L1210克隆细胞肿瘤动物模型生物学特性研究

目的　对L12 10细胞及其 4株克隆细胞建立的肿瘤动物模型的某些生物学特性进行比较研究 ,从中筛选出基本符合L12 10细胞生物学特性且一致性更好的克隆细胞。方法　北京肿瘤所L12 10细胞和 4株克隆细胞腹腔接种DBA 2小鼠 ,观察产生腹水的性质、腹水瘤细胞浓度和致小鼠死亡时间 ;皮下接种DBA 2小鼠 ,观察瘤块的生长情况 ;腹腔注射化疗药物环磷酰胺 (CY) ,比较对CY治疗的敏感性。结果　腹腔接种DBA 2小鼠均能生长腹水 ,其中克隆细胞L2H8、L3B12产生血性腹水 ,L3F9的腹水微血性 ,L3E11与肿瘤所L12 10细胞为无血性腹水 ;腹水瘤细胞的浓度及小鼠生存时间亦有差别。肿瘤所L12 10细胞及克隆细胞L3F9、L2H8、L3E11、L3B12第 10天瘤重依次为 1 9± 0 4 6、1 5± 0 3 8、0 75± 0 5 2、2 6± 0 3 0、2 0± 0 3 3g ;用CY治疗的抑瘤率分别是 4 8 7% ,81 3 % ,86 0 % ,78 7%及 67 1%。结论　 4株克隆细胞的生物学特性基本符合L12 10细胞 ,对化疗药物CY的敏感性均高于L12 10细胞     

香菇C91-3菌LP1蛋白在小鼠体内的 抗肿瘤免疫作用

目的通过观察注射C91-3菌LP1蛋白对H22荷瘤小鼠的影响,探讨LP1蛋白在小鼠体内的抗肿瘤免疫作用。方法使用鼠肝癌H22细胞接种于BALB/C小鼠右腋下,建立小鼠H22实体瘤模型。取上述建立成功的H22实体瘤模型小鼠64只,体重20~25g;分为A、B两组,每组32只。A组再分为LP1实验Ⅰ组(300μg/只)、LP1实验Ⅱ组(100μg/只)、PBS对照组和顺铂对照组(4 mg/kg),每组8只,各组隔日给药1次,共给药5次。A组用于检测LP1蛋白作用后在小鼠体内对H22肿瘤的抑瘤作用、血清中IL-2含量以及脾中NK细胞活性等生理指标。B组按同样的方法分组,隔日给药1次,直至荷瘤小鼠死亡,记录各组小鼠的生存期,计算生命延长率。结果 LP1蛋白可以延长H22荷瘤小鼠的生存期,LP1实验组生存期达16.6d,较PBS对照组13.2d有明显提高。LP1蛋白在体内对H22实体瘤具有一定的抑制作用,对H22实体瘤进行病理切片、HE染色观察后发现,LP1实验组中H22肿瘤组织较PBS对照组肿瘤组织内出现炎性细胞浸润,局部可见坏死现象。使用ELISA法和LDH法分别检测H22荷瘤小鼠血清中IL-2含量以及NK细胞活性,发现LP1实验组IL-2水平和NK细胞活性较PBS对照组和顺铂对照组显著提高。结论 LP1蛋白可延长H22荷瘤小鼠的生存期限,提高小鼠的生存质量,具有一定的肿瘤抑制作用。其抑制作用主要是由增强H22荷瘤小鼠自身免疫力,提高NK细胞活性,发挥机体自身肿瘤免疫功能造成的。     

珍奥酵母核酸对环磷酰胺致小鼠免疫功能低下的影响

目的 通过环磷酰胺致小鼠免疫功能低下,建立BALB/C小鼠免疫功能低下模型,评价珍奥酵母核酸对小鼠免疫功能低下的作用.方法 选用BALB/C小鼠,随机分组,分别给予相应的处理,选择T淋巴细胞亚群CD69+/CD3+比值、NK细胞亚群CD69+/NKG2D+比值、淋巴细胞转化率及血清IL-2含量作为细胞免疫的指标.结果 核酸各剂量组和添加剂组均可使免疫低下小鼠外周血和脾的T淋巴细胞亚群CD69+/CD3+比值、NK细胞亚群CD69+/NKG2D+比值提高,同时可提高免疫低下小鼠淋巴细胞转化率及IL-2水平,尤以高、中剂量核酸组和添加剂组明显(P＜0.05).结论 珍奥酵母核酸可以提高免疫低下小鼠的免疫功能,以其为珍奥酵母核酸的临床应用及提高机体免疫力提供了实验依据.     

黄芪多糖的分离及其免疫活性的研究

本文报道了黄芪多糖的分离纯化方法、理化性质、组成并进行免疫作用的研究,黄芪水提,经732(H~+)树脂初步纯化,得粗多糖,再经超滤,Sephadex G-150,透析等方法进一步纯化,得白色粉末状多糖M wt:37500。证明为α-糖甙键连接,水解多糖检出葡萄糖、半乳糖和阿拉伯糖,克分子比为:葡萄糖:半乳糖:阿拉伯糖=1:0.95:0.70。体外试验结果表明:(1)黄芪多糖可刺激小鼠脾细胞增殖,但与ConA联合刺激脾细胞时,未见有协同作用;(2)未见黄芪多糖有诱生脾细胞IL-2的作用;(3)黄芪多糖和IL-2均能增加人体LAK细胞活性,且两者合用,效果更佳,体内试验结果表明:(1)黄芪多糖可促使小鼠外周血白细胞数量增加,并且能完全纠正环磷酰胺引起的白细胞数量下降;(2)黄芪多糖对体内淋转无明显促进作用,但对CY所致免疫功能低下有一定的纠正作用;(3)黄芪多糖可增强NK细胞活性,并可完全纠正CY引起的免疫功能低下;(4)黄芪多糖可促进1g G的产生,与PWM无协同作用。     

板蓝根多糖体内抗肿瘤作用与免疫功能调节实验研究

本研究主要探讨板蓝根多糖(RIP)对荷瘤小鼠的抗肿瘤作用及其对免疫功能的影响。通过建立S180小鼠移植瘤和腹水瘤模型,以环磷酰胺(CTX)为阳性对照药,观察RIP对其的影响。连续给药12 d后,测定移植瘤小鼠的瘤重,计算肿瘤生长抑制率和胸腺、脾脏指数;检测脾淋巴细胞的转化功能和NK细胞杀伤活性以及血清中的TNF-α、INF-γ、IL-2水平;并对肿瘤组织进行HE染色和细胞周期分析;对进行相同给药周期的腹水瘤小鼠继续正常饲养,记录各组小鼠自然死亡的时间。结果显示,不同剂量的RIP均可明显抑制小鼠肿瘤的生长,其100 mg/kg和50 mg/kg剂量组的抑瘤率分别为35.4%,38.5%;各剂量组移植瘤小鼠胸腺指数和脾指数与对照组比较有所提高,还能刺激脾淋巴细胞的转化及增强NK细胞的杀伤活性,升高血清中TNF-α、INF-γ和IL-2的含量,其50 mg/kg组与模型对照组相比有统计学差异(P0.01)。此外,移植瘤组织HE染色观察可见各给药组肿瘤组织坏死面积呈不同比例增大,流式细胞仪检测出给药后G_0/G_1期细胞比例增加,S期细胞比例降低,G_2/M期细胞周期未见明显变化。由此提示,RIP能够增强荷瘤小鼠的免疫功能,对荷瘤小鼠具有抗肿瘤作用,能延长荷瘤小鼠的生存时间。     

益气补肾方药对肾虚小鼠细胞因子IL-1、IL-2及IL-12基因表达的影响

目的　探讨益气补肾中药对醋酸可的松致肾虚小鼠腹腔巨噬细胞IL 1及脾脏细胞因子IL 2、IL 12活性及脾脏IL 1、IL 2、IL 12mRNA表达的影响。方法　用醋酸可的松制备肾虚动物模型 ,经益气补肾方药灌胃给药 6周后 ,生物学方法观察腹腔巨噬细胞IL 1、脾脏淋巴细胞IL 2、IL 12的活性水平 ,RT PCR方法观察脾脏IL 1、IL 2及IL 12mRNA的表达。结果　模型动物IL 1、IL 2及IL 12的活性水平较正常小鼠下降 ,其mRNA表达均受到抑制 ,与正常对照组比差异显著 (P <0 0 5 ) ;经益气补肾方药治疗后 ,三种细胞因子活性水平及其mRNA表达均有不同程度的提高。结论　益气补肾方药可能是改善外源糖皮质激素所致肾虚及由此而导致的免疫衰老较理想的方法     

双歧杆菌总DNA对小鼠IL-2、NK活性影响的研究

目的　从双歧杆菌、大肠杆菌提取 DNA,用 DNA免疫小鼠 ,观察免疫功能的变化 ,探讨双歧杆菌 DNA对小鼠免疫功能的影响 ,并作对比研究。方法　肌肉注射提取的双歧杆菌 DNA、大肠杆菌 DNA,颈椎处死后 ,检测脾细胞的免疫功能 ,同时提取 IEL细胞与 DNA共孵育 ,检测它对 IEL细胞的激活情况及细胞因子产生情况 ,以自然杀伤细胞 (NK)活性 ,白细胞介素 2 (IL - 2 )产生能力为指标 ,测定小鼠上述各项指标变化。结果　双歧杆菌 DNA、大肠杆菌 DNA肌肉注射后 ,小鼠以上两项指标与相应对照组相比较均明显提高 (P<0 .0 5 )。双歧杆菌 DNA提高小鼠 NK活性与 IL - 2水平程度大于大肠杆菌 DNA的作用(P<0 .0 1)。结论　双歧杆菌 DNA可快速激活 NK活性 ,提高体内 IL - 2水平。其效能优于大肠杆菌DNA。     

大豆提取物（CKBN）对免疫低下小鼠免疫功能的影响

目的观察大豆提取物（CKBN）对免疫低下小鼠免疫功能的影响。方法腹腔注射环磷酰胺（cyclophosphamide,CTX）建立免疫功能低下小鼠模型,观察1、25、50、100 mg/kg剂量CKBN对免疫低下小鼠免疫功能的影响。结果25 mg/kg组的CKBN可显著增加免疫低下小鼠的脾指数;25、50、100 mg/kg组均能明显抑制环磷酰胺对小鼠外周血白细胞数量的影响,1 mg/kg组可显著提高单核细胞百分率,50 mg/kg组可显著提高中性粒细胞百分率;100 mg/kg组的IgG2a水平高于环磷酰胺组;1、25、50 mg/kg可显著提高腹腔巨噬细胞的吞噬功能;25 mg/kg组可显著提高NK细胞杀伤活性。结论CKBN能显著增强CTX造成的免疫低下小鼠的免疫功能。     

不同来源H22细胞株的生物学特性比较研究

目的　对不同研究单位保存的小鼠肝癌H2 2 细胞株的基本生物学特性进行比较研究。方法　从国内3个不同研究单位 (武汉大学典型培养物保藏中心 ,山东省医学科学院药物研究所以及中国医学科学院药物研究所 )引进小鼠肝癌H2 2 瘤株 (分别简称武汉H2 2 、山东H2 2 、北京H2 2 ) ,KM小鼠腹腔传代 ,然后对其体外培养特性、体内生长特征、病理形态、治疗学特征进行了比较分析。结果　 3株H2 2 细胞在体内、体外生长速度明显不同 ,武汉H2 2 生长速度较其他瘤株快 (P <0 .0 1) ,接种一致性好 ;而山东H2 2 则在 10 4 个细胞 只小鼠时即可接种成功。荷瘤小鼠体内未发现明显转移灶 ,但肿瘤形态各不相同。环磷酰胺治疗时 ,山东H2 2 抑瘤率最高为 74 6%。结论　不同研究单位H2 2 瘤株的生物学特性有很大不同 ,虽为同一起源 ,但经不同单位保存使用一定时间后 ,它们之间的生物学特性已存在较大的差异     

人IL-12和B7-1基因对HuPBL-SCID小鼠模型中人源肿瘤的协同抑制作用

人IL 12 (hIL 12 )对鼠源的免疫细胞作用较弱 ,进行hIL 12抗瘤研究缺乏有效的动物模型。为此利用荷人瘤的HuPBL SCID小鼠模型 ,将改良的Winnassay细胞免疫功能分析方法应用于评价hIL 12和hB 1协同抗瘤作用。用商业化的非脂质转基因试剂配制单独的hIL 12、hB7 1或hIL 12联合hB7 1的基因转染液。将上述三种基因转染液分别瞬时转基因入人恶性黑色素瘤A375细胞 ,转基因 30min后 ,按组别 (hIL 12组、hB7 1组、hIL 12 hB7 1组、rhIL 2对照组、HuPBL对照组和肿瘤对照组 )同人外周血淋巴细胞混合接种于SCID小鼠皮下 ,2 0天后处死实验小鼠 ,测得hIL 12和hB7 1的抑瘤率分别为 74 .0 6 %和 6 6 .98% ,联合作用达 93.4 0 % ,rhIL 2和HuPBL对照组无抗瘤作用。同时 ,在此模型上hIL 12联合hB7 1基因对人大肠癌LoVo和人肺癌SPC的抑制率分别为 98.37%和 97.39%。实验建立的各组HuPBL SCID小鼠 2 0天的外周血都含有人IgG(>0 .5mg/L)和极少量人CD3 淋巴细胞 (>0 .5个 /10 0个有核细胞 )。hIL 12、hB7 1和hIL 12 hB7 1组的瘤灶内人淋巴细胞浸润生长 ,肿瘤细胞残存 ,而rhIL 2和HuPBL对照组的瘤灶内人淋巴细胞“似团样”生长 ,肿瘤生长旺盛。表明此HuPBL SCID小鼠模型上的抗瘤机制为局部免疫反应。结果表明以此动物模型可跨     

Improved therapeutic effects of interleukin 2 after the accumulation of lymphokine-activated killer cells in tumor tissue of mice previously treated with cyclophosphamide

Summary We investigated the combined effects of human recombinant interleukin 2 (IL-2) and cyclophosphamide (CY) on s.c. transplanted 3LL lung carcinoma in C57BL/6 mice. A total of 95% of the tumors were competely cured when CY (150 mg/kg, i.v.) was given on day 5 (5 days after tumor implantation) and IL-2 (5×10⁴ Jurkat Units/day, i.p.) was then combined with it between day 6 and day 15. CY alone brought about the complete regression of tumors, although 60% of the mice died of local recurrence and pulmonary metastasis; IL-2 alone had no therapeutic effect. Satisfactory effects from the combination of CY and IL-2 were also obtained by 5 days administration of IL-2 between days 11 and 15, initiated 6 days after CY treatment, but not by that given before CY (days 1–5) or 1 day after CY (days 6–10). No therapeutic effects from IL-2 were observed when it was combined with other types of chemotherapy that showed not therapeutic effects by themselves. Nor were we able to observe any transplantation resistance to the rechallenge of 3LL tumor in cured mice. We particularly examined the lymphokine-activated killer (LAK) cells as we suspected that these were responsible for the development of active effector cells in the treated mice. LAK cell activity in fresh spleen cells was detected in mice treated with IL-2 alone but not in untreated mice nor in those treated with CY alone or CY plus IL-2. The number of LAK precursor cells in the spleen had increased on day 8 and on day 13 in untreated mice with 3LL, as compared with the incidence in normal mice, while the number of cells had decreased by day 18. On the other hand LAK precursor cells were suppressed on day 8 and tended to recover thereafter in CY-treated mice. Adoptively transferred LAK cells were found to accumulate in CY-treated tumors 2.5 times more densely than in untreated tumors. The preferential accumulation of LAK cells that had been activated systemically by the appropriately timed administration of IL-2 in tumor tissue was followed by the improved effects obtained by combined treatment with CY and IL-2.Supported in part by Grants-in-Aid for Cancer Research from the Japanese Ministry of Education, Science and Culture and from the Japanese Ministry of Health and Welfare     

Stimulation of the natural immune system in normal mice by polysaccharide from maitake mushroom

 Maitake D-Fraction is a polysaccharide extracted from the maitake mushroom (Grifola frondosa S.F. Gray). It is a β-glucan with a β-1,6 main chain with β-1,3 branches. Using normal C3H/Hej mice, its effects on the natural immune system, including macrophages, dendritic cells, and natural killer (NK) cells, were investigated. NK cells attack cells infected with pathogens such as bacteria and virus and produce cytokines, such as interferon-gamma (IFN-γ), that can modulate natural and specific immune responses. D-Fraction was administered to the mice intraperitoneally for 3 consecutive days; spleen cells containing macrophages and dendritic cells were then cultured and the culture supernatants were analyzed for IL-12. At the same time, IFN-γ expression in splenic NK cells was investigated. The levels of these cytokines were increased by D-Fraction. To elucidate NK cell activation by D-Fraction, CD69 expression on the surface of activated NK cells was examined, resulting in an increase in CD69-positive ratio for splenic NK cells. These results indicate that D-Fraction stimulates the natural immunity related to the activation of NK cells indirectly through IL-12 produced by macrophages and dendritic cells. Therefore, administration of D-Fraction to healthy individuals may serve to prevent infection. Received: August 1, 2002 / Accepted: February 10, 2003     

Virulizin, a novel immunotherapy agent, activates NK cells through induction of IL-12 expression in macrophages

Virulizin, a novel biological response modifier, has demonstrated significant antitumor efficacy in a variety of human tumor xenograft models including melanoma, pancreatic cancer, breast cancer, ovarian cancer and prostate cancer. The significant role of macrophages and NK (Natural killer) cells was implicated in the antitumor mechanism of Virulizin where expansion as well as increased activity of macrophages and NK cells were observed in mice treated with Virulizin. Depletion of macrophages compromised Virulizin-induced NK1.1⁺ cell infiltration into xenografted tumors and was accompanied by reduced antitumor efficacy. In the present study, involvement of macrophages in NK cell activation was investigated further. We found that depletion of NK cells in CD-1 nude mice by anti-ASGM1 antibody significantly compromised the antitumor activity of Virulizin. Cytotoxicity of NK cells isolated from Virulizin-treated mice was enhanced against NK-sensitive YAC-1 cells and C8161 human melanoma cells, but not against NK-insensitive P815 cells. An increased level of IL-12 was observed in the serum of mice treated with Virulizin. IL-12 mRNA and protein levels were also increased in peritoneal macrophages isolated from Virulizin-treated mice. Moreover, Virulizin-induced cytotoxic activity of NK cells isolated from the spleen was abolished when an IL-12 neutralizing antibody was co-administered. In addition, depletion of macrophages in mice significantly impaired Virulizin-induced NK cell cytotoxicty. Taken together, the results suggest that Virulizin induces macrophage IL-12 production, which in turn stimulates NK cell-mediated antitumor activity.     

Studies of the mechanisms for the induction of in vivo tumor immunity. VI. Induction of specific and nonspecific cell-mediated immunity in tumor-bearing hosts and its correlation with transplantation tumor immunity

Studies were performed to determine the development of cell-mediated cytotoxic response at tumor site in C57BL/6 mice bearing progressively growing FBL-3 ascites leukemia. The effectors isolated from tumor ascites are found to be highly cytotoxic for leukemic target cells. The levels of cytotoxicity obtained with effectors isolated from tumor site are generally higher than those obtained with immune mice. This cytotoxicity is both specific and nonspecific. The specific cytotoxicity against tumor-associated antigen is mainly mediated by T cells and the nonspecific cytotoxicity against unrelated tumor cells is mediated largely by macrophages. The T-cell-enriched preparation did not give significant natural killer activity. When testing the ability of these effectors to produce in vivo immunity against the challenge of FBL-3, it was found that only T cells could confer the transplantation-type immunity, but the immunity was transient. The macrophage-enriched preparation isolated from tumor ascites failed to give in vivo protection. These findings indicate that in FBL-3 system, mice with progressively growing tumors are able to develop immune response against tumor cells. However, this immunity is probably interfered with by a suppressor factor(s) or suppressor cells which restrict their activity to eliminate the tumor cells effectively.     

Heat-killed Lactobacillus gasseri TMC0356 protects mice against influenza virus infection by stimulating gut and respiratory immune responses

This study investigated whether heat-killed Lactobacillus protects host animal against influenza virus infection and stimulates their immunity. Heat-killed Lactobacillus gasseri TMC0356 was orally administered to BALB/c mice for 19 days; the mice were intranasally infected with Flu A/PR/8/34 (H1N1) on day 14, and clinical symptoms were monitored. After 6 days, the mice were sacrificed, and pulmonary virus titres were determined. Splenic activation of natural killer (NK) cells and the mRNA expression of cytokines and other immune molecules in the lung and Peyer's patch (PP) were analysed. Clinical symptom scores of mice orally fed TMC0356 ameliorated significantly (P < 0.01); their pulmonary virus titres decreased significantly compared with those of control mice (P < 0.05); their mRNA expression of interleukin (IL)-12, IL-15 and IL-21 in PP and the pulmonary mRNA expression of IFN-γ, TNF, IL-12a, IL-12rbl, IL-2rb and perforin 1 increased significantly (P < 0.05). Oral administration of heat-killed lactobacilli may protect against influenza virus infection by stimulating local and systemic immune responses. Cellular components of lactobacilli may be pivotal in protecting against viral infection by enhancing gut and respiratory immune responses.     

Immunomodulatory activity of polysaccharide isolated from Angelica sinensis

The immunomodulatory activities of an Angelica sinensis polysaccharide (AP), purified from the fresh root of A. sinensis Diels, were investigated in vitro in relation to the specificity to immune cells. AP consisted of rhamnose, arabinose, mannose, glucose, galactose with the molar ratio of 1.00:4.54:2.98:11.09:7.45. Cell proliferation results showed that proliferation of total spleen cells, macrophages and T cells were promoted by the action of AP. The treatment of AP increased the production of IL-2 and IFN-γ, while that of IL-4 was decreased. RT-PCR analysis displayed that the IL-2 and IFN-γ gene expression were enhanced but the IL-4 gene expression was decreased. Some differences in cytokines secretion pattern were also detected, the expression of IFN-γ was rapidly augmented while that of IL-2 responded later. The flow cytometry results showed that the percentage of CD4⁺T cell in total spleen cells was remarkably increased by AP, while that of CD8⁺T cell was slightly decreased. In conclusion, AP has immunomodulatory activity by regulating expression of Th1 and Th2 related cytokines. The time–effect relation of cytokines response also suggests that macrophages and natural killer cells involved in nonspecific immunity were primary activated, and helper T cell were secondarily affected by AP.     

IL-22 is induced by S100/calgranulin and impairs cholesterol efflux in macrophages by downregulating ABCG1

S100A8/9 and S100A12 are emerging biomarkers for disease activity of autoimmune and cardiovascular diseases. We demonstrated previously that S100A12 accelerates atherosclerosis accompanied by large cholesterol deposits in atherosclerotic lesions of apoE-null mice. The objective of this study was to ascertain whether S100/calgranulin influences cholesterol homeostasis in macrophages. Peritoneal macrophages from transgenic mice expressing human S100A8/9 and S100A12 in myeloid cells [human bacterial artificial chromosome (hBAC)/S100] have increased lipid content and reduced ABCG1 expression and [³H]cholesterol efflux compared with WT littermates. This was associated with a 6-fold increase in plasma interleukin (IL)-22 and increased IL-22 mRNA in splenic T cells. These findings are mediated by the receptor for advanced glycation endproducts (RAGE), because hBAC/S100 mice lacking RAGE had normal IL-22 expression and normal cholesterol efflux. In vitro, recombinant IL-22 reduced ABCG1 expression and [³H]cholesterol efflux in THP-1 macrophages, while recombinant S100A12 had no effect on ABCG1 expression. In conclusion, S100/calgranulin has no direct effect on cholesterol efflux in macrophages, but rather promotes the secretion of IL-22, which then directly reduces cholesterol efflux in macrophages by decreasing the expression of ABCG1.     

新加良附方对移植性小鼠肝癌抑制率及其凋亡影响研究

目的:观察新加良附方对移植性小鼠肝癌(H22)生长抑制作用及其对肿瘤组织中Bcl-2和Bax表达影响。方法:建立移植型H22动物模型,并将动物模型随机分模型对照、环磷酰胺(CTX)与新加良附方大、中、小剂量5组。新加良附大、中、小剂量组给药量分别为10g/kg、5g/kg和2.5g/kg;CTX组给药计量为17mg/kg;模型组给予等量无菌生理盐水。连续给药、给水12天处死模型小鼠分离肿瘤,检测肿瘤大小、称重计算肿瘤抑制率,并将肿瘤组织切片,免疫组化法检测Bcl-2和Bax基因。结果:新加良附大剂量组肿瘤抑制率为48.5%,与模型对照组比较,有统计学意义(P<0.01);新加良附大、中剂量可降低肿瘤组织中Bcl-2蛋白基因表达,升高Bax蛋白基因表达,与模型组比较,有显著性差异(P<0.01,P<0.05)。结论:新加良附方可抑制H22瘤体生长,且下调Bcl-2蛋白基因表达,上调Bax基因,提示新加良附方在抗肿瘤方面具有进一步深入研究价值。     

Silkworm powder containing manganese superoxide dismutase regulated the immunity and inhibited the growth of Hepatoma 22 cell in mice

The effects of SOD contained silkworm powder on immune regulation and inhibition against Hepatoma 22 tumor cells in vivo were investigated. The activity of natural killer cell (NK) and the ConA-stimulated spleen proliferation were measured. The results found that the SOD-contained silkworm powder caused an enhancement on NK cell activity, which implied this material modulated the immune system in mice in vivo. The NK cell activities of Hepatoma 22 tumor modeled mice treated with silkworm powder including SOD were increased significantly compared to a modeled control and silkworm powder without SOD, reaching 36.18%. In addition, the ConA-stimulated spleen proliferation of SOD treated mice was higher than that of the controls. The treatment of SOD contained silkworm powder presented 40.3% of average inhibition rate to Hepatoma 22 tumor, showing stronger inhibition against tumor. There were no significant difference in body weight between modeled control and SOD silkworm powder feeding in Hepatoma 22 tumor modeled mice, suggesting the SOD silkworm powder is safety as an inhibitant to tumor. In conclusion, these findings demonstrate that administration of silkworm powder containing SOD results in activation of NK cells and immunity, suggesting the silkworm powder containing SOD plays a positive role in tumor inhibition.     

Effects of a plum (Prunus mume Siebold and Zucc.) ethanol extract on the immune system in vivo and in vitro

The effect of a plum ethanol extract (PEE) on immunity was analyzed. An oral administration of PEE increased the interleukin (IL)-12p40 concentration in the serum and T-cell ratio in the spleen. In vitro studies revealed that PEE stimulated IL-12p70 production in peritoneal macrophages and natural killer activity. These findings suggest that PEE enhanced the immune function by stimulating innate immune cells.