何首乌对老龄大鼠免疫功能的影响

目的:了解何首乌对老龄大鼠免疫功能的影响。方法:采用溶血素测定法检测何首乌对老龄大鼠溶血素抗体产生的影响;参照LDH法检测何首乌对老龄大鼠NK细胞活性的影响;采用3H-TdR掺入法检测何首乌对老龄大鼠淋巴细胞增殖活性的影响;采用姬姆萨染色法检测老龄大鼠腹腔巨噬细胞的吞噬功能。结果:药物实验组与老龄对照组比较,溶血素抗体产生水平明显增加(P<0.01);NK细胞的细胞毒活性明显增强(P<0.01);T、B淋巴细胞的转化增殖活性增强(P<0.05;P<0.01);腹腔巨噬细胞吞噬功能也明显增强。结论:何首乌能增强老龄大鼠的免疫功能。     

毛蚶多肽提取物的体外免疫活性

目的考察毛蚶多肽提取物(PEAS)的体外免疫活性。方法 MTT法测定PEAS对小鼠脾淋巴细胞增殖的影响及对小鼠NK细胞杀伤活性的影响;中性红吞噬法测定PEAS对小鼠腹腔巨噬细胞吞噬功能的影响;流式细胞术测定PEAS所致小鼠脾淋巴细胞周期的变化;双抗体夹心ELISA法测定PEAS对主要细胞因子IFN-γ和IL-4分泌水平的影响。结果 PEAS能够显著促进小鼠脾淋巴细胞增殖(P<0.05或0.01),能够增强小鼠腹腔巨噬细胞吞噬中性红活性和小鼠NK细胞杀伤活性(P<0.05或0.01);PEAS能够促进脾淋巴细胞G0/G1期向DNA合成期(S期)转化;PEAS协同Con A作用,能够增加IFN-γ的分泌(P<0.05或0.01),并且能够抑制IL-4的分泌(P<0.05或0.01)。结论 PEAS体外可促进小鼠脾淋巴细胞、腹腔巨噬细与NK细胞的免疫功能,其机制可能与促进脾淋巴细胞DNA合成,增加IFN-γ的分泌量有关。     

何首乌多糖对免疫功能低下小鼠的免疫保护作用

目的:探讨何首乌多糖(PPM)对免疫功能低下小鼠的免疫保护作用。方法:小鼠腹腔注射环磷酰胺建立小鼠免疫功能低下模型后,灌胃PPM 0.4,0.8,1.6 g.kg-1,qd,连续给药10 d,另设模型对照组和正常对照组。采用显微镜观察腹腔巨噬细胞的吞噬百分率、吞噬指数和T淋巴细胞酯酶阳性率;用分光光度测定血清溶血素含量;用3H-TdR掺入法测定脾细胞淋巴细胞增殖率。结果:PPM能显著拮抗环磷酰胺所致免疫功能低下小鼠的免疫器官重量减轻和白细胞数量减少,明显增加小鼠腹腔巨噬细胞的吞噬率及吞噬指数,显著增加血清溶血素含量,且能明显促进T淋巴细胞酯酶阳性率和ConA诱导的脾T淋巴细胞增殖反应。结论:何首乌多糖对免疫功能低小鼠的免疫功能有明显的增强作用。     

羊胎盘免疫调节因子对小鼠腹腔巨噬细胞免疫功能的影响

目的探讨羊胎盘免疫调节因子(GPIF)对小鼠腹腔巨噬细胞免疫功能的影响。方法采用巨噬细胞体外培养的方法。分3个实验组,对腹腔巨噬细胞分别给予0 .0 5 ,0 .1和0 .5mg/mlGPIF进行体外培养,培养结束后,测定腹腔巨噬细胞吞噬中性红的能力、对溴化四唑蓝(MTT)的还原能力,以及分泌一氧化氮(NO)和白细胞介素 1(IL-1)的量。结果与对照组比较,各浓度GPIF均有促进腹腔巨噬细胞吞噬中性红能力作用,且能显著提高腹腔巨噬细胞对MTT的还原能力,增加NO和IL-1的分泌量(P <0 .0 5 )。结论GPIF具有非特异性免疫增强作用     

生姜对小鼠免疫功能影响的实验研究

目的:了解生姜对小鼠免疫功能的影响。方法:①PFC法检测小鼠脾细胞抗体生成水平;②常规法检测小鼠腹腔巨噬细胞吞噬活性;③3H-T dR摄入法检测小鼠腹腔巨噬细胞细胞毒活性;④乳酸脱氢酶(LDH)释放法检测小鼠脾脏NK细胞杀伤活性。结果:与空白对照组比较,在有效剂量范围内,生姜能促进脾细胞抗体的生成,能增加小鼠腹腔巨噬细胞吞噬活性及细胞毒活性,能增强NK细胞杀伤活性。结论:生姜具有调节机体免疫功能的作用。     

茶多酚影响老年小鼠免疫功能的实验研究

目的观察茶多酚对老年小鼠免疫功能的影响,判定茶多酚对老年小鼠的免疫作用。方法测定老年小鼠脾悬液中淋巴细胞转化率和腹腔液中巨噬细胞吞噬率。结果茶多酚(0.25、0.5g·kg-1)可显著提高老年小鼠淋巴细胞增殖反应、巨噬细胞吞噬百分率及吞噬指数(P<0.01)。结论茶多酚可增强老年小鼠细胞免疫功能,提高机体巨噬细胞吞噬功能。     

三肽化合物酪丝亮肽对巨噬细胞吞噬及肿瘤细胞杀伤功能的影响

目的：研究三肽化合物酪丝亮肽(YSL)对巨噬细胞(M(?))吞噬功能、肿瘤细胞杀伤功能和细胞因子分泌功能的影响。方法：通过碳粒廓清实验观察YSL对小鼠M(?)吞噬功能的影响,采用MTT法观察YSL对腹腔M(?)杀伤人肝癌细胞BEL-7402和小鼠黑色素瘤细胞B16-F10作用的影响,用ELISA法观察YSL对M(?)株RAW264．7分泌细胞因子IL-1β和NO功能的影响。结果：YSL 80,160,320μg·kg~(-1)·d~(-1)均能够明显增强小鼠M(?)的吞噬功能(P＜0．01),YSL各浓度(0．1,1,10,100 mg·L~(-1))在体外明显增强小鼠腹腔M(?)对肿瘤细胞BEL-7402和B16-F10的杀伤作用(P＜0．01)。YSL可以促进细胞毒效应分子IL- 1β和NO的分泌合成,NO和IL-1β水平分别在YSL作用12 h,24 h时达到高峰。结论：YSL可以增强M(?)吞噬功能,增强对肿瘤细胞的杀伤作用,促进细胞因子IL-1β和NO分泌。     

多抗甲素对小鼠巨噬细胞功能的影响

对多抗甲素体外影响小鼠腹腔巨噬细胞吞噬中性红染料作用、对Ｌ９２９细胞的细胞毒活性，分泌ＴＮＦ、ＩＬ－１功能等方面进行了探讨。结果表明，ＰＡ能显著增强淀粉刺激的ＭΦ的吞噬功能、细胞毒作用、ＩＬ－１及ＴＮＦ的分泌功能（Ｐ＜０．０５），且呈良好剂量依赖关系。ＰＡ对正常小鼠ＭΦ吞噬功能几乎无明显促进作用（Ｐ＞０．０５），但能明显增强其细胞毒活性（Ｐ＜０．０５）、ＰＡ能协同ＬＰＳ促进ＩＬ－１的分泌（Ｐ＜０．０５），但不能联合ＬＰＳ、ＩＦＮ－ｒ促进ＴＮＦ的分泌（Ｐ＞０．０５）。     

草乌甲素对Balb/c小鼠的部分免疫功能的抑制作用

目的:研究草乌甲素对Balb/c小鼠部分免疫功能的影响。方法:Balb/c小鼠随机分为空白对照组、草乌甲素3个剂量(0.08、0.16、0.32 mg·kg~(-1),肌注7d)组、氢化可的松组(阳性对照药,10mg·kg~(-1))。小鼠d7处死,检测药物对小鼠胸腺指数、脾脏指数的影响;测定小鼠T、B淋巴细胞转化功能;酶联免疫法(ELISA)测定小鼠血清总IgG水平;中性红比色法测定小鼠腹腔巨噬细胞吞噬功能;硝酸还原酶法测定巨噬细胞培养上清一氧化氮(NO)水平。结果:草乌甲素0.32 mg·kg~(-1)能抑制致裂原刺激T、B淋巴细胞增殖(P<0.01),降低腹腔巨噬细胞培养上清中NO水平(P<0.05)。草乌甲素(0.16、0.32 mg·kg~(-1))降低小鼠的胸腺指数,降低小鼠血清中总IgG水平(P<0.05,P<0.01),草乌甲素还能抑制腹腔巨噬细胞吞噬功能(P<0.05,P<0.01)。结论:草乌甲素对Balb/c小鼠的免疫功能有一定的抑制作用。     

小叶黑柴胡多糖对小鼠腹腔巨噬细胞功能的影响

目的研究小叶黑柴胡多糖（BPs）对巨噬细胞免疫功能的影响。方法收集KM小鼠腹腔巨噬细胞,用不同质量浓度的BPs溶液(10、100、200 mg·L^-1)刺激,检测巨噬细胞吞噬E.codi、趋化和分泌一氧化氮（NO）的功能。结果 HPs各个浓度组均能显著促进巨噬细胞吞噬E.codi和趋化作用（P<0.001）,但对巨噬细胞分泌NO无明显影响;BPs 100、200 mg·L^-1可明显抑制脂多糖诱导的巨噬细胞分泌NO（P<0.05）。结论 BPs可增强巨噬细胞免疫功能,但能抑制脂多糖诱导的炎症介质分泌。     

肉苁蓉多糖的巨噬细胞活化作用

目的观察肉苁蓉多糖(CDPS)对巨噬细胞的活化作用。方法采用中性红法测定吞噬活性;Griess试剂法测定NO释放量;L929细胞法及小鼠胸腺细胞法测定TNF-α及IL-1释放。结果CDPS在6.25～50mg.L-1剂量范围内可剂量依赖性地增强BALB/c小鼠腹腔巨噬细胞吞噬中性红能力和促进NO释放;在2.8～100mg.L-1剂量范围内可使正常和免疫抑制的RAW264.7细胞NO释放明显增加;在0.56～7.2mg.L-1或3.6～10mg.L-1范围促进RAW264.7细胞TNF-α或IL-1产生,均具有良好的量效关系。结论CDPS可明显提高巨噬细胞吞噬及分泌功能,活化巨噬细胞。肉苁蓉免疫增强作用可能与此有关。     

枸杞糖缀合物和糖链对小鼠巨噬细胞功能的影响

目的确定巨噬细胞是枸杞糖缀合物和糖链免疫作用的靶细胞之一。方法应用中性红吞噬实验和鸡红细胞吞噬实验测定了枸杞糖缀合物LbGp4和糖链LbGp4-OL对小鼠腹腔巨噬细胞吞噬功能的影响;用硝酸根还原法、酶联免疫吸附实验(ELISA)和生物活性测定法测定了巨噬细胞产生一氧化氮(NO)、IL-1β和TNF-α含量和生物活性的变化。结果LbGp4和LbGp4-OL在(10~100)mg.L-1剂量范围内均可剂量依赖性地促进静息巨噬细胞吞噬中性红的能力,增加活化的巨噬细胞吞噬鸡红细胞的吞噬率和吞噬指数;增加巨噬细胞培养上清NO、IL-1β和TNF-α的浓度,并增强对L929细胞的杀伤活性,促进胸腺细胞的增殖反应。结论LbGp4和LbGp4-OL对静息和活化的腹腔巨噬细胞的吞噬功能具有明显的促进作用,对巨噬细胞产生NO、分泌IL-1β和TNF-α的含量和生物活性亦具有明显的促进作用,表明巨噬细胞是LbGp4和LbGp4-OL免疫作用的靶细胞之一。     

The immunomodulatory effects of the herbicide simazine on murine macrophage functions in vitro.

We examined the immunomodulating effects of simazine, a triazine herbicide, on murine peritoneal macrophages after in vitro pre-exposure. When thioglycollate-elicited macrophages pre-exposed to simazine were stimulated with lipopolysaccharide (LPS), the antitumor activity induced by LPS was suppressed by simazine. Simazine also inhibited poly I:C-induced antiviral activity and interferon (IFN) production in macrophages. In addition, the production of nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) which have been known to be major effector molecules in macrophage-mediated cytotoxicity was decreased by simazine pretreatment in a dose-dependent manner. However, simazine had little effect on phagocytosis and the level of hydrogen peroxide (H(2)O(2)), interleukin-1 (IL-1) and IL-6 by LPS-stimulated macrophages. Taken together, these data indicate that simazine has a differential immunomodulating effect on macrophage secretory and cellular activities.     

Contribution of crotoxin for the inhibitory effect of Crotalus durissus terrificus snake venom on macrophage function.

Previous work of our group demonstrated that Crotalus durissus terrificus venom has a dual effect on macrophage function: it inhibits spreading and phagocytosis and stimulates hydrogen peroxide and nitric oxide production, antimicrobial activity and glucose and glutamine metabolism of these cells. Crotalid venom also induces analgesia and this effect is mediated by opioid receptors. The involvement of opioidergic mechanism and the determination of the active component responsible for the inhibitory effect of crotalid venom on macrophage function were investigated. The venom reduced the spreading and phagocytic activities of peritoneal macrophages. This effect was observed in vitro, 2 h after incubation of resident peritoneal macrophages with the venom, and in vivo, 2 h after subcutaneous injection of the venom. The inhibition of phagocytosis was not modified by naloxone, an antagonist of opioid receptors. Venom neutralization with crotalid antivenom abolished the inhibitory effect of the venom, indicating that venom toxins are involved in this effect. Crotoxin, the main toxin of crotalid venom, s.c. injected to rats or added to the medium of peritoneal cell incubation, inhibited macrophage function in a similar manner to that observed for crude venom. The present results suggest that crotoxin causes a direct inhibition of macrophage spreading and phagocytic activities and may contribute to the inhibitory effect of crotalid venom on macrophage function.     

康乐霉素C与环孢素对小鼠免疫抑制作用的比较

AIM: To study inhibitory effects of kanglemycin C (Kan) on the mouse immune system, and compare with the effects of ciclosporin (Cic). METHODS: Delayed hypersensitivity (DH) and cyclophosphamide-potentiated DH induced by dinitrofluorobenzene (DNFB); heart allograft and skin allograft; hemolysin; the phagocytosis of the peritoneal macrophage. RESULTS: Kan (12.5, 25, 50 mg.kg-1.d-1, ig, 8 d) markedly inhibited DH and cyclophosphamide-potentiated DH induced by DNFB (P < 0.01), prolonged survival times of heart and skin allografts (P < 0.01), and decreased the content of hemolysin (P < 0.01), but had no significant effect on the neutral-red phagocytosis of the peritoneal macrophage (P > 0.05). CONCLUSION: Kan had marked suppressive effects on cell-mediated and humoral-mediated immune responses, but no effect on phagocytosis of macrophage.     

管花肉苁蓉麦角甾苷对衰老小鼠端粒酶活性和免疫功能的影响

目的观察管花肉苁蓉麦角甾苷(CTWA)对实验性衰老小鼠心、肝和脑组织中丙二醛(MDA)含量、端粒酶活性和免疫功能的影响。方法小鼠sc 10%D-半乳糖10mL·kg-1,每天1次,连续8周,建立亚急性衰老模型。给药组小鼠从造模第9周起,分别ig给予CTWA 10,20和40mg·kg-1,每天1次,连续2周。硫代巴比妥酸比色法检测MDA含量;PCR-ELISA法检测端粒酶活性;[3H]TdR掺入法测定淋巴细胞增殖反应;中性红实验测定小鼠腹腔巨噬细胞吞噬功能;放射免疫法测定外周血白细胞介素2(IL-2)含量。结果模型组小鼠心、肝和脑MDA含量明显增加,心和肝端粒酶活性明显降低,淋巴细胞增殖反应、腹腔巨噬细胞吞噬功能和外周血IL-2含量均显著下降。给予CTWA 2周,小鼠心、肝和脑MDA含量明显降低,CTWA 40mg·kg-1组小鼠心和脑组织端粒酶活性明显升高,淋巴细胞增殖反应、腹腔巨噬细胞吞噬功能和外周血IL-2含量明显升高。结论CTWA能拮抗自由基损伤,增强衰老小鼠心和脑组织端粒酶活性和机体免疫功能,这些可能与CTWA的抗衰老作用有关。     

松果菊苷对衰老小鼠免疫功能和线粒体DNA相对含量的影响

目的观察肉苁蓉提取物松果菊苷(ECH)对实验性小鼠免疫功能和肝细胞线粒体DNA相对含量的影响。方法小鼠皮下注射10%D-半乳糖10ml.kg-1,每天1次,连续8wk,建立亚急性衰老模型。阳性组和松果菊苷各组同时灌胃给于维生素E40mg·kg-1和ECH20、40、60mg·kg-1,每天1次。采用酶联免疫吸附试验(ELISA)法测定血清中IL-2、IL-6含量;中性红实验测定小鼠腹腔巨噬细胞吞噬功能;MTT法检测ConA诱导的小鼠脾淋巴细胞增殖转化;SDS碱变性法测定肝细胞线粒体DNA相对含量。结果与正常组比较,模型组小鼠血清IL-2含量,小鼠腹腔巨噬细胞吞噬功能和淋巴细胞增殖反应均下降,IL-6和肝脏线粒体DNA相对含量升高。ECH各剂量组和维生素E阴性对照组均能提高衰老小鼠血清IL-2含量、小鼠腹腔巨噬细胞吞噬功能和淋巴细胞增殖反应,降低IL-6和肝细胞线粒体DNA相对含量。结论松果菊苷能够提高机体的免疫功能,降低衰老小鼠肝细胞线粒体DNA相对含量,可能是其延缓衰老的作用机制之一。     

Modulation of murine macrophage function by methamphetamine

The abuse of methamphetamine (MA) is an increasingly growing problem globally and produces serious side effects. In the present study, the immunomodulating effects of MA were examined on murine peritoneal macrophages after MA (5 mg/kg body weight) was administered daily orally for 2 wk. When purified macrophages were stimulated with lipopolysaccharide (LPS), the tumoricidal activity induced by LPS was significantly suppressed by MA. MA also inhibited poly I:C-induced antiviral activity in macrophages and decreased the number of peritoneal macrophages. FACS analysis showed that the expression of CD14 was markedly decreased by MA in LPS-stimulated macrophages. The production of nitric oxide (NO) and tumor necrosis factor (TNF)-alpha: which are known to be major effector molecules in macrophage-mediated cytotoxicity, was decreased by MA. MA produced a significant effect on phagocytosis and interleukin-1 (IL-1) and IL-6 at 14 d. In addition, the level of hydrogen peroxide (H2O2) was not altered by MA. Taken together, these data indicate that MA has a differential immunomodulating effect on macrophage secretory and cellular activities.