怀槐异黄酮抗妊娠小鼠肝损伤的作用

目的观察怀槐异黄酮对雌激素诱导小鼠肝损伤的保护作用并探讨其作用机制。方法选择BALB/c孕鼠随机分为正常组、溶剂组、肝损伤模型组和大、中、小剂量异黄酮给药组,每组10只,给药组从受孕第7天开始分别灌胃异黄酮,每天1次,共7 d。除正常组外,各组从妊娠10 d起连续4 d皮下注射17-α-乙炔雌二醇1.0μg/g体重。常规检测孕鼠血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)活性水平和肝脏组织病理。结果给异黄酮的孕鼠血清ALT、AST活性水平显著下降,与肝损伤模型孕鼠比较差异有统计学意义(P<0.05),其肝脏组织病理学结果也证实给药孕鼠肝脏病理明显改善。结论怀槐异黄酮对雌激素诱导的小鼠肝损伤有显著保护作用。     

同种与异种胎胸腺混合移植诱导供者皮肤移植免疫耐受

目的:探讨同种异种胎胸腺混合移植达到供者皮肤移植的耐受。方法:实验于2003-03/12在第三军医大学创伤、烧伤、复合伤实验室完成。将F344大鼠胎胸腺和C57BL/6小鼠胎胸腺混合移植到BALB/C裸小鼠的双肾包膜下4个月后,用流式细胞仪技术检测裸小鼠外周血中CD3+和CD4+T细胞,用单向混合淋巴细胞培养了解T细胞对ConA以及同种异种淋巴细胞的反应性,异基因皮肤移植观察皮肤移植物存活期。结果:①混合移植胎胸腺4个月后,受者裸小鼠外周血中CD3+和CD4+T细胞占总白细胞的25.9%,正常裸小鼠外周血中CD3+和CD4+量极少(2.43%)。②受者T细胞对ConA以及无关的SD鼠异种淋巴细胞的反应性强(刺激指数分别为23.23与12.75),而对供者F344及C57BL/6淋巴细胞不发生增殖反应(刺激指数分别为1.12与0.98)。③受者对供者F344及C57BL/6鼠皮肤移植物86d不发生排斥,而对无关的SD鼠皮肤移植物15d即发生排斥。结论:受体对胸腺供体来源的F344和C57BL/6皮肤及宿主本身的BALB/C皮肤移植耐受,而对无关的SD鼠皮肤移植物较短时间内即发生了排斥,并且抗DNA自身抗体水平与正常鼠相似。表明同种和异种胸腺混合移植后受体可重建有免疫功能的T淋巴细胞,并能诱导供者特异性免疫耐受的发生。     

不同时段剂量腹腔注射百草枯致小鼠肺损伤及肺纤维化效果评价

目的 观察不同时段、剂量腹腔注射百草枯(PQ)对于小鼠肺损伤及肺纤维化诱导效果的区别,以期建立更为合适、操作简便且结果稳定的肺损伤和/或肺纤维化动物模型.方法 8～10周龄雄性C57BL/6J小鼠,分别采取腹腔注射单次给药(40 mg/kg、50 mg/kg、60 mg/kg),连续给药(10 mg/kg、12.5 mg/kg、15 mg/kg),以及间断给药(20 mg/kg、22.5 mg/kg、25 mg/kg)的方法,同组随机(随机数字法)匹配生理盐水对照组.分别于末次给药后1周、2周处死小鼠.监测小鼠一般情况,体质量状况及病死率.收获日检测肺功能指标;肺泡支气管灌洗液(BALF)细胞计数及分类;羟脯氨酸浓度;以及组织病理学分析.结果 单次或间断腹腔注射不同剂量PQ,均可诱导部分小鼠发生急性肺损伤,早期观察时间点的炎症表现随剂量增高而加重;晚期观察点少量存活小鼠可发生肺间质纤维化.病理切片见损伤部位主要集中在背后段、外周及胸膜下.但以上两组给药方式早期均有较高病死率,故晚期肺纤维化致病率较低.小剂量PQ连续给药法在各时间点诱导C57BL/6J小鼠的肺部病变缺乏显著意义.结论 单次大剂量或间断中等剂量腹腔注射作为PQ全身性给药的方法之一,可以成功诱导出早期小鼠急性肺损伤,但研究终点肺纤维化的致病率较低.PQ小剂量连续给药法致C57BL/6J鼠系肺损伤及肺纤维化的效果不明显.     

不同品系小鼠幽门螺杆菌感染实验模型的建立及其病理特征的比较

目的应用不同的HP菌株感染不同遗传背景小鼠,观察HP的感染状况及病理特征。方法SPF级C57BL/6及BALB/C小鼠预先灌饲0.5 ml NaHCO3(0.1M),随后分别接种HP SS1、NCTC11637菌液0.5 ml(1×109CUF/ml)连续4次,间隔48 h,对照组灌饲相同剂量的PBS。于末次接种后4、8、12周处死小鼠,胃黏膜行快速尿素酶检测、HP培养以及病理组织学检查。结果C57BL/6小鼠接种HP SS1后4、8及12周HP感染率均为100%,HP主要定植在胃窦部及胃窦/胃体交界部,黏膜下可见淋巴细胞及单核细胞浸润。C57BL/6小鼠接种HP NCTC 11637、BALB/C小鼠接种HP SS1或NCTC 11637,HP感染率低,胃黏膜HP定植量低,病理组织学改变轻。结论C57BL/6小鼠接种HP SS1可获得较好的HP感染模型。     

链脲佐菌素诱导C57BL/6小鼠糖尿病瘙痒模型的建立

[目的]探讨链脲佐菌素(streptozotocin , STZ)诱导C57BL/6小鼠糖尿病瘙痒模型的最佳剂量.[方法]24只雄性8周C57BL/6野生型小鼠,体重20～28 g,随机分为四组: A组(对照组)单次腹腔注射等剂量柠檬酸钠溶液 10 mL/kg,pH=4.5;B组STZ单次大剂量腹腔注射STZ 160 mg/kg;C组STZ腹腔注射40 mg/kg,连续注射5 d,每次给药时间间隔24 h;D组STZ两次中剂量注射,腹腔注射STZ 85 mg/kg+65 mg/kg,两次间隔时间24 h.从给药前4周开始,A组正常饮食,B、C、D组高脂饮食喂养至实验结束.注射STZ前1 d、注射STZ后1、2、3、4周测定动物的空腹血糖(FBG)、体重,采用录像记录30 min搔抓次数.[结果]与A组相比,B、C、D组造模后血糖升高并在不同时间点达到糖尿病标准(>200 mg/dL)(P<0.05),B组体重较A、C、D组下降(P<0.05),D组在STZ注射后第2、3周搔抓次数较A、B、C增多(P<0.05).[结论]腹腔分两次、间隔24 h注射STZ 85 mg/kg+65 mg/kg并配合高脂饮食是建立糖尿病并发瘙痒小鼠模型的合适方法.     

不同浓度顺铂对C57BL/6小鼠卵巢功能的影响

目的:通过研究不同浓度顺铂对C57BL/6小鼠卵巢功能的影响,探讨能够引起C57BL/6小鼠卵巢早衰的最低有效浓度,从而为临床研究提供一种安全、可靠、便捷的早发性卵巢功能不全(POI)模型构建方案。方法:随机选择SPF级雌性C57BL/6小鼠(6~8周)60只,随机分为对照组、剂量1.0组(1 mg/kg)、剂量1.5组(1.5 mg/kg)、剂量2.0组(2 mg/kg),给药组均连续腹腔注射7 d顺铂。结果:1.0组小鼠卵巢受损较轻,卵巢组织形态、卵泡计数及血清激素水平与对照组相比,变化程度较小,无法用于建模;1.5组小鼠卵巢受损较重,体质量下降平稳,一般状态好,死亡率低,动情周期恢复率低,卵巢组织形态、卵泡计数及血清激素水平与对照组差异均有统计学意义(P<0.05),但变化较为平缓,适宜建立POI模型;2.0组小鼠卵巢受损严重,体质量下降明显,全身状况差,出现持续的动情间期,卵巢组织形态、卵泡计数及血清激素水平与对照组差异均有统计学意义(P<0.05),但变化大,不利于实验研究。结论:1.5 mg/kg为建立C57BL/6小鼠POI模型的合适有效浓度,采用该给药方案建立的模型,卵巢组织损伤较为稳定,能够较好地模拟POI患者的激素水平变化,动物耐受性好,有利于治疗研究的开展,适用于POI治疗方案的评价。     

维甲酸诱导BALB／C近交系小鼠产生腭裂的剂量研究

目的：研究维甲酸诱导BALB／C近交系小鼠产生腭裂所需的剂量。方法：将40只BALB／C近交系小鼠分成四组,每组10只,在妊娠10d时分别给予不同剂量的维甲酸,给药后观察所有孕鼠的反应,在妊娠15d时解剖部分孕鼠,取胎鼠头部,行冠状切片,苏木精一伊红染色法（HE染色）,进行观察。剩余孕鼠任其自然分娩,观察子鼠情况。结果：给予70mg／kg维甲酸后,孕鼠组绝大多数表现腭裂动物模型所需特征。结论：70mg／kg剂量维甲酸能够诱导BALB／c近交系小鼠产生可靠的腭裂动物模型。     

同种与异种胎胸腺混合移植诱导供者皮肤移植免疫耐受

目的：探讨同种异种胎胸腺混合移植达到供皮肤移植的耐受。方法：实验于2003—03／12在第三军医大学创伤、烧伤、复合伤实验室完成。将F344大鼠胎胸腺和C57BL／6小鼠胎胸腺混合移植到BALB／C裸小鼠的双肾包膜下4个月后。用流式细胞仪技术检测裸小鼠外周血中CD3^ 和CD4^ T细胞，用单向混合淋巴细胞培养了解T细胞对ConA以及同种异种淋巴细胞的反应性，异基因皮肤移植观察皮肤移植物存活期。结果：①混合移植胎胸腺4个月后，受裸小鼠外周血中CD3^ 和CD4^ T细胞占总白细胞的25．9％，正常裸小鼠外周血中CD3^ 和CD4^ 量极少(2．43％)。②受T细胞对ConA以及无关的SD鼠异种淋巴细胞的反应性强(刺激指数分别为23．23与12．75)，而对供F344及C57BL／6淋巴细胞不发生增殖反应(刺激指数分别为1．12与0．98)。③受对供F344及C57BL／6鼠皮肤移植物86d不发生排斥，而对无关的SD鼠皮肤移植物15d即发生排斥。结论：受体对胸腺供体来源的F344和C57BL／6皮肤及宿主本身的BALB／13皮肤移植耐受，而对无关的SD鼠皮肤移植物较短时间内即发生了排斥，并且抗DNA自身抗体水平与正常鼠相似。表明同种和异种胸腺混合移植后受体可重建有免疫功能的T淋巴细胞，并能诱导供特异性免疫耐受的发生。     

C57BL／6小鼠胚胎成纤维细胞生物学特性及饲养层制备

背景：昆明小鼠胚胎成纤维细胞是目前最常用的饲养层细胞,C57BL/6小鼠胚胎成纤维细胞作为饲养层的研究鲜有报道。目的：体外分离和培养C57BL/6小鼠胚胎成纤维细胞,制备饲养层,力求扩大小鼠胚胎成纤维细胞的来源。方法：用不同浓度胰蛋白酶分步消化法体外分离和培养C57BL/6小鼠胚胎成纤维细胞,观察其生物学特性,研究其生长规律,并制备小鼠胚胎成纤维细胞饲养层,检测干细胞在所制备饲养层上的生长状态。结果与结论：不同浓度胰蛋白酶分步消化法制备的C57BL/6小鼠胚胎成纤维细胞生长状态好,获得的成纤维细胞数量多,增殖活跃。在细胞冻存后1,2周、1,3,6个月内复苏的细胞存活率差异无显著性意义。C57BL/6小鼠胚胎成纤维细胞在第2-5代增殖旺盛,第6代以后细胞增殖出现明显下降。种植到培养皿上的C57BL/6小鼠饲养层细胞在种植后3 d内活力高,种植4 d以后细胞活力急剧下降。所以C57BL/6小鼠胚胎成纤维细胞来源的饲养层的最佳使用时间为灭活后3 d内,C57BL/6小鼠胚胎成纤维细胞饲养层和昆明小鼠胚胎成纤维细胞饲养层一样,能很好地支持胚胎干细胞及诱导多能干细胞生长。     

雷公藤甲素延缓糖尿病肾病进展的实验研究

目的初步探讨雷公藤甲素对C57BL/6-Ins2Akita小鼠的安全剂量和延缓糖尿病肾病的作用效果。方法选择8周龄雄性C57BL/6-Ins2Akita小鼠和C57BL/6J野生鼠,每4周检测体血糖和体质量,每8周收集24 h尿液和血液,检测和对比糖尿病肾病相关指标,确定C57BL/6-Ins2Akita小鼠糖尿病肾病的评估和形成时机。另取8周龄C57BL/6-Ins2Akita小鼠以100、200、400、800μg·kg~(-1)·d~(-1)分成4个剂量组灌胃14 d,观察急性毒性反应,通过改良寇氏法计算LD50。以25、50、100μg·kg~(-1)·d~(-1)这3个剂量干预24周龄C57BL/6-Ins2Akita小鼠,并设置空白对照组和野生型对照组,干预8周,期间收集尿液检测24 h尿蛋白排泄率,处死后收集血液检测肌酐、尿素氮、血清清蛋白等指标,组织取材进行病理检查。结果 C57BL/6-Ins2Akita小鼠的24 h尿蛋白排泄率、血糖、三酰甘油在8周龄开始即高于C57BL/6J野生型小鼠(P0.05),血清蛋白低于C57BL/6J野生型小鼠(P0.05),且随周龄增加差距逐渐明显,但肌酐未出现升高趋势。急性毒性实验中改良寇氏法计算LD50值为356.45μg·kg~(-1)·d~(-1)。雷公藤甲素干预高、中、低剂量组的24 h尿清蛋白排泄率均较对照降低,其中高剂量组与对照组差异有统计学意义(P0.05)。随蛋白尿的减少,血清清蛋白水平得到提高,HDG组较CON组血清清蛋白水平提高约2.5 g/L,差异有统计学意义(P0.05)。对于体质量、24 h尿量、肾脏重量、血糖、血肌酐、尿素氮、三酰甘油、胆固醇等指标,实验组与空白对照组之间未发现差异有统计学意义。与此同时,病理检查发现高剂量组的系膜面积/毛细血管襻面积和肾小球系膜扩张比例均明显低于空白对照组(P0.05),中、低剂量组差异无统计学意义。结论 100μg·kg~(-1)·d~(-1)的雷公藤甲素可减少C57BL/6-Ins2Akita小鼠的蛋白尿,提高血清蛋白水平,减少系膜区系膜基质的聚积,增大剂量可能引起毒性反应。     

Does prolonged biliary obstructive jaundice sensitize the liver to endotoxemia?

Biliary obstructive jaundice (OJ) is an important clinical consideration concerning high bacteremic risk. Hepatocyte apoptosis is one of the causes of cholestatic liver injury. The aim of the current study was to examine the precise pathway and time course of hepatocyte apoptosis during OJ with LPS administration and to determine if OJ sensitizes the liver to endotoxemia. Male C57BL/6 mice were subjected to bile duct ligation and division and were administered with LPS at 3 (OJ3) or 14 (OJ14) days after surgery. Fas ligand expression, poly (adenosine diphosphate-ribose) polymerase p85 fragment immunohistochemistry, activation of caspases 3, 8, and 9, serum alanine aminotransferase levels, and hepatic adenosine triphosphate (ATP) contents were examined. Survival after LPS administration in male C57BL/6 or gld/gld (Fas ligand-deficient) mice was determined. The expression of Fas ligand increased during OJ. After LPS administration, the expression of cleaved caspases 3 and 8 increased in Sham3, Sham14, OJ3, and OJ14 mice, and it significantly increased in OJ14 compared with other mice. Poly (adenosine diphosphate-ribose) polymerase p85 immunohistochemistry showed significant hepatocyte apoptosis after LPS administration in OJ14 mice relative to OJ3. In OJ14 with LPS administration, ATP contents significantly decreased and alanine aminotransferase levels increased. Hepatocyte apoptosis was decreased in gld/gld OJ14 mice compared with C57BL/6 OJ14. All C57BL/6 OJ14 mice with LPS died, but survival in gld/gld OJ14 significantly ameliorated. In prolonged OJ with LPS administration, hepatocyte apoptosis depending on Fas ligand expression significantly increased in association with a decrease in ATP contents, thus resulting in liver necrapoptosis.     

骨髓间充质干细胞治疗ConA诱导的小鼠急性肝损伤的有效性研究

为了探讨骨髓原间充质千细胞（mesenchymal stem cells,MSC）治疗急性肝损伤的可行性及有效性,本研究分离培养小鼠MSC,并建立刀豆蛋白A（concanavalin A,ConA）诱导的小鼠急性肝损伤模型。在ConA静脉注射后立即给予MSC静脉输注,24小时后进行小鼠血清转氨酶、肝脏组织病理学和原位细胞凋亡检测,并用实时定量RT—PCR的方法检测小鼠肝脏组织内炎症介质表达变化。结果显示,ConA静脉注射后立即给予MSC静脉输注,小鼠血清丙氨酸氨基转移酶（alanine aminotransferase,ALT）和天门冬氨酸氨基转移酶（aspartate aminotransferase,AST）水平降低（p〈0．05）,肝脏坏死和肝细胞凋亡减轻,肝脏组织内TNF—α、IFN-γ的水平明显降低（P〈0．05）,iNOS、IL-2和IL-10的表达水平基本不受影响（P〉0．05）。结论：静脉输注MSC能减轻ConA诱导的小鼠急性肝损伤。     

Mechanism of Liver Injury during Obstructive Jaundice: Role of Nitric Oxide, Splenic Cytokines, and Intestinal Flora

To elucidate the roles of enteric bacteria and immunological interactions among liver, spleen and intestine in the pathogenesis of liver injury during obstructive jaundice, we studied the effects of antibiotics and splenectomy on bile-duct-ligated C57BL mice. When animals were subjected to bile-duct-ligation (BDL), plasma levels of bilirubin, alanine aminotransferase and aspartate aminotransferase increased markedly. However, the increases in plasma transaminases were significantly lower in splenectomized or antibiotics-treated groups than in the control BDL group. Histological examination revealed that liver injury was also low in the two groups. BDL markedly increased plasma level of interferon-gamma (IFN-gamma) and the expression of inducible nitric oxide synthase (iNOS) in liver and spleen. These changes were suppressed either by splenectomy or administration of antibiotics. Kinetic analysis revealed that BDL-induced liver injury and the increase of interleukin-10 (IL-10) and INF-gamma were lower in iNOS(-/-) than in wild type animals. BDL markedly increased the expression of IgA in colonic mucosa. These observations suggest that enteric bacteria, nitric oxide and cytokines including IFN-gamma and IL-10 derived from spleen and intestines form a critical network that determines the extent of liver injury during obstructive jaundice.     

Bias in macrophage activation pattern influences non-alcoholic steatohepatitis (NASH) in mice

In humans, there is large inter-individual variability in the evolution of NAFLD (non-alcoholic fatty liver disease) to NASH (non-alcoholic steatohepatitis). To investigate this issue, NASH was induced with an MCD (methionine-choline-deficient) diet in C57BL/6 and Balb/c mice that are characterized by different biases in Th1/Th2 and macrophage (M1/M2) responses. Following 4?weeks on the MCD diet, steatosis and lobular inflammation were prevalent in C57BL/6 (Th1, M1 oriented) than in Balb/c (Th2, M2 oriented) mice. Consistently, hepatic TNFα (tumour necrosis factor α) mRNA expression and circulating TNFα levels were higher in MCD-fed C57BL/6 than in MCD-fed Balb/c mice. The Th1/Th2 bias did not account for the increased NASH severity, as in both strains MCD feeding did not significantly modify the liver mRNA expression of the Th1 markers IFNγ (interferon γ) and T-bet or that of the Th2 markers IL-4 (interleukin 4) and GATA-3. Conversely, MCD-fed C57BL/6 mice displayed higher liver mRNAs for the macrophage M1 activation markers iNOS (inducible NO synthase), IL-12p40 and CXCL10 (CXC chemokine ligand 10) than similarly treated Balb/c mice, without effects on the M2 polarization markers IL-10 and MGL-1 (macrophage galactose-type C-type lectin-1). Circulating IL-12 was also higher in MCD-fed C57BL/6 than in MCD-fed Balb/c mice. The analysis of macrophages isolated from the livers of MCD-fed animals confirmed an enhanced expression of M1 markers in C57BL/6 mice. Among all of the MCD-treated mice, liver iNOS, IL-12p40 and CXCL10 mRNA levels positively correlated with the frequency of hepatic necro-inflammatory foci. We concluded that the macrophage M1 bias in C57BL/6 mice may account for the increased severity of NASH in this strain, suggesting macrophage responses as important contributors to NAFLD progression.     

Reduced toxicity, attenuated immunogenicity and efficient mediation of human p53 gene expression in vivo by an adenovirus vector with deleted E1-E3 and inactivated E4 by GAL4-TATA promoter replacement.

A recombinant adenovirus with deleted E1 and E3, and E4-inactivated by replacing the E4 promoter with a synthetic promoter composed of a minimal TATA box and five consensus yeast GAL4-binding site elements was developed and used to express the human tumor suppresser gene p53. The toxicity and immunogenicity of this vector and vector-mediated p53 gene expression in vivo were studied in immunocompetent C3H and C57BL/6 mice. Expression of the late viral gene product, hexon protein, was observed in C3H and C57BL/6 mice injected with E4 wild-type adenovirus constructs Adv-cmv-beta-Gal (BG), Adv-cmv-hp53 (WT), and empty E1- vector Adv-E4 (EW) 3 to 28 days after injection, but was undetectable in mice treated with E4 modified empty E1- vector Adv-GAL4 (EG) or Adv-cmv-hp53-GAL4 (G4). Expression of the p53 gene was observed in both WT- and G4-injected C3H and C57BL/6 mouse livers from days 3 to 28. Ten weeks after injection, p53 gene expression was still detected in G4-treated C57BL/6 mice at similar levels, but was not detectable in WT-treated mice. Vector-induced liver toxicity was evaluated by analyzing serum transaminases (SGOT and SGPT) activities. In all cases, SGOT and SGPT activities were markedly decreased in EG-treated C3H and C57BL/6 mice compared with those in EW-treated mice on days 3, 7 and 14 after injection. In C57BL/6 mice, the total anti-adenoviral CTL activities were two- to three-fold higher in animals treated with EW vector than in those treated with EG vector. These results suggest that inactivation of the E4 promoter efficiently diminished the viral replication and the late viral gene expression, reduced host immune response and consequently reduced toxicity and prolonged the duration of transgene expression in vivo.     

超声生物显微镜成像对正常小鼠心血管的初步研究

目的探讨超声生物显微镜对小鼠心血管成像的方法及价值。方法选择8、16、24及32周龄C57BL／6健康成年雄性小鼠32只，每组各8只，采用Visualsonics公司Vevo770小动物超声成像系统，经胸骨左缘、心尖、胸骨右缘及胸骨上窝等扫查窗口，观察并分析小鼠心脏、大血管的结构及血流频谱，并对左心收缩及舒张功能进行评价。结果经上述扫查窗口，可获得左心室长轴、左心室短轴、升主动脉长轴、主动脉弓长轴、主动脉短轴、右心室流人道、肺动脉长轴等切面，仅心尖切面显示不满意。通过这些切面能清晰显示左心房、左心室、二尖瓣、主动脉及主动脉弓、室间隔、右心房、右心室、三尖瓣、肺动脉、无名动脉及左颈总动脉等结构，进而测量其内径，并可顺利获得各瓣口的血流频谱。各切面心脏及大血管二维径线测值及各瓣口血流脉冲多普勒测值比较显示，各周龄组相关测量数据间差异无统计学意义（P〉0．05）。结论超声生物显微镜可很好地应用于小鼠心脏及大血管成像，采用适当的扫查窗口和切面可获得满意的图像。超声医师经过短期培训即可熟练掌握该技术，因而具有很好的应用前景。     

Effects of the Cellcultured Acanthopanax senticosus Extract on Antioxidative Defense System and Membrane Fluidity in the Liver of Type 2 Diabetes Mouse

This study examined the effect of cellcultured Acanthopanax senticosus (A. senticosus) extract on the antioxidative defense system, oxidative stress and cell membrane fluidity in the liver of type 2 diabetes in the C57BL/6J mouse as an animal which is genetically prone to develop insulin resistance and obesity/diabetes. C57BL/6J mice were randomly divided, control diet (N-C), high fat diet (DM-C), control diet plus A. senticosus extract (N-CASM), and high fat diet plus A. senticosus extract (DM-CASM). The mice were orally administered an A. senticosus extract (0.5 g/kg body weight) in the N-CASM and DM-CASM groups once a day for 12 weeks, and distilled water in the N-C and DM-C groups. Cellcultured A. senticosus extract was found to be excellent for strengthening the antioxidative defense system, reducing the generation of reactive oxygen species (ROS) and damaging oxidative substances, and maintaing membrane fluidity (MF) in the liver of type 2 diabetes mouse.