谷胱甘肽可拮抗环磷酰胺和丙烯醛诱导的小鼠PC3细胞毒性和免疫抑制作用。

X L Liu, K Chen, Y P Ye, X Y Peng, B C Qian
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引用次数: 0

摘要

目的:研究谷胱甘肽(GSH)对环磷酰胺(Cyc)和丙烯醛(Acr)诱导的PC3细胞毒性的拮抗作用及对Cyc引起的免疫抑制作用。方法:采用四氮唑(MTT)法和考马斯亮蓝法测定脾细胞、PC3细胞增殖及细胞蛋白含量。测定正常小鼠和s -180小鼠血清抗srbc溶血素、凝集素和脾细胞增殖。对肿瘤进行称重。结果:GSH 2 mmol预处理。L-1使脾细胞增殖抑制从18.64%、49.72%降低到6.78%、18.36% (Cyc 1、5 mmol.L-1诱导),PC3细胞增殖抑制从27.7%、45.3%、74.6%降低到14.6%、18.8%、49.1% (Cyc 1、3、5 mmol.L-1诱导),从62.6%、85.4%、90.6%降低到41.9%、57.7%、86.4% (Acr 10、25、50 mmol.L-1诱导)。正常小鼠,s.c.谷胱甘肽75或150毫克。kg-1次,每次服药后5天,周期40毫克。小鼠红细胞溶血素和脾细胞增殖均明显高于正常小鼠。公斤。s -180小鼠溶血素、血清凝集素和脾细胞增殖的变化。kg-1次,每次服药后10天,周期40毫克。kg-1也明显高于单剂量给予s -180的小鼠。但根据肿瘤重量,GSH不干扰s -180小鼠Cyc的抗肿瘤活性。结论:谷胱甘肽对Cyc和Acr均有保护作用,但对Cyc的抗肿瘤作用无影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Glutathione antagonized cyclophosphamide- and acrolein-induced cytotoxicity of PC3 cells and immunosuppressive actions in mice.

Aim: To study the antagonistic effect of glutathione (GSH) on toxicity of PC3 cell induced by cyclophosphamide (Cyc) and acrolein (Acr) and on immunosuppressive actions caused by Cyc.

Methods: Splenocyte, PC3 cell proliferation and cell protein content were measured by tetrazolium (MTT) assay and Coomassie brilliant blue assay. Serum anti-SRBC hemolysin, agglutinin, and splenocyte proliferation were measured in normal and S-180-bearing mice. Tumors were weighed.

Results: Pretreatment with GSH 2 mmol.L-1 reduced splenocyte proliferation inhibition from 18.64%, 49.72% to 6.78%, 18.36% (induced by Cyc 1, and 5 mmol.L-1), and PC3 cell proliferation inhibition from 27.7%, 45.3%, and 74.6% to 14.6%, 18.8%, and 49.1% (induced by Cyc 1, 3, and 5 mmol.L-1), and from 62.6%, 85.4%, and 90.6% to 41.9%, 57.7%, and 86.4% (induced by Acr 10, 25, and 50 mumol.L-1), respectively. In normal mice, s.c. GSH 75 or 150 mg.kg-1 b.i.d. x 5 d after i.p. Cyc 40 mg.kg-1, the hemolysin and the splenocyte proliferation were higher than those in normal mice i.p. Cyc 40 mg.kg-1 alone. Hemolysin, serum agglutinin, and splenocyte proliferation in S-180-bearing mice given s.c. GSH 150 mg.kg-1 b.i.d. x 10 d after i.p. Cyc 40 mg.kg-1 were also markedly higher than those in S-180-bearing mice given i.p. Cyc alone. But, according to tumor weight, GSH did not interfere the antitumor activity of Cyc in S-180-bearing mice.

Conclusion: GSH exhibited protective effects against Cyc and Acr, but had no effect on the antitumor action of Cyc.

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