急性氟中毒大鼠肾损害及其机理研究

本研究以NaF 0、30、60,90mg/kg灌胃,观察大鼠48小时急性氟中毒尿氟排泄规律、肾损害情况及其与LPO的关系。结果发现:中毒大鼠尿氟浓度在中毒3小时显著升高,中毒6小时达高峰;肾损害指标尿AKP活性显著增强,峰值分别在12、24小时;尿蛋白含量显著升高,峰值在36小时;肾匀浆MDA含量显著升高,肾匀浆GSH含量显著降低,肾G—6—Pase活性显著下降,以上三指标均存在显著的剂量效应关系,肾SDHase活性显著降低。提示氟中毒可损害肾脏;其损害的机理之一是LPO;损害亚细胞部位可能在线粒体和微粒体。     

外环境氟砷含量分布研究

目的　研究外环境氟、砷含量的分布规律 ,为制定科学有效的防治策略提供可靠依据。方法　采集砷中毒病区饮用井水样 ,测定水中的砷含量、氟含量。结果　高砷、高氟现象并存 ,含有不同含量砷的水中水氟含量不同 (F =2 1.83,P <0 .0 1) ,水砷含量有随井深增加而呈增高的趋势 (F =187.5 3,P <0 .0 1) ,水氟含量有随井深增加而呈降低的趋势 (F =2 7.98,P <0 .0 1)。结论　外环境中水砷含量与水氟含量呈负相关关系 ,低氟低砷水源多埋深于 5 0m左右 ;因地制宜地选择安全水源 ,以保证综合的降氟除砷改水工程防治措施的顺利实施。     

知母皂苷对D-半乳糖衰老模型小鼠的作用

目的研究知母皂苷对D 半乳糖所致小鼠学习记忆能力下降和各项衰老指标的对抗作用 ,以期探讨知母皂苷的抗衰老作用机制。方法以D 半乳糖衰老模型小鼠为实验对象 ,以其体质量、免疫器官质量、肝脑丙二醛 (MDA)和脂褐素 (LF)的含量、全血谷胱苷肽过氧化氢酶 (GSH PX)、红细胞过氧化氢酶 (CAT)和脑中超氧化物歧化酶 (SOD)的活力、脑中谷氨酸水平为指标 ,全面考察知母皂苷的抗衰老作用。结果知母皂苷 (10 0、2 0 0、4 0 0mg·kg-1,ip) ,能对抗连续 6周给予 5 0g·L-1D 半乳糖 (0 0 2 5mL·g-1)所致小鼠脑组织中LPO、LF含量的升高 ;提高全血GSH PX、红细胞CAT和脑中SOD的活力 ;对抗小鼠体质量、脾脏及胸腺指数下降。结论知母皂苷能有效地对抗D 半乳糖所致的小鼠多项衰老指标的出现 ,促进衰老小鼠的学习记忆能力     

肺癌患者化疗前后血清SOD、LPO、GSH—PX水平的变化及临床意义

目的探讨肺癌患者化疗前后血清SOD、LPO、GSH—PX含量的变化及意义。方法应用放射免疫分析法和生化法对31例肺癌患者进行了化疗前后血清SOD、LPO、GSH—PX含量的检测，并与35名正常人作比较。结果肺癌患者化疗前血清SOD、GSH—PX水平明显低于正常人组（P〈O．01），而LPO则明显高正常人组（P〈0．01），化疗后6个月复发者SOD、LPO、GSH—PX水平持续异常，未复发者SOD、LPO、GSH—PX水平接近正常。结论观察肺癌患者血清SOD、LPO、GSH—PX含量的变化与患者的预后密切相关。     

光气致小鼠肺水肿及肝脏过氧化损伤的实验研究

目的　探讨小鼠光气染毒剂量与肺水肿形成的关系及其对肝脏的过氧化损伤。方法　 5 0只小鼠 ,雌雄各半 ,随机分为 5组。正常对照组小鼠放置染毒柜中 5min ,染毒组小鼠分别给予 3 2、3 9、46、5 3mg L的光气 (各 10只 ) ,染毒时间为 5min。染毒后 4h ,测定各组小鼠肺脏的湿干比、肝脏的丙二醛 (MDA)含量、总超氧化物歧化酶 (T SOD)活力及进行肝脏HE染色。结果　随着光气染毒剂量的增加 ,小鼠肺脏的湿干比增加 ;当染毒剂量为 3 2mg L ,肝脏的MDA含量[(2 10 3 1± 44 61) μmol g]和T SOD活力 [(3 2 5 1± 6 10 )U g]比正常组 [(15 7 2 1± 18 17) μmol g ,(2 2 3 8± 6 0 2 )U g]升高 (P <0 0 5 ) ;光镜下 ,光气染毒的肝组织肝细胞呈现空泡样变性。结论　光气染毒可造成小鼠肺水肿 ,引起肝脏过氧化损伤。     

葡萄籽原花青素对砷致小鼠肝脏毒性预防保护作用的研究

目的观察葡萄籽提取物原花青素(GSPE)对三氧化二砷(As2O3)所致肝脏毒性的预防保护效果,揭示其可能机制。方法将84只昆明种小鼠,随机分为35 d空白组、70 d空白组、35 d GSPE组、70 d GSPE组、砷染毒组、GSPE预防组和GSPE干预组,每组12只,雌雄各半,以GSPE 400 mg/kg、As2O35 mg/kg为剂量灌胃给药。测定小鼠体重、肝重、肝脏系数、肝匀浆中丙二醛(MDA)含量、谷胱甘肽(GSH)含量、超氧化物歧化酶(SOD)活力、总抗氧化能力(T-AOC)水平,血清中天冬氨酸转氨酶(AST)与丙氨酸转氨酶(ALT)活力。结果砷染毒组ALT和AST活性、MDA含量显著高于70 d空白组,SOD活性、GSH含量、T-AOC水平显著低于70 d空白组(P0.05);砷染毒组与GSPE干预组、70 d GSPE预防组相比,血清ALT、AST活力增高(P0.05);70 d GSPE预防组ALT及AST活性、MDA含量均低于35 d GSPE干预组(P0.05),SOD活性、GSH含量、T-AOC水平均高于35 d GSPE干预组(P0.05);GSPE干预组和GSPE预防组较砷染毒组,SOD活力、T-AOC水平、GSH含量均升高,MDA含量均降低(P0.05)。结论砷染毒前35 d对小鼠进行GSPE预防性干预,可提高肝脏组织抗氧化能力,有效减轻砷致肝脏毒性作用。     

姜黄素对汞致大鼠肾损伤保护作用的实验研究

目的探讨姜黄素对汞致大鼠肾损伤的影响,为汞中毒的发病机制和防治提供实验依据。方法 Wistar大鼠30只按体重随机分为5组,每组6只,雌雄各半。分别为对照组、低剂量染汞组、中剂量染汞组、高剂量染汞组和姜黄素预处理组。1~4组大鼠予皮下注射0.9%氯化钠溶液,第5组大鼠给予皮下注射100 mg/kg姜黄素;2 h后,第1组腹腔注射生理盐水,第2~5组大鼠分别腹腔注射2.2、4.4、8.8和8.8μmol/kg氯化汞溶液,连续干预与染毒3 d。第3天染毒2 h后将动物放入代谢笼,收集24 h尿液测定尿汞和尿蛋白含量,以及尿碱性磷酸酶(ALP)、β-N-乙酰氨基葡萄糖苷酶(NAG)和乳酸脱氢酶(LDH)活力;用乙醚将大鼠麻醉,腹主动脉采血测定血清尿素氮(BUN);切取肾皮质,测定肾皮质汞、还原型谷胱甘肽(GSH)和丙二醛(MDA)的含量及超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)活力。结果与对照组比较,随着染汞剂量的增加,肾皮质汞、尿汞、尿蛋白和BUN含量均升高;尿NAG、LDH和ALP活力均升高;肾皮质GSH和MDA含量明显升高而GSH-Px和SOD活力显著下降,差异具有统计学意义(P0.05)。姜黄素预处理组与高剂量氯化汞染毒组比较,各项指标均有不同程度的改善,差异有统计学意义(P0.05)。结论姜黄素对汞致大鼠肾损伤具有一定的保护作用。     

低砷染毒对小鼠的一般作用研究

目的动态观察低剂量砷染毒小鼠后其一般情况的变化。方法 96只健康雄性KM小鼠随机分组,设0、50、500和5 000μg/L 4个染毒组,再将每个剂量组分4、6和8周3个染毒时间点,经饮水染毒,测定饮水量、饲料消耗量及主要的脏器系数,用原子荧光吸收光谱法测血、肝和肾的总砷含量。结果体重在低和中剂量染毒4周明显增高,高剂量组8周则显著降低。肝脏和肾脏系数均是随染毒时间和染毒剂量的增加出现先增高后降低的现象。脾脏和心脏系数均随染毒时间和染毒剂量的增加而增加(P0.05),肺脏系数在中剂量有明显增高(P0.05)。血砷、肝砷、肾砷含量随着染毒时间和染毒剂量的增加而逐渐增高,差异有统计学意义(P0.05)。结论短时间低剂量砷可以诱导小鼠代偿性反应,随着染毒时间和剂量的增加,主要脏器出现损伤。     

抗氧化药物在肺心病治疗中的意义

本研究在观察慢性肺心病血VitE、脂质过氧化物（LPO）、谷优甘肽过氧化物酶（GSH－PX）、过氧化氨酶（CAT）、超氧化物歧化酶（SOD）、血栓素入（TXA2）、前列腺素I2（PGI2）变化的基础上，并观察了复方丹参、甘糖酯注射液对LPO与抗氧化酶活性的影响。结果表明：VitE含量与GSH－PX、GSH－PX／LPO呈正相关，VitE与LPO、TXB2／6-k-PGF1a呈负相关；复方丹参组治疗后LPO的降低，GSH－PX的增高，甘糖酯组治疗后LPO的降低，CAT的增高，以及两组GSH－PX／LPO增高均较常规组有明显差异。     

丙溴磷对家兔组织中血管内皮活性物质的影响

目的　探讨丙溴磷对组织中血管内皮活性物质的影响及意义。方法　对不同染毒剂量、不同染毒时间家兔进行了全血胆碱酯酶 (ChE)活力 ,以及大脑、肝和肾组织中的内皮素 (ET)、一氧化氮 (NO)浓度的测定。结果　与染毒前和对照组比较 ,染毒后家兔全血ChE活力显著下降 (P <0 0 1) ;染毒后家兔组织中ET浓度 [( 9 2 1～ 12 65 )pg ml]较染毒前 [( 7 98～ 10 2 5 )pg ml]有明显增高趋势 ,而染毒后NO浓度 [( 10 3 8～ 17 3 6)nmol ml]较染毒前 [( 15 44～ 2 5 64 )nmol ml]有明显下降趋势 (P <0 0 5 ,P <0 0 1) ,且随染毒时间延长变化更明显。结论　丙溴磷所致的血管内皮活性物质的紊乱 ,可能是丙溴磷抑制ChE活力以外的毒性表现     

Effects of acetaminophen on reactive oxygen species and nitric oxide redox signaling in kidney of arsenic-exposed rats

We examined whether acetaminophen could alter renal oxidative stress induced by arsenic; also whether withdrawal of acetaminophen treatment can increase susceptibility of kidney to arsenic toxicity. Acetaminophen (400 and 1600 mg/kg) was co-administered orally to rats for 3 days after preexposure to arsenic (25 ppm) for 28 days (Phase-I) and thereafter, acetaminophen was withdrawn, but arsenic exposure was continued for another 28 days (Phase-II). Acetaminophen enhanced arsenic-induced lipid peroxidation, GSH depletion and ROS production and further decreased superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase activities. Increased peroxidation did not alter kidney weight, but increased serum urea nitrogen and creatinine. Arsenic did not alter basal, iNOS-mediated NO production or iNOS expression. Arsenic decreased cNOS-mediated NO release and eNOS expression in Phase-II. Acetaminophen increased their expressions and NO production in Phase-I. In Phase-II, arsenic-mediated effects on NO remained mostly unaffected with acetaminophen. Results reveal that acetaminophen enhanced the risk of arsenic-mediated oxidative stress in kidney. Discontinuation of acetaminophen administration also increased the susceptibility of kidney to nephrotoxic effect of arsenic. It appeared ROS were primarily responsible for oxidative stress in both the phases. NO may have a minor role in Phase-I, but does not contribute to redox signaling mechanism in Phase-II.     

Oxidative stress and hepatic stellate cell activation are key events in arsenic induced liver fibrosis in mice

Arsenic is an environmental toxicant and carcinogen. Exposure to arsenic is associated with development of liver fibrosis and portal hypertension through ill defined mechanisms. We evaluated hepatic fibrogenesis after long term arsenic exposure in a murine model. BALB/c mice were exposed to arsenic by daily gavages of 6 μg/gm body weight for 1 year and were evaluated for markers of hepatic oxidative stress and fibrosis, as well as pro-inflammatory, pro-apoptotic and pro-fibrogenic factors at 9 and 12 months. Hepatic NADPH oxidase activity progressively increased in arsenic exposure with concomitant development of hepatic oxidative stress. Hepatic steatosis with occasional collection of mononuclear inflammatory cells and mild portal fibrosis were the predominant liver lesion observed after 9 months of arsenic exposure, while at 12 months, the changes included mild hepatic steatosis, inflammation, necrosis and significant fibrosis in periportal areas. The pathologic changes in the liver were associated with markers of hepatic stellate cells (HSCs) activation, matrix reorganization and fibrosis including α-smooth muscle actin, transforming growth factor-β1, PDGF-Rβ, pro-inflammatory cytokines and enhanced expression of tissue inhibitor of metalloproteinase-1 and pro(α) collagen type I. Moreover, pro-apoptotic protein Bax was dominantly expressed and Bcl-2 was down-regulated along with increased number of TUNEL positive hepatocytes in liver of arsenic exposed mice. Furthermore, HSCs activation due to increased hepatic oxidative stress observed after in vivo arsenic exposure was recapitulated in co-culture model of isolated HSCs and hepatocytes exposed to arsenic. These findings have implications not only for the understanding of the pathology of arsenic related liver fibrosis but also for the design of preventive strategies in chronic arsenicosis.     

Effect of cysteine, methionine, ascorbic acid and thiamine on arsenic-induced oxidative stress and biochemical alterations in rats

Oxidative stress due to enhanced production of free radicals has been incriminated as one of the several mechanisms involved in arsenic-induced toxic effects in different organs. In the present study, ameliorative potential of certain amino acids like cysteine, methionine and vitamins like ascorbic acid and thiamine on some of the parameters indicative of oxidative stress in liver, kidney and blood and of hepatic and renal infliction was investigated in arsenic exposed rats. Rats were given 0 ppm (group I healthy controls) or 10 ppm arsenic in drinking water ad lib for a period of 12 weeks. During oral exposure to arsenic rats of different groups received daily oral dose of placebo, cysteine, methionine, ascorbic acid or thiamine at 25mg/kg body weight. After the end of the experimental period, animals were sacrificed under light anesthesia and blood, liver and kidney were collected. Samples were processed for estimation of arsenic, biochemical parameters indicative of oxidative stress and hepatic and renal function. Arsenic exposure resulted in significantly (P<0.05) higher accumulation of arsenic in blood, liver and kidney. It was associated with significant (P<0.05) rise in lipid peroxide level and decrease in superoxide dismutase and catalase activities in liver and kidneys. However, alterations in biochemical parameters did not reach statistical (P>0.05) significance. Treatment with vitamins and amino acids resulted in reversal of oxidative stress with significant (P<0.05) decline in tissue arsenic burden. All the treatment produced tissue specific changes in lipid peroxide level, antioxidant enzyme activities and tissue arsenic burden.     

FPBC对猪血清及组织LDH同工酶影响的现场研究

燃煤染氟8个月时,E组猪血清及组织样品经凝胶电泳,发现与C组相比:(1)E组血清LDH_1、LDH_2下降,伴LDH_5升高,有显著性差异(P<0.05);(2)心肌以LDH_2极显著升高(P<0.0l)、LDH_1/LDH;比值显著降低(P<0.05)为其特征,(3)肾组织LDH_6下降而LDH_1代偿性升高(P<0.05);(4)骨骼肌LDH_(2、3、5)不同程度升高,使其TLDH显著升高(P<0 05)。综上表明受氟影响较早,且较敏感的器官组织是骨骼肌和心肌,其次是排氟器官肾脏,建议血清LDH同工酶酶谱可以作为研究人及动物氟中毒时的早期敏感指标。     

Protein oxidative damage in arsenic induced rat brain: influence of DL-alpha-lipoic acid

A body of evidence has accumulated implicating free radical generation and reaction of arsenic with protein thiols in the biochemical and molecular mechanisms of arsenic toxicity. Brain readily undergoes oxidative damage, so it is important to determine whether arsenic-induced changes in rat brain may be associated with oxidative events. An increase in oxidative stress may contribute to the development of protein damage in rat brain. Present experiments were performed to study the effect of arsenic (sodium arsenite, 100 ppm mixed in drinking water) on protein oxidation and further to demonstrate the potential of dl-alpha-lipoic acid (70 mg/kg body weight) against arsenic-induced changes in different anatomic regions (cortex, striatum, cerebellum, hypothalamus and hippocampus) of the brain of male Wistar rats. We report here that arsenic treated rats had a significantly higher level of oxidised protein as assessed by increased carbonyl residues and decreased protein thiols (protein sulfhydryls) as compared to control rats in all five regions studied, with the most notable changes occurring in the cortex, striatum and hippocampus. Coadministration of lipoic acid along with arsenic resulted in reversal of the arsenic induced trends in carbonyl and sulfhydryl concentrations. The results of the study showed, lipoic acid treatment reduces oxidative protein damage in arsenic intoxicated rat brain regions, which is associated with its antioxidant activity that combines free radical scavenging and metal chelating properties.     

Oxidative stress indices and plasma biochemical parameters during oral exposure to arsenic in rats.

An experiment was conducted to study the response of rat tissues to low level exposure of arsenic (III) for different time periods. Rats were exposed to 0 (Gr. I, healthy control, n=18) or 10 ppm arsenic (Gr. II, positive control, n=18) through drinking water ad lib for a maximum period of 12 weeks. Six rats were sacrificed from each group under light chloroform anesthesia at the end of 4, 8 and 12 weeks of arsenic exposure for collection of blood, liver and kidneys. Samples were processed for estimation of oxidative stress indices and biochemical variables indicative of hepatic and renal functions. Tissue arsenic burden was measured at the end of 12 weeks of exposure. Arsenic treated rats (Gr. II) had comparatively poor body weight gain over time, and the mean body weights of these rats were significantly (P<0.05) lower from 10th weeks onwards. Oral exposure to arsenic for a period of 12 weeks significantly (P<0.05) increased arsenic burden in blood, liver and kidney from arsenic treated rats. This was associated with exposure duration-dependent rise (P<0.05) in lipid peroxidation in these tissues. Superoxide dismutase (SOD) and catalase (CAT) activities increased initially (P<0.05) in all the tissues followed by a declining trend and at the end of 12 weeks, the activities were non-significantly (P>0.05) lower than respective controls. Alterations in most of the biochemical parameters did not reach statistical significance (P>0.05). It was concluded from the present study that low dose arsenic exposure for a shorter period caused activation of intrinsic antioxidant defense whereas a prolonged insult suppressed it. However, biochemical parameters indicative of hepatic and renal dysfunction remained well within the normal range.     

Hepatic damage caused by chronic arsenic toxicity in experimental animals

OBJECTIVE: Noncirrhotic fibrosis of the liver is common in subjects chronically consuming ground water geologically contaminated with arsenic, but the mechanism of the hepatic fibrosis is not known. Because lipid peroxidation has been implicated in the development of several other forms of hepatic fibrosis, including iron and copper overload, we have explored the roles of oxidative stress and lipid peroxidation in the causation of hepatic fibrosis in a murine model of chronic arsenic toxicity. METHODS: Male BALB/c mice were given drinking water contaminated with arsenic (3.2 mg/L) or arsenic-free (<0.01 mg/L, control) ad libitum. Mice were sacrificed at 3, 6, 9, 12, and 15 months for examination of hepatic histology and assays of hepatic reduced glutathione content, lipid peroxidation, enzymes of the antioxidant defense system, and membrane-bound sodium/potassium ATPase (Na+/K+ ATPase). RESULTS: After 12 months of arsenic feeding, the liver weights increased significantly as did serum aspartate aminotransferase and alanine aminotransferase. After 6 months of arsenic feeding, hepatic glutathione and the enzymes glucose-6-phosphate dehydrogenase and glutathione peroxidase were significantly lower than those of the control group. Hepatic catalase activity was significantly reduced at 9 months in the arsenic-fed group, while glutathione-S-transferase and glutathione reductase activities were also significantly reduced at 12 and 15 months. Plasma membrane Na+/K+ ATPase activity was reduced after 6 months while lipid peroxidation increased significantly after 6 months of arsenic feeding. Liver histology remained normal for the first 9 months, but showed fatty infiltration after 12 months of arsenic feeding. Histologic evidence of fibrosis was observed after 15 months. CONCLUSION: We have demonstrated hepatic fibrosis due to long-term arsenic toxicity in an animal model. Initial biochemical evidence of hepatic membrane damage, probably due to reduction of glutathione and antioxidant enzymes, may be seen by 6 months. Continued arsenic feeding resulted in fatty liver with serum aminotransferase and alanine aminotransferase elevated at 12 months and hepatic fibrosis at 15 months. The murine model is proposed as relevant to epidemic human toxicity in areas of arsenic contamination.     

抗血小板药物的非血流灌注依赖性神经保护作用及其性别差异研究

目的　探讨抗血小板药物的非血流灌注依赖性神经保护作用及其性别差异。方法　在无血流因素影响的小鼠海马脑片观察乙酰水杨酸 (ASA)、噻氯匹啶和氯吡格雷预处理前后群峰电位波幅 (PSA)在缺氧和恢复供氧时的变化 ,以及不同性别小鼠ASA预处理前后PSA和还原型辅酶I(NADH)荧光强度缺氧前后的变化。结果　对照组缺氧后PSA恢复为 (2 5 9± 11 6 ) % ,ASA、噻氯匹啶和氯吡格雷预处理组缺氧后PSA恢复分别为 (74 7± 35 7) % (P <0 0 5 )、(6 7 8± 38 4 ) % (P <0 0 5 )和 (77 8± 2 6 5 ) % (P <0 0 1)。ASA预处理在雌雄性动物显示不同的保护效果 ,雌性组PSA缺氧后恢复为 (48 4± 34 0 ) % (与雌性对照组比较P <0 0 5 ,与雄性ASA预处理组比较P <0 0 5 ) ;缺氧时NADH增加幅度在雄性和雌性动物分别由对照组的 (14 1 8±9 9) %和 (2 0 4 9± 74 1) %降至ASA预处理后的 (117 9±10 3) % (P <0 0 5 )和 (12 4 0± 11 0 ) % (P <0 0 1)。结论　抗血小板药物的神经保护机制涉及非血流灌注依赖途径 ,该作用存在性别差异 ,差异的形成与NADH相关的氧化能量代谢有关     

Renal, hepatic, pulmonary and adrenal tumors induced by prenatal inorganic arsenic followed by dimethylarsinic acid in adulthood in CD1 mice

Inorganic arsenic, an early life carcinogen in humans and mice, can initiate lesions promotable by other agents in later life. The biomethylation product of arsenic, dimethylarsinic acid (DMA), is a multi-site tumor promoter. Thus, pregnant CD1 mice were given drinking water (0 ppm or 85 ppm arsenic) from gestation day 8 to 18 and after weaning male offspring received DMA (0 ppm or 200 ppm; drinking water) for up to 2 years. No renal tumors occurred in controls or DMA alone treated mice while gestational arsenic exposure plus later DMA induced a significant renal tumor incidence of 17% (primarily renal cell carcinoma). Arsenic plus DMA or arsenic alone also increased renal hyperplasia over control but DMA alone did not. Arsenic alone, DMA alone and arsenic plus DMA all induced urinary bladder hyperplasia (33-35%) versus control (2%). Compared to control (6%), arsenic alone tripled hepatocellular carcinoma (20%), and arsenic plus DMA doubled this rate again (43%), but DMA alone had no effect. DMA alone, arsenic alone, and arsenic plus DMA increased lung adenocarcinomas and adrenal adenomas versus control. Overall, DMA in adulthood promoted tumors/lesions initiated by prenatal arsenic in the kidney and liver, but acted independently in the urinary bladder, lung and adrenal.     

乌头碱对小鼠腹腔巨噬细胞Ia抗原表达影响的研究

目的：观察乌头碱（ＡＴＮ）对正常小鼠和皮质酮所致阳虚模型小鼠腹腔巨噬细胞（ＭΦ）在干扰素（ＩＮＦ－γ）诱导下，其表面Ｉａ抗原表达的改变。方法：采用流式细胞技术测定。结果：正常小鼠腹腔注射ＡＴＮ（１．５、３．０和６．０μｇ·ｋｇ－１·ｄ－１）７ｄ后，其ＭΦ在３００Ｕ·Ｌ－１浓度ＩＮＦ－的诱导下Ｉａ抗原表达明显增强，反映Ｉａ抗原表达的荧光强度从对照组的９３．０１±１３．３０增加到１０８．９０±８．６３、１１３．０１±１２．８０和１１３．５７±１０．１３（Ｐ＜０．０５）。阳虚模型小鼠腹腔ＭΦ在ＩＦＮ－诱导下的Ｉａ抗原表达明显低于正常小鼠（９０．８０±７．３６和１０９．９６±１０．３７，Ｐ＜０．０５），但ＡＴＮ治疗可使阳虚模型小鼠ＭΦ的Ｉａ抗原表达增强到１１１．１１±１４．４８、１１７．８９±１４．６４和１１５．６１±１３．７４，与模型组相比差异显著（Ｐ＜０．０５和Ｐ＜０．０１）。结论：说明ＡＴＮ能够提高正常小鼠和皮质酮免疫抑制阳虚模型小鼠ＭΦＩａ抗原的表达，从而增强ＭΦ递呈抗原能力，促进免疫应答反应。