盐水，3个SPA组分别给予20mg、40mg和80mg/kg的SPA，FT-207组给予150mg/kg的FT-207，连续给药10天。检测SPA对Lewis肺癌的抑制活性，采用MTT法检测经SPA处理的A549肿瘤细胞的增殖情况。（2）将新西兰兔随机分为对照组、500mg/kg的SPA组和100mg/kg的CTX组。采用血清药理学方法，进行体内外抗肿瘤实验。用不同浓度含SPA血清孵育A549细胞后，通过流式细胞术检测细胞的生长、凋亡、细胞周期、凋亡率以及凋亡相关基因如p53和bcl-2的表达。
（1）SPA显著抑制体内植入的Lewis肺癌生长，且呈剂量依赖性。SPA对C57BL小鼠植入Lewis肺癌的抑制率分别为35.27%（P<0.01）、48.29%（P<0.01）和65.41%（P<0.01），呈剂量依赖性。直接添加到培养基中的SPA在体外既不诱导A549肺癌细胞凋亡，也不抑制其增殖。（2）含SPA血清显著诱导A549肺癌细胞凋亡并抑制其增殖，p53表达增加，bcl-2阳性蛋白表达降低，呈时间和剂量依赖性关系。
SPA对动物模型肺癌和肺癌细胞株具有显著的抑制活性。SPA的抗肿瘤活性被认为源于诱导凋亡，这可能与p53表达增加和bcl-2阳性蛋白表达降低有关。
