Effects of Ganoderma lucidum polysaccharides on proliferation and cytotoxicity of cytokine-induced killer cells

AIM: To study the effects (and the mechanisms thereof) of Ganoderma lucidum polysaccharides (Gl-PS) on the proliferation and the anti-tumor activity of cytokine-induced killer (CIK) cells, and to make use of CIK cells as a means to investigate the interactions between Gl-PS and cytokines. METHODS: CIK cells were prepared by using the standard protocol as a positive control. Experimental groups also underwent the standard protocol, except that Gl-PS (400 mg/L or 100 mg/L) was added and the dose of anti-CD3 and interleukin-2 they received was reduced by 50% and 75%, respectively. For negative controls, Gl-PS in the experimental protocol was replaced with soluble starch or methylcellulose (400 mg/L or 100 mg/L). CIK cell proliferation, cytotoxicity, and phenotype were determined by using the Trypan blue exclusion method, MTT assay, and flow cytometry. RESULTS: By synergizing cytokines, Gl-PS (400 mg/L or 100 mg/L) could decrease the amount of cytokine in lymphokine activated killer (LAK) cells and CIK cells culture, but had no significant effect on the proliferation, cytotoxicity, or phenotype of LAK cells, or CIK cells induced by cytokines at higher doses alone, in which CIK cells expanded about 80-fold and the main effectors, CD3+NK1.1+ cells, expanded by more than 15%. The cytotoxicity of CIK cells in experimental groups was 79.3%+/-4.7%, 76.9%+/-6.8% versus the positive control 80.7%+/-6.8% against P815 (P>0.05) and 88.9%+/-5.5%, 84.7%+/-7.9% versus the positive control 89.8%+/-4.5% against YAC-1 (P>0.05). The activity of Gl-PS could mostly be blocked by anti-CR3. CONCLUSION: Gl-PS was shown to be a promising biological response modifier and immune potentiator. The effect of Gl-PS on CIK cells is possibly mediated primarily through complement receptor type 3.     

Ganoderma lucidum polysaccharides reduce methotrexate-induced small intestinal damage in mice via induction of epithelial cell proliferation and migration

Aim:

To study the effects of Ganoderma lucidum polysaccharides (Gl-PS) on methotrexate (MTX)-induced small intestinal damage in mice and the underlying mechanisms.

Methods:

BALB/c mice were used for in vivo study. The mice were administered with Gl-PS (50, 100, or 200 mg/kg, ig) for 10 d, and injected with MTX (50 mg/kg, ip) on d 7 and 8 to induce intestinal damage, and then sacrificed on d 11 for morphological study and tissue malondialdehyde (MDA) and superoxide dismutase (SOD) measurements. Before sacrificing, blood samples were collected to analyze immunoglobulin A (IgA). Rat intestinal IEC-6 cells were used for in vitro study. Cell proliferation and migration were assessed using MTT method and an in vitro wounding model, respectively. Transforming growth factor β (TGFβ) protein expression was determined using ELISA assay. Ornithine decarboxylase (ODC) and c-Myc mRNA expression profiles were determined using RT-PCR.

Results:

MTX treatment caused severe mucosal damage, significantly increased small intestine MDA levels, and decreased SOD and serum IgA levels in BALB/c mice. Gl-PS (100 and 200 mg/kg) markedly reversed the MTX effects. In IEC-6 cells, Gl-PS (0.1, 1, and 10 μg/mL) significantly stimulated the cell proliferation. Furthermore, Gl-PS (10 μg/mL) significantly stimulated the cell migration. In addition, Gl-PS (10 and 20 μg/mL) significantly increased the expression of ODC and c-Myc mRNAs. However, Gl-PS (up to 20 μg/mL) had no effect on the expression of TGFβ protein.

Conclusion:

The results suggest that Gl-PS protects small intestine against MTX-induced injury via induction of epithelial cell proliferation and migration.     

段木栽培及袋栽灵芝多糖对体外培养小鼠脾淋巴细胞增殖活性的比较

目的 比较段木栽培灵芝多糖(wood-cultured Ganoderma lucidum polysaccharides, GL-PS-WC) 及袋栽灵芝多糖(bag-cultured Ganoderma lucidum polysaccharides, GL-PS-BC)对体外培养小鼠脾淋巴细胞增殖活性的影响,探讨袋栽灵芝多糖替代段木栽培灵芝多糖的可能性。 方法检测两种灵芝多糖对混合淋巴细胞培养(MLC)反应的影响;观察对刀豆蛋白A (Con A)、细菌脂多糖(LPS)诱导淋巴细胞增殖的影响以及对环孢素A (CsA)、丝裂霉素C(Mit C)、足叶乙苷(VP-16) 等抑制MLC反应的影响。结果当质量浓度为0.2～12.8 mg·L^-1时,两种灵芝多糖均可促进MLC反应,增强Con A或LPS诱导的淋巴细胞增殖,并拮抗CsA, Mit C或VP-16对MLC反应的抑制作用。未发现两种多糖之间有显著性差异。结论GL-PS-WC及GL-PS-BC对体外培养脾淋巴细胞的增殖活性有类似作用。     

灵芝多糖对体外树突状细胞诱导细胞毒性T-淋巴细胞的调节作用(英文)

目的:研究灵芝多糖(Gl-PS)在抗原提呈阶段对体外培养树突状细胞(DC)诱导特异性细胞毒性T-淋巴细胞(CTL)功能的调节及其机制。方法:体外培养小鼠骨髓来源DC经P815肿瘤细胞冻融抗原冲击致敏,并与不同浓度Gl-PS(0.8,3.2,或12.8 mg/L)共培养。成熟DC与脾淋巴细胞共培养诱导P815特异性CTL生成。第5天收集各组悬浮细胞及培养上清,采用乳酸脱氢酶法比较CTL特异性杀伤活性;RT-PCR法测定T扰素γ(IFNγ)及颗粒酶B mRNA在CTL的表达;ELISA或Western blot法检测IFNγ或颗粒酶B蛋白的表达。结果:3种浓度的Gl-PS均可增高培养上清中释放的LDH活性(P<0.01);增加CTL表达IFN7及颗粒酶B mRNA(IFNγ:Gl-PS 12.8 mg/L组与RPMI-1640组,P<0.05;颗粒酶B:P<0.01);促进CTL培养上清中IFNγ蛋白生成(P<0.05)以及CTL表达颗粒酶B蛋白(Gl-PS 12.8 mg/L组与RPMI-1640组,P<0.05)。结论:Gl-PS可在抗原提呈阶段促进P815肿瘤冻融抗原冲击致敏DC所诱导的特异性CTL的杀伤活性,其机制可能是通过IFNγ及颗粒酶B途径的调节。     

灵芝多糖肽对自由基所致的腹腔巨噬细胞早期损伤的影响

目的　以膜电位方法进一步研究灵芝多糖肽(GLPP)对自由基损伤的巨噬细胞线粒体的影响。方法　以叔丁基氢过氧化物(tBOOH)为氧化剂,建立小鼠巨噬细胞体外氧化损伤模型,以罗丹明1 2 3(Rh1 2 3 )为荧光染色剂,以激光共聚焦显微镜检测细胞线粒体膜电位改变。结果　tBOOH氧化剂可损伤线粒体膜,使线粒体膜电位降低,GLPP体内( 1 0 0mg·kg- 1 ig 5d)及体外给药(GLPP 1 0mg·L- 1)均可对抗tBOOH自由基损伤,可使因自由基损伤而降低的巨噬细胞线粒体膜电位恢复。结论　GLPP体内体外给药可减轻自由基损伤,使损伤的线粒体膜电位恢复     

灵芝多糖对小鼠腹腔巨噬细胞活性氧自由基的影响

为进一步探讨灵芝多糖 ( GLP)免疫调节作用机理 ,采用激光扫描共聚焦显微镜技术 ,动态监测灵芝多糖均一体 GLB7对小鼠腹腔巨噬细胞 ( M )活性氧自由基含量的影响 .以 GLB7( 2 0 mg· L-1)刺激 M ,发现探针 DCHF- DA的荧光强度明显下降 ,与静息水平相比 ,平均下降 ( 36± 6) % ( n=6,P<0 .0 5) ;同时还能拮抗 PMA引起的 M 呼吸爆发 ,荧光强度下降幅度为 ( 1 9± 4) % ( n=6,P<0 .0 5) .结果证明 :GLB7能减少 M 内活性氧自由基的生成 ,具有清除活性氧的作用 ,这也是 GLB7产生免疫增强和抗衰老作用的重要途径 .     

灵芝菌丝体多糖对K562细胞的抑制作用及免疫调节作用研究

目的研究灵芝菌丝体多糖（ganoderma lucidum mycelia polysaccharides,GLMP）对K562白血病细胞及小鼠体外脾淋巴细胞增殖的影响。方法 MTT法检测不同浓度GLMP对K562白血病细胞增殖及对小鼠体外脾淋巴细胞增殖的作用;血细胞计数方法绘制生长曲线。结果不同浓度的GLMP处理K562细胞48h后,50mg/L及以上浓度抑制率与对照组比较差异有统计学意义（P〈0.01）,而且随浓度的增加抑制率增加。作用48h的IC50为270.2mg/L。生长曲线也表明随时间的延长和浓度的增加,细胞增殖能力下降。GLMP作用小鼠体外脾淋巴细胞48h后,在多糖浓度为50、100mg/L和25、50、100mg/L时能显著刺激静止性和激活型细胞的增殖。结论 GLMP可以抑制K562白血病细胞增殖而且具有免疫调节能力。     

灵芝多糖对大鼠胰岛细胞分泌胰岛素功能的影响

目的 :探讨灵芝多糖 (Gl PS)对胰岛细胞分泌胰岛素的影响。方法 :分离大鼠胰岛细胞 ,分别观察在葡萄糖为 5 .6和 1 6.7mmol·L- 1 时 ,Gl PS对胰岛细胞分泌胰岛素的影响。进一步加入不同的抑制剂观察Gl PS对胰岛细胞分泌胰岛素的影响。采用Westernblotting观察Gl PS对胰岛细胞葡萄糖转运蛋白 2 (GLUT2 )表达的影响。结果 :在 5 .6mmol·L- 1葡萄糖时 ,1 0 0mg·L- 1 的Gl PS可明显促进胰岛细胞胰岛素的分泌 ;当葡萄糖浓度为 1 6.7mmol·L- 1 时 ,5 0和 1 0 0mg·L- 1 的Gl PS均可明显促进胰岛细胞胰岛素的分泌。维拉帕米或维拉帕米 +EGTA均可显著抑制 5 .6和 1 6.7mmol·L- 1 葡萄糖时胰岛素的分泌 ,维拉帕米只能部分抑制Gl PS的促胰岛素分泌作用 ,而维拉帕米 +EGTA则可完全抑制Gl PS的这种作用。在葡萄糖浓度为 5 .6和 1 6.7mmol·L- 1 时 ,Gl PS 5 0和 1 0 0mg·L- 1 均能明显促进胰岛细胞GLUT2的蛋白表达。结论 :Gl PS可能通过促进胰岛细胞GLUT2蛋白的表达从而有助于葡萄糖转运入B细胞 ,促进葡萄糖的代谢 ,引起胰岛细胞外Ca2 + 内流而起到促胰岛素释放的作用     

党参白术提取物分别和合用诱导IEC-6细胞增殖分化的作用

目的　观察党参提取物 (D h)和白术提取物 (B t)对小肠隐窝细胞 (IEC 6 )增殖、分化的作用及其二者配伍对IEC 6细胞增殖的影响。方法　IEC 6细胞培养 2 4h ,加入不同剂量的D h、B t及二者的配伍溶液 ,2 4h后用MTT法观察细胞增殖 ,显微镜观察细胞分化的形态特征。结果　D h在 2 5 0mg·L-1以下剂量时对细胞增殖无影响 ,剂量提高到 5 0 0mg·L-1和 10 0 0mg·L-1时 ,明显促进细胞的增殖。B t各剂量均无促进细胞增殖的作用 ,在 5 0 0mg·L-1和10 0 0mg·L-1剂量时 ,细胞增殖反见减弱。二药配伍后 ,促进细胞增殖的作用明显增强 ,具有一定的剂量依赖关系 ,其效果优于D h ;IEC 6细胞在B t作用下 ,分化程度增高 ,低倍镜下细胞呈典型的上皮细胞形态 ,细胞排列呈条索状 ,部分呈腺管状排列。高倍镜下可观察到隐约有细胞连接样结构 ,上皮细胞似有微绒毛形成的趋势。D h处理的细胞分化程度较低 ,镜下所见多为未分化的梭状细胞 ,且排列不规则 ,无任何形成腺管的趋势和有细胞连接样结构。结论　D h能促进细胞增殖 ,B t可促进细胞分化 ,二者配伍后促进细胞增殖作用明显增强 ,有协同作用     

唐古特大黄多糖促进IEC-6细胞增殖、移行作用及其可能的机制研究

目的观察唐古特大黄多糖组分之一(RTP1)对大鼠小肠隐窝上皮细胞株(IEC-6)细胞增殖、移行及其对细胞内鸟氨酸脱羧酶(ODC)活性和ODC蛋白表达的影响,观察其对胃肠黏膜的修复作用并探讨可能的机制。方法采用MTT法和体外肠上皮细胞移行模型,观察不同剂量的RTP1(10、30、100mg·L-1)处理IEC-6细胞24h后,细胞增殖和移行情况;Western blot检测ODC蛋白表达;通过测定L-[1-14C]鸟氨酸释放14CO2的量来检测ODC活性变化。结果RTP1在10、30、100mg·L-1时均可明显促进IEC-6细胞的增殖和移行,可增加ODC蛋白表达和ODC活性,并具有剂量依赖性,与空白对照组相比差异具有显著性(P<0·05或0·01)。结论RTP1可促进肠上皮细胞的增殖和移行,提示RTP1可能对肠黏膜的损伤修复具有直接作用。其作用机制可能与鸟氨酸脱羧酶表达增加和(或)活性增大有关。     

高效液相色谱法检测小肠上皮细胞多胺含量

目的建立检测小肠上皮细胞(IEC-6)多胺含量的方法,为病理生理及药理研究中检测该细胞多胺含量提供参考。方法采用苯甲酰氯柱前衍生反相高效液相色谱法,以多胺(腐胺、精脒和精胺)含量为指标,苯甲酰氯为衍生化试剂,采用ODS-C18柱,考察和优化衍生化条件以及色谱条件。结果当衍生温度为50℃,衍生时间为8 h时,各指标成分的峰面积均较大;在柱温为25℃、流动相为甲醇∶水(55∶45)、流速1.0 ml.min-1、检测波长234 nm的条件下,各指标成分峰分离良好。线性范围:腐胺0.054～1.35 nmol,精脒0.046～1.15 nmol,精胺0.080～2.00 nmol,r2≥0.9995;高、中、低浓度的日内精密度:腐胺RSD 1.5%～3.2%,精脒RSD 1.2%～4.5%,精胺RSD 1.3%～4.1%;日间精密度:腐胺RSD 1.2%～2.7%,精脒RSD 1.0%～3.5%,精胺RSD0.8%～3.9%;高、中、低浓度的回收率:腐胺85%～110%,精脒88%～110%,精胺90%～108%。结论建立的苯甲酰氯柱前衍生高效液相色谱法适用于小肠上皮细胞中多胺含量的测定。     

灵芝孢子粉对癫痫大鼠皮质和海马区NMDAR1免疫反应影响的研究

目的:观察灵芝孢子粉对癫痫大鼠模型皮质和海马区NMDAR1含量及神经元形态学的影响,探索癫痫发病机制以及灵芝孢子粉对癫痫的干预作用.方法:采用戊四氮(PTZ)腹腔注射制作Wistar大鼠慢性点燃模型,并将其分为空白对照组、癫痫模型组和灵芝孢子粉干预组,点燃后断头取脑,行免疫组化染色观察NMDAR1含量的变化及神经元形态学的改变.结果:所有大鼠均达到癫痫模型点燃标准.使用灵芝孢子粉的中药干预组与癫痫模型组相比,脑内NMDAR1含量明显下降(P<0.05),同时神经元形态学改变明显好转.结论:灵芝孢子粉能够有效降低皮质和海马区兴奋性氨基酸受体NMDAR1的含量,使神经元兴奋性减弱,抑制癫痫的发作,从而减轻癫痫发作给神经系统带来的损伤, 以达到抗癫痫作用.所以灵芝孢子粉可能具有减轻痫性发作、保护神经元的作用.     

灵芝孢子粉抑制人卵巢癌细胞增殖及诱导凋亡的体外研究

目的研究灵芝孢子粉对人卵巢癌OV2008细胞增殖及凋亡的影响,并探讨其作用机制。方法采用WST-1比色法及显微镜观察法研究灵芝孢子粉对OV2008细胞生长抑制作用及细胞形态的改变;流式细胞仪检测细胞周期分布情况;Hoechst-33258染色方法评估细胞凋亡并采用western blot方法测定凋亡相关蛋白的表达。结果 WST结果表明灵芝孢子粉可以抑制OV2008细胞的生长,并呈剂量和时间依赖性;流式细胞术结果提示灵芝孢子粉可使卵巢癌细胞生长阻滞于G1期。Hoechst-33258染色结果显示灵芝孢子处理细胞后可以检测出凋亡细胞。Western blot方法检测到凋亡抑制蛋白bcl-2、bcl-xl随灵芝孢子浓度增加而下降,而促凋亡蛋白bax及P27、casep具有抑制卵巢癌细胞生长及诱导凋亡的作用,其机制是作用于细胞周期的ase-3逐渐升高。结论灵芝孢子粉可以抑制卵巢细胞生长,使细胞生长阻滞于G1期,并可以通过上调bax、P27,下调bcl-2并活化casepase-3而发挥其作用。     

Polysaccharides isolated from Ganoderma lucidum occurring in Southern parts of India, protects radiation induced damages both in vitro and in vivo

The in vivo and in vitro radioprotective property of the polysaccharides isolated from Ganoderma lucidum were determined by survival studies, induction of micronucleus in reticulocytes of mice, strand breaks in plasmid pBR322 DNA and inhibition of lipid peroxidation (TBARS assay). Polysaccharides were administered as a single dose after whole body exposure to 10 Gy ⁶⁰Co γ-radiation to Swiss albino mice. At a dose of 500 μg/kg body wt, the polysaccharides were most effective in protecting animals from radiation induced loss of lethality. Administration of 500 μg/kg body wt to animal exposed to 10 Gy gamma radiation resulted in more than 60% survival on the 30th day compared to the dose of 300 mg/kg/body wt administration of amifostine, a clinically used radioprotective drug. The induction of micronuclei was reduced by the administration of polysaccharides. The decrease in micronuclei induction was dose dependent. Thus following 4 Gy exposure the micronuclei in polychromatic erythrocytes (MNCE) was reduced from 28.16 ± 3.049 to 16.0243 ± 2.074 and 6.30 ± 2.422 by polysaccharides at doses of 250 μg/kg body wt and 500 μg/kg body wt, respectively, and to 10.4 ± 2.581 by amifostine at a dose of 300 mg/kg body wt. The results indicate the significant protective effect of Ganoderma polysaccharides against radiation induced damages. The findings thus suggest the potential use of Ganoderma polysaccharides as novel radioprotective agent.     

灵芝多糖体外对小鼠脾细胞IL-2,IL-3 mRNA表达的影响

目的观察灵芝多糖体外对小鼠脾细胞ＩＬ－２、ＩＬ－３ｍＲＮＡ的表达水平是否有影响。方法逆转录多聚酶链式反应（ＲＴ－ＰＣＲ）检测ｍＲＮＡ表达，凝胶图象光密度分析系统进行相对定量。结果在原代小鼠脾细胞培养开始时加入不同浓度的灵芝多糖ＧＬＢ７（５，１０，２０，４０ｍｇ·Ｌ－１），培养１２ｈ及２１ｈ后观察ＧＬＢ７与ＩＬ－２及ＩＬ－３ｍＲＮＡ表达水平之间的量效关系。发现在一定范围内，随着ＧＬＢ７浓度的升高，ＩＬ－２及ＩＬ－３ｍＲＮＡ表达水平也相应提高，对ＩＬ－２ｍＲＮＡ的提高率分别为１０．４％，２１．９％，３７．８％，４６．６％；对ＩＬ－３ｍＲＮＡ的提高率分别为１５．４％，３５．２％，５２．４％，７４．５％。１９９８－０４－０８收稿，１９９８－０７－２６修回＊国家自然科学基金资助课题，Ｎｏ３９４００１６５作者简介：王庆彪，男，２６岁，硕士；雷林生，男，３８岁，医学博士，副教授培养１２ｈ和３０ｈ的上清液中ＩＬ－２样活性及ＩＬ－３样活性处理组与对照组相比亦有明显升高，且有一定的浓度依赖关系。结论灵芝多糖的免疫增强作用与其在转录水平上促进ＩＬ－２及ＩＬ－３ｍＲＮＡ的表达有关     

肉灵芝提取物调控长链非编码RNA BRCA1相邻基因2/双特异性磷酸酶4/细胞外信号调节激酶通路对肝癌细胞Hep3B增殖及凋亡的影响

目的 探讨肉灵芝提取物是否可通过长链非编码RNA BRCA1相邻基因2(LncRNA NBR2)/双特异性磷酸酶4/细胞外信号调节激酶(DUSP4/ERK)通路而影响肝癌HepB细胞增殖及凋亡。方法 体外培养肝癌HepB细胞,分为1 mg/L肉灵芝提取物组、2 mg/L肉灵芝提取物组、4 mg/L肉灵芝提取物组、si-NC组、si-LncRNA NBR2组、pcDNA-NC组、pcDNA-LncRNA NBR2组、肉灵芝提取物+si-NC组、肉灵芝提取物+si-LncRNA NBR2组;采用MTT检测肝癌HepB细胞增殖;流式细胞术检测肝癌HepB细胞凋亡;RT-qPCR检测LncRNA NBR2的表达量;蛋白质印迹法(Western blotting)检测增殖细胞核抗原(PCNA)、活化的含半胱氨酸的天冬氨酸蛋白水解酶3(Cleaved-caspase-3)、DUSP4、p-ERK蛋白表达量。结果 肉灵芝提取物可明显降低肝癌HepB细胞增殖率与PCNA、DUSP4、p-ERK蛋白水平(P<0.05),提高肝癌HepB细胞凋亡率、Cleaved-caspase-3蛋白水平及Lnc...     

松杉灵芝菌丝体多糖(FI_0-b)对人组织瘤细胞和人外周血白细胞产生炎症性细胞因子的影响(Ⅰ)(英文)

目的:比较研究松杉灵芝水溶性多糖(Fl_0-b)及其甲酸修饰产物(FI_0-b-H)对人炎症性细胞因子产生的影响.方法:用放射免疫分析法(RIA)及逆转录聚合酶链反应(RT-PCR)分析法研究FI_0-b和Fl_0-b-H对人组织瘤细胞(THP-1)和人外周血单核细胞(PBMC)分泌的各种与炎症有关的细胞因子(白介素-1 α,6,8,肿瘤坏死因子α)及对白介素-1α,肿瘤坏死因子αmRNA表达的影响.结果:FI_0-b和FI_0-b-H(浓度分别为4,40,400 mg/L)显著抑制LPS 10 mg/L协同PMA 200 nmol/L诱导的THP-1细胞和PBMC细胞产生IL-1α和TNF α的量.当低浓度刺激剂(LPS 1mg/L协同PMA 200 nmol/L)刺激THP-1细胞时,FI_0-b-H明显提高白介素-8的产生;但当高浓度刺激剂(LPS 10 mg/L协同200 nmol/L PMA)刺激THP-1-细胞时,FI_0-b-H却明显抑制白介素-8的产生.FI_0-b-和FI_0-b-H对THP-1细胞白介素-1α和肿瘤坏死因子α的mRNA表达有显著作用.结论:与FI_0-b相比,FI_0-b-H在人炎症性细胞因子的产生方面表现出较强的活性.松杉灵芝菌丝体水溶性多糖在不同的刺激条件下,具有双向免疫调节作用,并具有一定的剂量依赖关系.     

Antioxidant activities of Ganoderma lucidum polysaccharides and their role on DNA damage in mice induced by cobalt-60 gamma-irradiation

In this study, the radio-protective effects of Ganoderma lucidum polysaccharides (GLP) were investigated in a mouse animal model exposed to (60)Co gamma-irradiation. Each of three batches of mice were divided into five groups (negative control, positive gamma irradiated control, and low, middle and high dosage GLP groups). Different batches of animals were used to evaluate the impact of GLP on peripheral white blood cell count, immune organ index; DNA damage, lipid peroxidation; micronuclei formation, and nucleated cell count in bone marrow induced by (60)Co gamma-irradiation. DNA strand-break and micronuclei frequency were significantly reduced and glutathione peroxidase activity and nucleated cell count in bone marrow were significantly increased by GLP treatment in a dose-dependent manner. GLP intervention also increased the activity of superoxide dismutase and decreased the level of malondialdehyde in middle and high GLP treatment groups. No adverse effects were observed on peripheral white blood cells and immune organ or body weight in either the control groups or GLP treated gamma exposed mice. These findings suggest that GLP possesses marked antioxidant capacity which plays an important role in the prevention of radiation damage in mice induced by (60)Co gamma-irradiation.     

唐古特大黄多糖促进肠上皮细胞的增殖、移行和分化

目的　观察唐古特大黄多糖对正常人肠上皮细胞(HIEC)增殖、移行和分化的影响,探讨其肠粘膜可能的修复机制。方法　HIEC细胞接种后24h,加入不同浓度的大黄多糖,加药后24h,MTT法观察细胞增殖情况,HE染色法和碱性磷酸酶活性的测定观察细胞分化情况,细胞接种后待长成单细胞层后,在细胞层上作一圆形损伤区,并加入大黄多糖,分别于加药后0、12、24、36、48h倒置显微镜下观察细胞移行情况并拍照,采用图像分析定量测定缺损区随时间变化的情况。结果　大黄多糖可剂量依赖性地促进HIEC细胞的增殖、移行和分化,与正常对照组比较,细胞增殖、移行以及碱性磷酸酶活性差异均具有显著性(P< 0 .05或P<0. 01)。结论　大黄多糖可能通过促进肠上皮细胞的增殖移行和分化来促进肠粘膜的损伤修复。