高脂饮食诱导肥胖大鼠胰腺中蛋白酪氨酸磷酸酶1B的表达和活性增高

目的：观察不同时间肥胖大鼠胰腺组织中蛋白酪氨酸磷酸酶1B（PTP-1B）的表达和活性变化，以及其底物蛋白IR和IRS-1经胰岛素刺激后磷酸化程度的变化，探讨肥胖大鼠胰岛胰岛素抵抗发生的可能机制。     

肉桂对高脂饮食诱导的肥胖性高血压大鼠症状的改善及Toll样受体的影响

目的探讨肉桂对高脂饮食诱导的肥胖性高血压大鼠症状的改善及Toll样受体的影响。方法采用高脂饮食诱导肥胖性高血压大鼠模型。将SD大鼠随机分为对照组、模型组、肉桂高、低剂量组(0.9、0.3 g生药/kg)。检测用药后2、4、6、8、10和12 w的收缩压和体重,检测12 w后的血清甘油三酯、总胆固醇水平、脂肪系数、不同部位(腹股沟、腹膜后、附睾、肠系膜)和全身的脂肪质量、计算Lee指数,脂肪的Toll样受体2(TLR2)和Toll样受体4(TLR4)的蛋白水平。结果与对照组相比,模型组的以上指标均显著升高(P<0.05);采用肉桂治疗,可降低升高的收缩压、体重,除2、4 w外,其余观察点的指标均与模型组有差异(P<0.05),治疗12 w的Lee指数、血清甘油三酯、总胆固醇水平、脂肪系数及不同部位和全身的脂肪质量,脂肪Toll样受体蛋白水平均低于模型组(P<0.05),且高剂量肉桂组的改善效果强于低剂量组(P<0.05)。结论肉桂可改善高脂饮食诱导的肥胖性高血压大鼠的高血压及肥胖症状,可能是通过下调脂肪中的Toll样受体水平来发挥作用的。     

髓样分化蛋白2对重症急性胰腺炎的影响

脂多糖（LPS）是革兰氏阴性菌（G-）细胞壁的主要成分,它能被Toll样受体4（TLR4）所识别,并且TLR4是LPS跨膜信号转导的主要受体。已有研究表明,TLR4的表达在发生胰腺炎的胰腺中存在上调趋势,且急性坏死性胰腺炎时,肝、肺等组织中TLR4 mRNA的表达明显增强。所以,在SIRS和早期MODS,TLR4受体的激动即可被认为是诱导炎症反应失控的最初因素之一。本文主要就髓样分化蛋白2（MD2）在TLR4信号转导过程中的重要作用,及在其诱导下产生的炎症反应对重症急性胰腺炎（SAP）的影响和临床意义加以阐述。     

绿茶多酚影响高脂饮食大鼠窖蛋白-1表达的实验研究

目的:探讨绿茶多酚单体表没食子儿茶素没食子酸酯(epigallcatechin gallate,EGCG)对高脂饮食所致肥胖及窖蛋白-1(caveolin-1,Cav-1)表达的影响。方法:30只雄性Wistar大鼠(体质量170~190g)随机分为3组,即高脂饮食组、高脂饮食加EGCG组和对照组。饲养15周,测量体质量、血糖及血脂;用RT-PCR及Western blot分别检测Cav-1mRNA及其蛋白表达。结果:高脂饮食可上调Cav-1mRNA和其蛋白表达;而EGCG可降低Cav-1mRNA和其蛋白的上调。结论:绿茶多酚降低高脂饮食大鼠Cav-1mRNA和其蛋白表达的作用,可能是绿茶及其多酚改善内皮功能和预防心血管疾病的分子机制之一。     

高脂饮食和追赶生长对大鼠胃排空及血浆胰高血糖素样肽-1浓度的影响

的病理生理变化有关.     

髓样分化蛋白-2及Toll样受体4在星形细胞瘤中的表达及临床意义

目的 检测不同级别星形细胞瘤中髓样分化蛋白-2(MD2)和Toll样受体4(TLR-4)的表达,并探讨其临床意义.方法 收集2019年1月 ～2020年8月于山东国欣颐养集团新汶中心医院接受手术切除治疗的低级别星形细胞瘤(LGA)患者50例及高级别星形细胞瘤(HGA)患者50例,所有患者的肿瘤组织样本于术中离体后立刻保...     

高脂饮食诱导的肥胖大鼠胰腺蛋白酪氨酸磷酸酶1B表达增高

目的观察高脂饮食诱导的肥胖大鼠胰腺中蛋白酪氨酸磷酸酶1B（PTP-1B）的表达。方法选取SD大鼠20只，随机分为正常对照组10只，给予常规饲料；肥胖模型组10只，给予高脂饲料，共喂养12周。测定大鼠空腹胰岛素、血糖、甘油三酯、总胆固醇，附睾脂肪垫重量；观察肝脏形态学改变；进行葡萄糖耐量试验和胰岛素释放试验；用免疫组化和蛋白印迹法检测大鼠胰腺组织中PTP-1B蛋白的表达。用免疫沉淀法检测胰岛素受体（IR）和胰岛素受体底物1（IRS-1）磷酸化程度。结果（1）肥胖组胰岛素敏感指数显著低于对照组（0．36±0．18 vs 0．91±0．28，P〈0．05）；（2）肥胖组大鼠葡萄糖耐量受损，葡萄糖刺激的胰岛素Ⅰ相分泌反应受损；（3）肥胖组大鼠胰腺中PTP-1B蛋白与对照组相比，含量增加86％（P〈0．01）。肥胖组胰腺中胰岛素诱导的IR和IRS-1磷酸化程度都降低。结论高脂饮食诱导的肥胖大鼠胰腺中PTP-1B蛋白表达量升高，从而使胰岛素诱导的IR和IRS-1磷酸化程度降低，可能是肥胖状态下引发胰岛产生胰岛素抵抗的机制之一。     

高脂饮食对实验性大鼠非酒精性脂肪肝UCP2表达的影响

目的:通过高脂饮食制作非酒精性脂肪肝(NAFLD)动物模型;观察高脂饮食对实验性大鼠NAFLD解偶联蛋白2(UCP2)的影响。方法:通过高脂饮食建立大鼠非酒精性脂肪性肝病模型。观察肝脏病理改变并检测肝脏UCP2表达情况。结果:与正常对照组相比,高脂饮食大鼠肝脏UCP2表达显著上升,肝组织广泛脂肪变性,形成单纯性脂肪肝。继续给予高脂饮食使肝脏UCP2表达水平进一步增加,肝脏发生进一步病理改变而形成脂肪性肝炎。结论:高脂饮食成功地复制了NAFLD动物模型;NAFLD时肝脏UCP2表达上调,可能是机体的一种适应性反应;但是UCP2过度表达,可能诱导或加剧肝脏病理改变。     

脂多糖对大鼠肺泡巨噬细胞Toll样受体4和髓样分化蛋白-2基因表达及炎性因子分泌的影响

目的 探讨脂多糖刺激大鼠肺泡巨噬细胞株NR8383细胞Toll样受体4(TLR4)、髓样分化蛋白-2(MD-2)mRNA表达和炎性因子分泌的影响,以及MD-2小干扰RNA(MD-2 siRNA)对脂多糖刺激下NR8383细胞炎性因子分泌的作用.方法 体外培养NR8383细胞,以不同浓度脂多糖(0.01～10 mg/L)刺激2 h,以1 mg/L脂多糖刺激2～24 h.运用脂质体Lipofectamine 2000将MD-2siRNA转染至细胞.半定量RT-PCR方法检测细胞TLR4和MD-2 mRNA的表达,酶联免疫吸附法检测细胞培养上清中肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6和IL-1β的含量.统计学处理采用单因素方差分析、独立样本t检验和Pearson相关分析.结果 对照组NR8383细胞TLR4和MD-2mRNA的相对表达量分别为0.52±0.05和0.44±0.09,0.01 mg/L浓度脂多糖刺激前后表达量无明显改变,0.1 mg/L浓度时表达增加,随脂多糖浓度的升高表达量进一步增加,10 mg/L刺激后相对表达量分别为0.72±0.06和0.65±0.10(F=17.26、6.04,P<0.01);TNF-αIL-6和IL-1β含量具有类似改变趋势,对照组分别为(25.8±3.4)ng/L、(62.4±4.7)ng/L和(31.6±1.7)ng/L;在10 mg/L脂多糖刺激下分别增加至(58.9±5.3)ng/L、(96.5±3.9)ng/L和(55.4±5.4)ng/L(F=29.55、54.47、31.45,P<0.01).在1 mr/L脂多糖刺激下,TLR4和MD-2 mRNA的表达量在2 h后明显增加,6 h达高峰,8 h开始回落,至24 h时仍高于基础值(F=5.28、4.11,P<0.01);TNF-α、IL-6和IL-1β含量具有类似变化(F=10.64、11.23、17.58,P<0.01),其中TNF-α和IL-1β含量在6 h达高峰,持续至8 h,IL-6含量在8 h达高峰,持续至12 h.TLR4和MD-2 mRNA表达呈正相关(r=0.513,P<0.01).MD-2 siRNA对NR8383细胞MD-2基因的干扰效率为67%,在脂多糖刺激下干扰组细胞培养上清液中TNF-α、IL-1β和IL-6水平未见明显升高.结论 高浓度脂多糖可较长时间上调大鼠肺泡巨噬细胞株NR8383细胞TLR4和MD-2基因的表达,并促进TNF-α、IL-6和IL-1β的分泌.MD-2 siRNA可抑制脂多糖刺激下NR8383细胞分泌TNF-α、IL-1 β和IL-6.     

高脂饮食促进病毒性肝炎小鼠肝内细胞因子表达

目的：研究高脂饮食对病毒性肝炎小鼠肝内细胞因子表达的影响。方法：选取C3H/HeN小鼠共152只，随机分为标准饮食组(32只)、高脂饮食组(32只)、标准饮食感染组(44只)、高脂饮食感染组(44只)。标准饮食组及标准饮食感染组持续予以标准饮食喂养，高脂饮食组及高脂饮食感染组持续予以高脂饮食喂养。喂养第12周末，标准饮食感染组及高脂饮食感染组予以腹腔注射3型鼠肝炎病毒(MHV-3)诱导病毒性肝炎。于感染后不同时间点，采用定量逆转录聚合酶链式反应(PCR)检测肝内肿瘤坏死因子(TNF-α)、白介素(IL)-1β、IL-6、IL-17A表达。结果：高脂饮食喂养12周诱导小鼠出现代谢异常。感染后第4天，标准饮食感染组小鼠肝内仅IL-6表达上调，而高脂饮食感染组TNF-α、IL-1β、IL-6、IL-17A表达上调(P均<0.05)。感染后第8天，标准饮食感染组及高脂饮食感染组小鼠肝内TNF-α、IL-1β、IL-6、IL-17A表达上调，且高脂饮食感染组表达水平显著高于标准饮食感染组(P均<0.05)。感染后第12天，标准饮食感染组小鼠肝内TNF-α、IL-17A表达回落至未感染...     

去酰基化胃饥饿素对高脂饮食诱导C57BL/6J小鼠的抗疲劳作用

目的探究去酰基化胃饥饿素(DAG)对高脂饮食(HFD)诱导的肥胖小鼠的抗疲劳作用。方法36只6周龄C57BL/6小鼠随机分为对照(NC)组、高脂(HFD)组、HFD+DAG组(每组各12只),分别予以标准饲料(NC组)、高脂饲料(HFD组、HFD+DAG组)喂养,并给予每日腹腔注射生理盐水(NC组,HFD组)和DAG(HFD+DAG组)。喂养16 w后行力竭测试和负重游泳实验,随后处死小鼠取血检测血清乳酸(LA)、乳酸脱氢酶(LDH)、尿素氮(BUN)水平;留取肝脏和股四头肌测定肝糖原和肌糖原水平。结果与NC组相比,HFD组体重上升,腓肠肌和股四头肌指数下降,力竭运动距离和游泳力竭时间均缩短,血清BUN、LA水平升高,血清LDH、肝糖原、肌糖原含量下降,差异有统计学意义(P<0.05,P<0.01)。与HFD组相比,HFD+DAG组力竭运动距离和游泳力竭时间延长,血清BUN、LA水平下降,血清LDH、肝糖原、肌糖原含量升高,差异有统计学意义(P<0.05,P<0.01)。结论长期应用DAG有助于提高肥胖小鼠的运动耐力与抗疲劳能力。     

苦龙胆酯苷拮抗高脂饮食所致的小鼠动脉粥样硬化

[目的]探究苦龙胆酯苷(MAG)对高脂饮食(HFD)所致动脉粥样硬化的拮抗作用及其机制。[方法]将30只ApoE^-/-小鼠随机分为对照组(正常饮食)、HFD组、HFD+MAG组,每组10只小鼠,其中HFD+MAG组每日予50 mg/kg MAG灌胃,持续12周。生物化学检测仪测定血脂水平;油红O染色观察主动脉斑块沉积情况;苏木精-伊红(HE)染色观察主动脉血管病理形态表现;Mac-3免疫组织化学染色观察主动脉巨噬细胞聚集情况;免疫荧光定位染色观察NOD样受体热蛋白结构域相关蛋白3(NLRP3)表达与分布;Western blot检测主动脉中NLRP3、凋亡相关斑点样蛋白(ASC)和Caspase-1亚基p20表达水平。[结果] HFD+MAG组血清甘油三酯、总胆固醇和低密度脂蛋白胆固醇水平分别降低至HFD组的88.39%、74.85%和64.97%(均P<0.05),高密度脂蛋白胆固醇水平升高至HFD组的142.18%(P<0.05),斑块面积减少至HFD组的45.16%(P<0.05),MAG能改善主动脉病理形态表现,使巨噬细胞沉积减少,斑块内...     

Effect of Carnitine and herbal mixture extract on obesity induced by high fat diet in rats

Background

Obesity-associated type 2 diabetes is rapidly increasing throughout the world. It is generally recognized that natural products with a long history of safety can modulate obesity.

Aim

To investigate the development of obesity in response to a high fat diet (HFD) and to estimate the effect of L-carnitine and an Egyptian Herbal mixture formulation (HMF) (consisting of T. chebula, Senae, rhubarb, black cumin, aniseed, fennel and licorice) on bodyweight, food intake, lipid profiles, renal, hepatic, cardiac function markers, lipid Peroxidation, and the glucose and insulin levels in blood and liver tissue in rats.

Method

White male albino rats weighing 80-90 gm, 60 days old. 10 rats were fed a normal basal diet (Cr), 30 rats fed a high-fat diet (HFD) for 14 weeks during the entire study. Rats of the HFD group were equally divided into 3 subgroups each one include 10 rats. The first group received HFD with no supplement (HFD), the 2^nd group HFD+L-carnitine and the third group received HFD+HMF. Carnitine and HMF were administered at 10^th week (start time for treatments) for 4 weeks. Body weight, lipid profile & renal function (urea, uric acid creatinine) ALT & AST activities, cardiac markers, (LDH, C.K-NAC and MB) the oxidative stress marker reduced glutathione (GSH), and Malondialdehyde (MDA) catalase activity, in addition to glucose, insulin, and insulin resistance in serum & tissues were analyzed.

Results

Data showed that feeding HFD diet significantly increased final body weight, triglycerides (TG), total cholesterol, & LDL concentration compared with controls, while significantly decreasing HDL; meanwhile treatment with L-carnitine, or HMF significantly normalized the lipid profile. Serum ALT, urea, uric acid, creatinine, LDH, CK-NAC, CK-MB were significantly higher in the high fat group compared with normal controls; and administration of L-carnitine or herbal extract significantly lessened the effect of the HFD. Hyperglycemia, hyperinsulinemia, and high insulin resistance (IR) significantly increased in HFD in comparison with the control group. The treatment with L-carnitine or HMF improved the condition. HFD elevated hepatic MDA and lipid peroxidation associated with reduction in hepatic GSH and catalase activity; whereas administration of L-carnitine or herbal extract significantly ameliorated these hepatic alterations.

Conclusion

HFD induced obesity associated with a disturbed lipid profile, defective antioxidant stability, and high values of IR parameters; this may have implications for the progress of obesity related problems. Treatment with L-carnitine, or HMF extract improved obesity and its associated metabolic problems in different degrees. Also HMF has antioxidant, hypolipidaemic insulin sensitizing effects. Moreover HMF might be a safe combination on the organs whose functions were examined, as a way to surmount the obesity state; and it has a distinct anti-obesity effect.     

Toll样受体2基因敲除对高脂饮食诱导的肥胖小鼠脂肪组织凋亡的影响

目的分析Toll样受体(TLR)2敲除对高脂饮食诱导的肥胖小鼠脂肪组织凋亡的影响。方法 C57BL/6J小鼠和TLR2基因敲除小鼠各16只,分为两组,给予普通饮食和高脂饮食喂养:正常对照组(NC)、肥胖组(OB)、TLR2基因敲除组(TK)和TLR2基因敲除肥胖组(TO)。16 w后检测各组空腹血糖(FPG),三酰甘油(TG),总胆固醇(TC),低密度脂蛋白(LDL)和高密度脂蛋白(HDL)水平及脂肪组织caspase3活性,bcl2和bax蛋白、mRNA表达量。结果与NC组相比,OB组小鼠脂肪组织caspase3活性升高,bax蛋白和mRNA水平升高,bcl2蛋白和mRNA水平降低;与OB组相比,TO组小鼠脂肪组织caspase3活性降低,bax蛋白和mRNA水平降低,bcl2蛋白和mRNA水平升高。结论 TLR2敲除减轻了高脂饮食诱导的肥胖小鼠脂肪组织的细胞凋亡。     

胰岛素治疗逆转糖尿病小鼠肝脏的脂肪沉积

观察胰岛素治疗对糖尿病小鼠脂肪肝的影响.C57BL/6J小鼠高脂饲养12周后,甘精胰岛素皮下注射4周.结果 显示,与高脂组相比,胰岛素组腹腔葡萄糖耐量试验所有时间点血糖及血总胆同醇、甘油三酯(TG)均显著改善(P相似文献   

马来酸罗格列酮干预高脂饲养大鼠脂肪肝的研究

目的观察高脂饲养所致正常SD大鼠脂肪肝与胰岛素抵抗的关系及罗格列酮干预脂肪肝的效果。方法将8周龄雄性SD大鼠随机分为三组，每组各11只：正常饲养组（NC）、高脂饲养组（HF）、高脂＋罗格列酮组（HF4-Ros）。饲养8周后取空腹血测定血糖、脂联素，胰岛素敏感性用正常血糖高胰岛素钳夹术稳态时的葡萄糖输注率（GIR）来评价，测定肝脏中TG含量，并对大鼠肝脏组织做HE染色。结果高脂饲养8周后，与NC组相比，HF组肝脏呈现明显脂肪肝，肝脏中TG明显增加达154．2％（NC组3．89mg／g，HF组9．89mg／g，P〈0．01）；与HF组相比，HF4-Ros组肝脏中TG显著降低达46．6％（5．28mg／g，P〈0．01），脂肪肝减轻。结论马来酸罗格列酮能明显改善高脂饲养大鼠的脂肪肝。     

Liraglutide及PTEN在高脂饮食诱导的大鼠胰岛细胞凋亡中的作用

目的观察高脂饮食的SD大鼠胰腺第10号染色体同源丢失性磷酸酶-张力蛋白基因（PTEN）表达量的变化,以及liraglutide对胰岛细胞凋亡的作用。方法20只雄性SD大鼠随机分为3组：正常饮食（ND）组（n=6）、高脂饮食（HFD）组（n=6）和高脂饮食并给予liraglutide（HL）组（n=8）。ND组给予正常饮食,HFD组和HL组给予高脂饮食持续20周后行0GTT试验。随后ND组和HFD组给予生理盐水0．2mg／kg,HL组给予liraglutide0．2mg／kg,早晚各1次,持续4周,给药终点再次行OG-TT试验,评估β细胞功能。应用实时定量PCR检测各组大鼠胰腺PTENmRNA相对表达量,TUNEL染色观察大鼠胰岛细胞凋亡的变化。结果与ND组相比,HFD组和HL组大鼠体重增加（P〈0．05）,血TG和TC升高（P〈0．01）,OGTT中胰岛素曲线下面积（AUCIns）增大（P〈0．05或P〈0．01）,且胰腺PTENmRNA表达量增多（P〈0．05）。与HFD组相比,HL组体重、进食量和血TC下降（P〈0．05或P〈0．01）,OGTT中60min和120min时胰岛素和血糖降低（P〈O．01）,胰岛细胞凋亡减少,β细胞功能得到一定改善,但胰腺PTENmRNA表达量的差异无统计学意义（P〉0．05）。结论高脂饮食时SD大鼠胰腺PTENmRNA表达增加,liraglutide对高脂饮食大鼠胰腺PTENmRNA表达没有影响,但可能通过Akt信号通路减少其胰岛细胞凋亡。     

Effect of high fat diet on body weight and mammary tumor latency in MMTV-TGF-alpha mice

OBJECTIVE: The role of high fat diets in breast cancer/mammary tumor (MT) development is controversial. This may be partially attributable to variable effects of high fat diets on body weight. Here, we used a moderately high fat diet (32.5% fat calories) expected to cause obesity in most mice, but predicted to result in some mice remaining in the weight range of mice fed the low fat diet (11% fat calories). This provided the opportunity to compare mice fed the high fat diet exhibiting different body weights and mice of similar weight consuming high vs low fat diets. EXPERIMENTAL METHODS: Transgenic MMTV-TGF-alpha mice, a model of postmenopausal breast cancer, consumed a low fat diet, that is, chow-fed (n=25) or a moderately high fat diet from 10 weeks of age (n=51). Body weight at 34 weeks of age was used to assign high fat diet mice to obesity-prone>overweight>obesity-resistant groups (n=17) (P<0.0001). Mice were euthanized when MTs developed or at 85 weeks of age. RESULTS: Final body weights were highest in obesity-prone>overweight >obesity-resistant=chow-fed mice. Fat pads and fat pad:carcass were heaviest in obesity-prone followed by overweight mice. However, obesity-resistant mice had fat pad weights and fat pad:carcass three-fold greater than chow-fed mice. All groups had MT incidences between 72 and 82%. Obesity-prone mice exhibited the shortest MT latency (P<0.0001), but obesity-resistant mice had significantly shorter latency than chow-fed mice. CONCLUSIONS: Consumption of a high fat diet increased adiposity and shortened MT latency in relation to its effect on body weight. These results indicate a complex role of dietary fat level on mammary tumorigenesis.     

Obesity induced by high fat diet attenuates postinfarct myocardial remodeling and dysfunction in adult B6D2F1 mice

Obesity is a major risk factor for cardiovascular morbidity and mortality. However, some studies suggest that among patients with established cardiovascular disease, obesity is associated with better prognosis, a phenomenon described as the obesity paradox. In this study we tested the hypothesis that obesity with hyperinsulinemia and without hyperglycemia attenuates the impact of transient coronary occlusion on left ventricular remodeling and function. B6D2F1 mice from both genders fed with a high fat diet (HFD) or control diet for 6 months were subjected to 45 min of coronary occlusion and 28 days of reperfusion. Left ventricular dimensions and function were assessed by serial echocardiography, and infarct size was determined by Picrosirius red staining. HFD mice developed obesity with hypercholesterolemia and hyperinsulinemia in the absence of hyperglycemia or hypertension. During the period of feeding, no changes were observed in ventricular mass, volume or function, or in vascular reactivity. HFD attenuated the consequences of transient coronary occlusion as shown by a marked reduction in infarct size (51%, P = 0.021) and cardiac dilation, as well as improved left ventricular function as compared to control diet animals. These effects were associated with enhanced reperfusion injury salvage kinases (RISK) pathway function in HFD hearts shown as increased Akt and GSK3β phosphorylation. These results demonstrate that dietary obesity without hyperglycemia or hypertension attenuates the impact of ischemia/reperfusion injury in association with increased insulin signaling and RISK activation. This study provides experimental support to the controversial concept of the obesity paradox in humans.     

祛湿化瘀方对高脂饮食诱导的小鼠非酒精性脂肪性肝炎的防治作用

目的：观察祛湿化瘀方治疗非酒精性脂肪性肝炎（NASH）的药效。方法：12周龄C57BL／6J雄性小鼠32只．SPF级。随机分为对照饮食组（n=16）和高脂饮食组（n：16）,对照饮食组小鼠给予10％热能来源于脂肪的对照饲料,高脂饮食组小鼠给予60％热能来源于脂肪的高脂饲料。12周末,对照饮食组和高脂饮食组再分,51j随机分为正常组（N,n=8）、正常给祛湿化瘀方组（NQ,n=8）、模型组（M,n=8）、模型给祛湿化瘀方组（Q,n=8）,分别以lml／100g鼠重灌胃给予祛湿化瘀方（生药含量0．93g／m1）和灭菌饮用水,16周末取材,观察各组小鼠体重、肝组织TG、血清ALT、肝组织HE染色、油红O染色等指标的变化。结果：模型组小鼠体重明显增加,肝组织甘油三酯（TG）含量、血清丙氨酸转氨酶（ALT）明显升高,肝脏HE染色见肝细胞明显的肿胀、脂肪变性和炎细胞浸润．油红O染色见肝脏显著脂滴沉着。肝脏脂肪变积分、炎症积分、气球样变积分均显著升高,并达脂肪性肝炎诊断标准。祛湿化瘀方组小鼠肝组织TG、血清ALT较模型组显著下降,同时肝脏病理组织变化改善,病理积分较模型组显著降低。结论：祛湿化瘀方能够有效防治高脂饮食诱导的C57BL／6J小鼠NASH。