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目的研究红芪总多糖(THPS)单用及与环磷酰胺(CTX)合用对荷瘤小鼠的抑瘤作用,并探讨其机制。方法昆明种小鼠90只,随机分10只为正常对照组,其余80只小鼠接种S180瘤株后随机分为荷瘤对照组、CTX组、THPS高、中、低剂量[400、200、100mg/(kg.d)]组及各与CTX合用组共8组。正常对照组和荷瘤对照组给予生理盐水,其余各组给予相应剂量THPS及CTX治疗,观察肿瘤的体积变化。14d后处死小鼠,观察瘤质量、抑瘤率;血球计数仪检测外周血白细胞、血小板、红细胞及血红蛋白;流式细胞仪检测CD3+T细胞和NK细胞。结果与荷瘤对照组相比,中剂量THPS明显抑制小鼠S180瘤质量增长(P<0.01)及体积增加(P<0.05),提高NK细胞水平(P<0.05)。与CTX组相比,THPS与CTX合用后,各剂量组均能明显抑制CTX所致的白细胞数量下降(P<0.01);而只有中剂量的THPS与CTX合用能够降低肿瘤的质量(P<0.05),并能明显抑制CTX所致的CD3+T细胞(P<0.01)和NK细胞(P<0.05)数量下降。结论中剂量的THPS能抑制S180瘤生长,具有降低CTX免疫抑制和骨髓抑制的作用,其机制与提高T细胞和NK细胞介导的免疫应答有关。
Objective To study the antitumor effect of total polysaccharide of Radix Hedysari (THPS) alone and combined with cyclophosphamide (CTX) on tumor-bearing mice and its mechanism. Methods Ninety Kunming mice were randomly divided into 10 normal control groups. The remaining 80 mice were randomly divided into tumor-bearing control group, CTX group, high, medium, low dose [400, 200, 100mg / (kg.d)] group and each with CTX combined group of 8 groups. The normal control group and the tumor-bearing control group were given normal saline, and the rest groups were given the corresponding dose of THPS and CTX treatment to observe the tumor volume changes. The mice were killed after 14 days, and the tumor mass and tumor inhibition rate were observed. The white blood cells, platelets, erythrocytes and hemoglobin were detected by hemacytometer. CD3 + T cells and NK cells were detected by flow cytometry. Results Compared with the tumor-bearing control group, the medium dose of THPS significantly inhibited the growth of S180 tumor (P <0.01) and increased the volume (P <0.05), and increased the level of NK cells (P <0.05). Compared with CTX group, CTX-induced leukocyte count decreased significantly (P <0.01) in THX group and CTX group, while only moderate-dose THPS combined with CTX reduced tumor mass (P <0.05) ), And significantly inhibited the decrease of CTX-induced CD3 + T cells (P <0.01) and NK cells (P <0.05). Conclusions The moderate dose of THPS can inhibit the growth of S180 tumor, and has the effect of decreasing CTX immunosuppression and myelosuppression. The mechanism is related to the enhancement of T cell and NK cell mediated immune response.