羧甲基茯苓多糖抗疲劳作用研究

研究羧甲基茯苓多糖(CMP)对小鼠抗疲劳作用。将雄性小鼠随机分为5组,分别为空白对照组、阳性对照组、CMP低剂量组(35 mg/(kg bw·d))、CMP中剂量组(70 mg/(kg bw·d))、CMP高剂量组(140 mg/(kg bw·d)),灌胃给药30 d后,测定小鼠负重的游泳时间、血清尿素氮和血乳酸等指标。结果表明,与空白对照组相比,CMP可以延长小鼠负重游泳时间(P0.05);CMP中、高剂量组可以显著降低血清尿素氮、血乳酸含量并提高肝脏SOD活性(P0.05)。CMP对小鼠具有很好的抗疲劳作用,其机制可能与降低血清尿氮素、血乳酸含量以及提高肝脏SOD活性有关。     

牦牛皮胶对环磷酰胺致贫血小鼠血象红系参数及脾脏结构的影响

探讨牦牛皮胶对环磷酰胺所致的贫血小鼠的血象红系参数和脾脏结构的影响。采用腹腔注射环磷酰胺建立小鼠贫血模型,造模4天后各给药组小鼠分别ig牦牛皮胶1、2、3、6 g/(kg·d),阿胶补血颗粒14.05 g/(kg·d),在给药后的第7、14、21天检测各组小鼠的外周血象,计算脾脏和胸腺系数,切片观察脾脏的形态结构。结果表明,与模型组相比,1 g/(kg·d)牦牛皮胶给药组给药7、14、21 d,血红蛋白显著升高(P 0.05); 2 g/(kg·d)牦牛皮胶给药组给药7、14、21天,红细胞数、血红蛋白、红细胞比容、平均血红蛋白量及平均血红蛋白浓度显著升高(P 0.05); 3g/(kg·d)牦牛皮胶给药组给药14、21天,红细胞数及平均血红蛋白浓度显著升高(P 0.05); 6 g/(kg·d)牦牛皮胶给药组给药7、14天,平均血红蛋白量显著升高(P 0.05);各给药组脾脏淋巴细胞增多,白髓与红髓的界限变清晰。综上,各浓度牦牛皮胶对贫血小鼠均有补血作用,其中2 g/(kg·d)的牦牛皮胶给药剂量,14天的给药时间的补血作用较为理想。     

大豆多糖联合环磷酰胺对S180荷瘤小鼠抗肿瘤增效作用研究

目的 从免疫学角度研究大豆多糖对环磷酰胺的减毒增效作用及其机制.方法 选用昆明种小鼠80只,随机分为阴性对照;大豆多糖(SSPS)组:50、100、200 mg/(kg· d);阳性对照:环磷酰胺(CP) 25 mg/(kg·d);大豆多糖联合环磷酰胺组:(1)CP 25 mg/(kg·d)+SSPS mg/(kg·d)、(2)CP 25 mg/(kg·d)+SSPS 100 mg/(kg·d)、(3)CP25 mg/(kg·d)+SSPS200 mg/(kg·d);0.2 mL/只,腋下接种S180,腹腔给药,连续给药10d.测定大豆多糖联合环磷酰胺对S180荷瘤小鼠瘤重、胸腺指数、脾指数的影响,ELISA法检测S180荷瘤小鼠外周血血清中细胞因子IL-2含量的影响.结果 大豆多糖能够抑制S180荷瘤小鼠的肿瘤生长,其抑瘤率分别为24.10％、35.39％和39.75％,与环磷酰胺合用后其抑瘤率为89.87％、91.91％和92.63％(P＜0.05,P＜0.01),q值0.99 ～1.00,具有协同作用;且合用后提高了环磷酰胺所致免疫低下小鼠的胸腺指数和脾指数;并促进S180荷瘤小鼠分泌IL-2.结论 大豆多糖通过增加荷瘤小鼠免疫功能而减轻环磷酰胺对机体的毒副反应,增强其抗肿瘤作用.     

金思维对东莨菪碱致记忆障碍小鼠脑胆碱能系统的影响

目的 通过建立东莨菪碱记忆障碍模型,采用中药复方金思维进行干预,观察金思维对东莨菪碱致记忆障碍模型小鼠行为学和胆碱能系统的影响,探讨该药的神经保护作用机制。方法 将ICR小鼠随机分为正常对照组;模型组,溶媒0.5%CMC;阳性对照组,多奈哌齐,0.92 mg/(kg·d);金思维大、中、小剂量组,20、10、5 mg/(kg·d)。每组18只,按0.1 mL/10 g小鼠体重连续灌胃给药30 d。末次给药后造模,对照组腹腔注射生理盐水,其余各组腹腔注射东莨菪碱3 mg/(kg·d),溶于0.9%生理盐水,按0.1 mL/10 g小鼠体重注射,进行Morris水迷宫实验。实验结束后取皮层和海马组织,分别测定皮层和海马中乙酰胆碱(Ach)含量、乙酰胆碱酯酶(Ach E)及胆碱乙酰转移酶(Ch AT)活性。结果 金思维可使模型小鼠游泳距离和游泳时间缩短及目标象限停留时间增长;金思维可使模型组小鼠脑内Ach含量升高、Ach E活性下降和Ch AT活性升高。结论 金思维可以改善东莨菪碱导致的记忆障碍模型小鼠学习记忆能力,其机制可能与胆碱能能系统有关。     

初步探讨鸟嘌呤核苷、姜黄素对AD双转基因小鼠学习记忆的影响

目的通过Morris水迷宫检测学习记忆和记忆保持能力,判断鸟嘌呤核苷、姜黄素对4月龄APPswe/PS1dE9双转基因小鼠认知功能的影响。方法将3月龄APPswe/PS1dE9双转基因小鼠随机分为模型组、盐酸多奈哌齐组0.92 mg/(kg·d)、鸟嘌呤核苷组20 mg/(kg·d)、姜黄素组200 mg/(kg·d)、姜黄素200 mg/(kg·d)和鸟嘌呤核苷组20 mg/(kg·d),每组12只;并以同月龄野生型C57/BL6J小鼠作对照。每天给药1次,连续给药1个月。应用Morris水迷宫进行行为学检测。结果鸟嘌呤核苷、姜黄素对空间探索、定位航行障碍有改善作用,尤其以姜黄素组明显。结论鸟嘌呤核苷、姜黄素能改善APPswe/PS1dE9双转基因小鼠的早期出现的认知障碍。     

硫丹及其主要代谢产物对紫色土中酶活性的影响

采用室内避光培养,研究了硫丹及其主要代谢产物(硫丹硫酸盐和硫丹二醇)在紫色土中的质量浓度变化及其对土壤酶活性的影响。结果表明,α-、β-硫丹在紫色土中的消解过程符合一级反应动力学方程,半衰期分别为32—99d和69—116 d。代谢产物硫丹硫酸盐浓度在前20 d增加较快,30 d后基本趋于稳定;硫丹二醇浓度先增加后减小,15 d时达到最大。5 mg/kg的硫丹处理5 d时对脲酶和硝酸还原酶活性起激活作用,随着培养时间的增加,硫丹处理对脲酶活性从无显著影响逐渐转向抑制,第60天时抑制作用达到最大;高浓度处理(100 mg/kg)强烈抑制脲酶活性,最大降幅达到94.5%。硫丹处理(除5 mg/kg外)对硝酸还原酶活性起抑制作用,浓度越大,抑制作用越强,最大降幅达到89.9%。5 mg/kg的处理抑制多酚氧化酶活性,10—20 mg/kg的处理30 d后由激活逐渐转向抑制;100 mg/kg的处理起激活作用,第15天时酶活性达到最大,随后持续下降,第60天时恢复到对照水平。偏相关分析表明,脲酶、硝酸还原酶活性与硫丹硫酸盐浓度呈显著负相关,硫丹硫酸盐抑制这两种酶的活性;多酚氧化酶活性与α-、β-硫丹、硫丹硫酸盐和硫丹二醇浓度的偏相关性不显著。     

牛大力多糖对小鼠抗疲劳作用的研究

本文以牛大力(Millettia speciosa Champ.)为对象,利用小鼠爬杆和负重游泳为实验模型,研究了其多糖的抗疲劳作用。实验随机将小鼠分为五组,分别为空白对照组、阳性药(人参蜂王浆,7 mL/kg)对照组、牛大力多糖低剂量组[212.5 mg/(kg·d)]、中剂量组[425 mg/(kg·d)]、高剂量组[850 mg/(kg·d)],灌胃给药14 d后,考察其对小鼠爬杆时间、负重游泳时间以及血乳酸(LD)、血乳酸脱氢酶(LD-H)、血中尿素氮(BUN)含量的影响。结果表明,牛大力多糖能延长小鼠爬杆时间,增加小鼠游泳耐力,降低LD、BUN的含量、提高血中LD-H含量。且中剂量的药效与阳性药对照组的基本相当。     

药物滥用者红细胞免疫功能的变化

通过检测红细胞C3b受体花环（RBC－C3bRR)、红细胞免疫复合物光环（RBC－ICR）、粘附增强因子活性（RFER）及抑制因子活性（RFIR）,观察了50例海洛因依赖者红细胞免疫功能的变化。结果表明,海洛因依赖者RBC－C3bRR、RFER明显下降（P＜0．01）,而RBC-ICR、RFIR则明显升高（P＜0．01）。本文对检测结果进行了初步探讨。     

青春期丙烯酰胺暴露对小鼠肺组织氧化损伤的影响

目的 探究丙烯酰胺(acrylamide, ACR)对小鼠肺组织的损伤及其可能机制。方法 以4周龄SPF级雄性小鼠为实验动物，随机分为对照组和ACR组(10 mg/(kg·d)组和20 mg/(kg·d)组),每组8只。对照组给予常规饮用水；ACR组按小鼠每日饮水5 mL来配制ACR的染毒浓度，每3 d更换1次，连续处理4周。实验结束后取肺组织制作切片，进行组织病理学分析；利用试剂盒检测其氧化损伤的相关指标；进一步利用免疫荧光与Western Blot技术检测Nrf2-ARE通路相关蛋白表达。结果 与对照组相比，随ACR摄入浓度的增加，小鼠体重逐渐下降(P<0.01);组织病理学分析发现，ACR组小鼠肺组织出现细支气管上皮肥大，肺泡上皮增生及肺泡腔面积明显减少，20 mg/(kg·d)组病理学改变更为明显；氧化应激指标检测发现，与对照组相比，随着ACR摄入浓度的增加，肺组织中GSH-PX活性逐渐下降(P<0.05)、SOD活力逐渐下降(P<0.05)、CAT活力逐渐下降(P<0.01),而MDA的含量明显上升(P<0.01);免疫荧光结果显示，与对照组相比...     

分枝杆菌L型感染与肺癌患者红细胞免疫功能改变的相关性

目的:研究分枝杆菌L型血行感染与肺癌患者红细胞免疫功能改变的相关性.方法:溶血离心培养法和滴片法检测血液中的分枝杆菌L型,常规方法测定红细胞沉降率(ESR)、红细胞C3b受体花环率(C3bRR)、免疫复合物花环率(ICRR)、血清红细胞C3b受体花环促进率(RFER)和抑制率(RFIR).结果:TBL( )与TBL(-)肺癌患者相比,C3bRR和ICRR两项指标均明显降低.TBL( )肺癌与TBL(-)肺癌患者相比,ESR增快更为显著.TBL(-)较TBL( )之RFER值的降低更为明显.RFIR差异未见有显著性.结论:分枝杆菌L型血行感染影响肺癌患者血沉和红细胞免疫功能改变.     

The effect of ethanol on erythrocyte carbonic anhydrase isoenzymes activity: an in vitro and in vivo study

The ethanol is a widely consumed as sedative-hypnotic drug throughout the world. In this study, the effects of ethanol were investigated on carbonic anhydrase (CA) enzyme activities both in vitro in human erythrocyte and in vivo in Sprague-Dawley rat erythrocyte. For in vitro study, the human carbonic anhydrase-I (HCA-I) and -II (HCA-II) are purified by Sepharose 4B-L-tyrosine-sulphanilamide affinity chromatography. In vivo CA enzyme activity was determined colorimetrically by using CO(2)-hydration method of Wilbur and Anderson. Rat blood samples were taken from each rat before and after the ethanol administration at different times (1 h, 3 h, and 5 h). Rat erythrocyte CA activity was significantly inhibited by pharmacological dosage of the ethanol (2 mL.kg(- 1)) for up to 3 h (p < 0.001) following intraperitoneally administration. The ethanol showed in vitro inhibitory effects on HCA-I and HCA-II hydratase activity, determined by colorimetrically using the CO(2)-hydratase method. The inhibitor concentrations causing up to 50% inhibition (IC(50)) were 2.09 M for HCA-I (r(2):0.9273) and 1.83 M for HCA-II (r(2):9749). In conclusion, it was demonstrated that carbonic anhydrase enzyme in erythrocytes was significantly inhibited by the ethanol both in in vitro and in vivo.     

The effect of therapeutic drugs and other pharmacologic agents on activity of porphobilinogen deaminase, the enzyme that is deficient in intermittent acute porphyria.

Drugs and toxins precipitate life-threatening acute attacks in patients with intermittent acute porphyria. These materials may act by directly inhibiting enzyme activity, thus further reducing porphobilinogen (PBG) deaminase activity below the ca. 50% level that results from the gene defect. To test this, we studied the effects of drugs that precipitate acute attacks (lead, phenobarbital, griseofulvin, phenytoin, sulfanilamide, sulfisoxazole, 17alpha-ethinyl estradiol, 5beta-pregnan-3alpha-ol-20-one), drugs that are safe (lithium, magnesium, chlorpromazine, promethazine), and those with uncertain effects (ethyl alcohol, imipramine, diazepam, haloperidol) on activity of PBG deaminase in vitro and in vivo. In the in vitro studies, of PBG deaminase from human erythrocytes from normals and individuals with IAP, only lead (> or = .01 mM) inhibited enzyme activity. Chlorpromazine (> or = .01 mM), promethazine (> or = .01 mM) and imipramine (1 mM) seemed to increase enzyme activity. In most in vivo experiments, male rats were injected intraperitoneally with test material twice daily for 3 days and once on day four; and erythrocyte and hepatic PBG deaminase activity was assayed thereafter. Effects on enzyme activity were observed only with 17alpha-ethinyl estradiol (0.05 microg/kg/day; reduction of 11% in erythrocyte enzyme [NS], and of 20% in liver enzyme [P=.02]), and imipramine (12.5 mg/kg/day; reduction in erythrocyte enzyme activity of 13% [P<.001]). Rats given lead acetate in their drinking water (10 mg/ml) for the first 60 days of life, resulting in high blood and liver lead levels, had increased erythrocyte PBG deaminase (167% of control; P=.004). Thus, enzyme inhibition by lead in vitro was not reflected in a similar in vivo inhibition. The only inhibitory effects in vivo, with ethinyl estradiol and imipramine, appear to be mild and biologically inconsequential. We conclude that inhibition of PBG deaminase activity by materials that precipitate acute attacks is an unlikely mechanism by which these materials exert their harmful effects in patients with IAP.     

Sublethal ammonia and urea concentrations inhibit rainbow trout (Oncorhynchus mykiss) erythrocyte glucose-6-phosphate dehydrogenase

In vitro and in vivo effects of sublethal ammonia and urea concentrations were assayed on glucose-6-phosphate dehydrogenase (G6PD) of rainbow trout (Oncorhynchus mykiss) erythrocyte. G6PD was purified from erythrocytes with a specific activity of 16.7 EU (mmol NADP+/min)/mg protein and approximately 1600-fold in a yield of approximately 60% by ammonium sulphate precipitation and 2',5'-ADP Sepharose 4B affinity chromatography. The purity of the enzyme was confirmed using SDS polyacrylamide gel electrophoresis. Experiments with ammonia (2.2-5.5 microM) and urea (20-50 microM) showed the inhibitory effects on the enzyme, in vitro. Inhibition effects were determined in vitro by Lineweaver-Burk and regression graphs. The dissociation constant of the enzyme inhibitor complex (Ki) and 50% inhibitory values were 2.26+/-1.21 and 2.86+/-3.51 microM for ammonia and 18.69+/-6.75 and 23.77+/-4.58 microM for urea, respectively. In vivo studies in rainbow trout erythrocytes showed significant (p < 0.01) inhibition of G6PD by ammonia and urea. However, ammonia inhibited more than urea since there were significant differences between the final values of erythrocyte G6PD activities.     

Plasmodium falciparum: Rosettes do not protect merozoites from invasion-inhibitory antibodies

Rosetting is a parasite adhesion phenotype associated with severe malaria in African children. Why parasites form rosettes is unknown, although enhanced invasion or immune evasion have been suggested as possible functions. Previous work showed that rosetting does not enhance parasite invasion under standard in vitro conditions. We hypothesised that rosetting might promote invasion in the presence of host invasion-inhibitory antibodies, by allowing merozoites direct entry into the erythrocytes in the rosette and so minimising exposure to plasma antibodies. We therefore investigated whether rosetting influences invasion in the presence of invasion-inhibitory antibodies to MSP-1. We found no difference in invasion rates between isogenic rosetting and non-rosetting lines from two parasite strains, R29 and TM284, in the presence of MSP-1 antibodies (P = 0.62 and P = 0.63, Student's t test, TM284 and R29, respectively). These results do not support the hypothesis that rosettes protect merozoites from inhibitory antibodies during invasion. The biological function of rosetting remains unknown.     

硫化氢合成酶抑制剂金丝桃素的体内外抗结肠癌作用研究

为研究金丝桃素对硫化氢合成酶活性的影响,探索金丝桃素作为胱硫醚-β-合成酶(CBS)抑制剂的体内外抗结肠癌作用。本研究通过亚甲蓝法测定金丝桃素和氨基氧乙酸(AOAA)对CBS产H2S活性的抑制作用,以HT29人结肠癌细胞和移植HT29细胞的裸鼠肿瘤模型为抗肿瘤研究对象,测定金丝桃素体内外抗肿瘤作用。结果表明,来源于贯叶连翘(Hypericum perforatum L.)的化合物金丝桃素是CBS的高效选择性抑制剂,其IC50为7.9±1.42μmol/L。金丝桃素能显著抑制HT29人结肠癌细胞的增殖,其IC50为22.2±2.25μmol/L。基因沉默实验表明CBS蛋白可能是金丝桃素在细胞内的潜在靶标之一。意外的是,目前普遍使用的CBS抑制剂AOAA抑制HT29细胞增殖作用非常弱,其IC50为152.5±35.68μmol/L。此外,不同剂量的金丝桃素(5~30mg/kg·d)均能显著减少裸鼠肿瘤体积和重量,30mg/kg·d剂量皮下给药2周后,和对照组相比肿瘤重量减少了68%。以上结果表明金丝桃素作为CBS的选择性抑制剂具有显著的抗结肠癌作用。     

Chemoprotective effects of carnosine against genotoxicity induced by cyclophosphamide in mice bone marrow cells

The protective effects of carnosine as a natural dipeptide were investigated in mouse bone marrow cells against genotoxicity induced by cyclophosphamide. Mice were injected with solutions of carnosine at three different doses (10, 50 and 100?mg kg(-1) bw) for five consecutive days. On the fifth day of treatment, mice were injected cyclophosphamide and killed after 24?h. The frequency of micronuclei in polychromatic erythrocytes and the ratio of polychromatic erythrocyte/polychromatic erythrocyte?+?normochromatic erythrocyte [PCE/(PCE?+?NCE)] were evaluated by May-Grunwald/Giemsa staining. Histopathology of bone marrow was examined in mice treated with cyclophosphamide and carnosine. Carnosine significantly reduced micronucleated polychromatic erythrocytes (MnPCEs) induced by cyclophosphamide at all three doses. Carnosine at dose of 100?mg kg(-1) bw reduced MnPCEs 3.76-fold and completely normalized the PCE/(PCE?+?NCE) ratio. Administration of carnosine inhibited bone marrow toxicity induced by cyclophosphamide. It appeared that carnosine with protective activity reduced the oxidative stress and genotoxicity induced by cyclophosphamide in bone marrow cells of mice. Copyright ? 2012 John Wiley & Sons, Ltd.     

Effects of some antibiotics on human erythrocyte 6-phosphogluconate dehydrogenase: an in vitro and in vivo study

The in vitro and in vivo effects of some antibiotics on human erythrocyte 6-phosphogluconate dehydrogenase were investigated. Human erythrocyte 6-phosphogluconate dehydrogenase was purified with ammonium sulphate precipitation, 2',5' ADP-Sepharose 4B affinity and gel filtration chromatography. Some antibiotics (netilmicin sulphate, cefepime, amikacin, isepamycin, chloramphenicol, ceftazidim, teicoplanin, ampicillin, ofloxacin, levofloxacin, cefotaxime, penicillin G, gentamicin sulphate, ciprofloxacin) inhibited enzyme activity in vitro but others (cefozin, decefin, streptomycin, combisid, and meronem) were devoid of inhibitory effects. For the drugs having low IC50 values (netilmicin sulphate and cefepime), in vivo studies were performed in rats. Netilmicin sulphate at 15-mg/kg inhibited enzyme activity significantly (p < 0.001) 1 h, 2 h, and 3 h after dosing and cefepime at 200-mg/kg very significantly (p < 0.001) inhibited the enzyme 1 h and 2 h after dosing. Netilmicin sulphate and cefepime inhibited rat erythrocyte 6-phosphogluconate dehydrogenase both in vivo and in-vitro.     

Copper activation of superoxide dismutase in rat erythrocytes

Several lines of evidence suggested that copper can activate a preexisting pool of superoxide dismutase (SOD) apoprotein in erythrocytes from copper-deficient rats. First, feeding adequate copper to copper-deficient rats raised initially low erythrocyte SOD activities to normal values in under one-third the time needed to replace the entire red cell population. Moreover, copper injection (1 mg Cu/kg, sc) doubled erythrocyte SOD activity levels in 16 h. Since protein synthesis is restricted in mature erythrocytes, these results imply that copper activated apoSOD in vivo. Furthermore, injected copper raised SOD activity contents of both young and old erythrocytes. Neither dietary copper status nor copper injection influenced red cell SOD immunoreactive protein levels. In contrast, copper injection increased the amount of copper associated with the SOD activity peak region resulting from gel filtration of hemoglobin-free erythrocyte proteins on Sephadex G-75. Copper ions (3 microM) elevated SOD activity levels in vitro by 63% in 4 h in intact red cells from copper-deficient rats. No activation took place in lysed red cells from the same rats or in intact cells from copper-adequate rats. These results all suggest that copper can activate SOD apoprotein in erythrocytes by a specific, saturable process.     

形态学与形态计量学观察大豆异黄酮对前列腺增生大鼠的作用

目的探讨不同剂量大豆异黄酮(SI)对前列腺增生大鼠组织形态学和超微结构的影响。方法应用丙酸睾酮诱导雄性SD大鼠前列腺增生,随机分为五组:正常对照组、模型组和3个大豆异黄酮剂量组,分别灌胃SI 60、120、240 mg/(kg.d),28 d后,光镜观察前列腺组织形态,同时结合图像分析系统检测前列腺腺体、间质的形态计量学改变,透射电镜观察前列腺细胞超微结构的变化。结果各剂量大豆异黄酮均可降低前列腺增生大鼠前列腺湿重、指数及体积,降低上皮细胞高度、腺体面积、腺体相对总体积、单位体积内腺体平均直径、平均体积、平均表面积和间质相对总体积,提高腺体数目、腺体数密度、腺体表面积/腺体体积和腺体平均曲率。结论大豆异黄酮具有抑制大鼠前列腺增生的作用。     

鳖甲育肝颗粒对乙醇性肝纤维化大鼠的影响*

目的:探讨鳖甲育肝颗粒对乙醇性肝纤维化大鼠的防治作用。方法:将SD大鼠随机分为空白对照组、模型对照组、鳖甲育肝颗粒对照组、秋水仙碱组、鳖甲育肝颗粒低剂量组和鳖甲育肝颗粒高剂量组(n=8),采用梯度乙醇灌胃法复制肝纤维化动物模型,即除了空白对照组及鳖甲育肝颗粒对照组灌胃等量纯净水外,其余各组大鼠第1～4周灌胃5 g/(kg·d)乙醇,第5～8周灌胃7 g/(kg·d)乙醇,第9～12周灌胃9 g/(kg·d)乙醇,第13～24周灌胃9.5 g/(kg·d)乙醇,其中乙醇剂量计算采用下列公式:乙醇剂量(g) = 无水乙醇体积(ml)×预配乙醇浓度(%)×0.8(g/ml),同时每天灌胃相应的药物:鳖甲育肝颗粒对照组灌胃鳖甲育肝颗粒5.55 g/kg、秋水仙碱组灌胃秋水仙碱0.1 mg/kg、鳖甲育肝颗粒低剂量组灌胃鳖甲育肝颗粒1.85 g/kg、鳖甲育肝颗粒高剂量组灌胃鳖甲育肝颗粒5.55 g/kg,空白对照组及模型对照组灌胃等量纯净水。实验第169日观测鳖甲育肝颗粒对大鼠肝脏脏器宏观变化、肝组织含水量及其纤维化病理变化、肝组织羟脯氨酸(Hyp)含量及α-平滑肌肌动蛋白(α-SMA)、CREB表达水平的影响。结果:1.85、5.55 g/kg鳖甲育肝颗粒能明显改善乙醇性肝纤维化大鼠肝脏脏器宏观变化及肝组织纤维化病理变化,降低肝组织含水量及Hyp的含量,下调α-SMA、CREB表达水平。结论:鳖甲育肝颗粒具有明显的抑制乙醇性肝纤维化的作用,而下调CREB是其抗肝纤维化的作用机制之一。