北柴胡及春柴胡挥发油的解热作用比较

目的：通过解热作用比较北柴胡及春柴胡挥发油的差异。方法：采用干酵母所致大鼠发热模型及内毒素所致家兔发热模型，观察北柴胡及春柴胡的解热作用。结果：北柴胡及春柴胡均可降低干酵母所致大鼠体温升高和降低内毒素所致家兔体温升高，与模型组比较差异有显著性（P〈0．05）。结论：北柴胡及春柴胡均具有良好的解热作用，提示春柴胡在临床上可以替换北柴胡。     

北柴胡及春柴胡挥发油的抗炎镇痛作用的实验研究

目的:比较北柴胡与春柴胡挥发油抗炎镇痛作用的差异.方法:采用小鼠耳廓肿胀和小鼠腹腔毛细血管通透性实验,比较北柴胡与春柴胡的抗炎作用;以热板法和扭体法比较北柴胡与春柴胡的镇痛作用.结果:北柴胡 10 g·kg-1剂量组、春柴胡 5 g·kg-1、10 g·kg-1剂量组可对抗二甲苯所致小鼠耳肿胀,可减少醋酸致小鼠毛细血管通透性增加,与模型组比较有显著性差异;北柴胡 10 g·kg-1剂量组、春柴胡 10 g·kg-1剂量组还可减少小鼠扭体次数,提高小鼠的痛阈值.结论:北柴胡和春柴胡均具有一定的抗炎作用,春柴胡抗炎疗效优于北柴胡.北柴胡和春柴胡对化学性和物理性刺激具有一定的镇痛作用,但两者疗效无显著性差异.     

北柴胡根及其地上部分解热、保肝药理作用的比较研究

目的合理开发和综合利用北柴胡药用植物资源。方法采用酵母致热法和CCl4致小鼠急性肝损伤实验,对北柴胡根及其地上部分解热、保肝药理作用进行比较研究。结果北柴胡根7.0g/kg剂量组在2 h时和北柴胡地上部分7.0 g/kg剂量组在2 h、4 h时与模型组比较有统计学差异,均可抑制酵母所致大鼠体温升高;北柴胡根2.5 g/kg、5.0 g/kg剂量组能够抑制CCl4所致小鼠ALT升高,与模型组比较有统计学差异;北柴胡根5.0 g/kg剂量组能够抑制CCl4所致小鼠AST升高,与模型组比较有统计学差异;北柴胡地上部分2.5 g/kg、5.0 g/kg剂量组均不能抑制CCl4所致小鼠ALT、AST升高。结论结果提示北柴胡根及其地上部分高剂量组均具有一定的解热作用;北柴胡根有保护CCl4所致小鼠急性肝损伤作用,而北柴胡地上部分无保护CCl4所致小鼠急性肝损伤作用。     

柴胡对大鼠实验性肝纤维化的预防作用

目的研究中药柴胡对肝纤维化的预防作用。方法采用四氯化碳(CCL4)诱发大鼠肝损伤,辅以高脂、低蛋白饲料和一定浓度乙醇饮料,复制肝纤维化模型,柴胡预防给药,观察其对大鼠血清及肝组织生化指标的影响。结果柴胡预防给药可显著降低四氯化碳所致慢性肝损伤大鼠血清ALT、AST和肝组织MDA、HyP,提高肝组织SOD活性。病理组织学观察显示,柴胡可使肝组织变性、坏死程度减轻。结论柴胡能预防四氯化碳致大鼠肝纤维化的发生与发展。     

丹参滴丸对二甲基亚硝胺诱导大鼠肝纤维化的治疗作用

目的观察丹参滴丸对二甲基亚硝胺诱导的大鼠肝纤维化的治疗作用。方法除对照组外,其余大鼠采用ip二甲基亚硝胺4周诱导大鼠肝纤维化,造模结束后,ig丹参滴丸175、350、700 mg/kg,设扶正化瘀胶囊为阳性对照组(1 500 mg/kg),对照组、模型组给予同体积蒸馏水,1次/d,连续给药4周。末次给药后1 h剖杀动物,测定血清生化(ALT、AST活性及TP、ALB、TBIL含量)、血清胶原(HA、LN、Ⅲ型前胶原、IV型胶原)水平、肝组织中蛋白、Hyp的含量。取肝组织固定,进行HE、Masson染色,镜下观察肝细胞组织结构和肝纤维化程度。结果丹参滴丸能够显著增加血清中TP和ALB水平,降低ALT、AST活性和TBIL水平;能显著降低LN、Ⅳ型胶原含量,明显降低HA含量,对Ⅲ型前胶原含量有一定的降低趋势;肝匀浆检测显示能显著增加肝组织中蛋白含量,对Hyp含量有一定的降低趋势;肝组织病理学HE染色和Masson染色显示,丹参滴丸能够改善弥漫性肝细胞变性、坏死及炎症反应,能显著抑制胶原增生、减轻肝纤维化程度。结论丹参滴丸能显著改善大鼠的肝功能、减少肝组织纤维的增生、对二甲基亚硝胺诱导的大鼠肝纤维化有一定的治疗作用。     

北柴胡对对乙酰氨基酚所致小鼠急性肝损伤的保护作用

目的：探讨北柴胡对对乙酰氨基酚所致小鼠急性肝损伤的保护作用。方法：采用0．5g·kg^-1对乙酰氨基酚灌胃造模，以血清中天冬氨酸氨基转移酶（AST），丙氨酸氨基转移酶（ALT），血清碱性磷酸酶（ALP），肿瘤坏死因子（TNF-α）含量为指标，观察北柴胡醇提物及北柴胡水提物对肝损伤的保护作用。结果：北柴胡醇提物及北柴胡水提物均能不同程度降低血清中AST，ATJT，AIJP和TNF-α含量，与水飞蓟素无明显差别。结论：北柴胡对对乙酰氨基酚所致小鼠急性肝损伤有一定的保护作用。     

埃克替尼对二甲基亚硝胺诱导肝纤维化大鼠的作用

目的观察埃克替尼对二甲基亚硝胺(DMN)大鼠实验性肝纤维化的影响。方法 48只雄性Wistar大鼠随机分为正常组(n=10)、模型组(n=14)、扶正化瘀组(n=12)与埃克替尼组(n=12)。模型组、扶正化瘀组和埃克替尼组以DMN 10μg·kg-1体重腹腔注射复制肝纤维化模型,每周连续3 d,连续4周;首次注射剂量为正常剂量2/3。自造模第3周开始,扶正化瘀组与埃克替尼组分别给予扶正化瘀胶囊4.0 g·kg-1、埃克替尼5 mg·kg-1灌胃,每周连续7 d,连续4周。HE染色与胶原染色观察肝组织炎症与胶原沉积,试剂盒检测血清肝功能水平,Jamall法测定肝组织羟脯氨酸(HYP)含量。荧光定量PCR检测肝组织α-平滑肌肌动蛋白(α-SMA)与转化生长因子-β(TGF-β)表达。结果与正常组相比,模型组大鼠的腹水发生率、血清总胆红素(T.Bil)含量、丙氨酸转氨酶(ALT)与天冬氨酸转氨酶(AST)活性、肝组织HYP含量均明显升高(P<0.01),血清白蛋白(Alb)含量明显减少,肝组织炎症及胶原沉积加重(P<0.01),肝组织α-SMA及TGF-βm RNA表达增多(P<0.05)。埃克替尼可明显减少造模大鼠腹水发生率,降低ALT、AST、T.Bil水平和肝组织HYP(P<0.05),减轻肝组织炎症及胶原沉积(P<0.05),下调肝组织α-SMA及TGF-βm RNA表达(P<0.05)。结论埃克替尼能够改善DMN诱导的大鼠实验性肝纤维化。     

柴胡合剂对实验性肝纤维化的防治作用

目的：研究柴胡合剂对大鼠四氯化碳肝纤维化模型作用,方法：２２只大鼠随机分为正常对照组（Ａ组）病组模型组（Ｂ组）和柴胡合治疗组（Ｃ组）。其中Ｂ和Ｃ两组动物皮下注射４０％四氯化碳橄榄油溶液,每周２次,共１１周,自第５周予以Ｃ组动物柴胡合剂稀释灌胃,每日１次,共７周,结果：柴胡合剂治疗组的血清Ⅲ型前胶原与透明质酸水平,肝匀浆羟脯氨酸含量明显低于病理模型组（Ｐ〈０．０１）。形态学观察显示柴胡合剂的治疗组的     

丹参粉针剂对二甲基亚硝胺所致大鼠肝纤维化进程的影响(英文)

丹参是一种传统的中草药,对多种疾病有治疗作用,丹参粉针剂主要由其水溶性成分组成。在本项研究中,大鼠腹腔注射二甲基亚硝胺诱导肝纤维化,每周注射3天,连续4周。在造模2周后,阳性药组大鼠皮下注射8×105IU/kg IFNα2b;各治疗组分别腹腔注射50,100和200 mg/kg丹参粉针剂,每周给药6天,连续4周。结果表明,IFNα2b及3个治疗组的大鼠体重和肝脾比明显增加,而且3个治疗组大鼠的脾脏指数降低。血清检测结果显示,IFNα2b和丹参粉针剂可降低谷丙转氨酶,总胆红素,透明质酸,和Ⅲ型前胶原水平,其中100和200 mg/kg剂量组还明显改善了谷草转氨酶、白蛋白水平。在组织学检查中发现,IFNα2b和丹参粉针剂可改善肝细胞的状态,较少的纤维增生和胶原沉积。免疫组织化学染色显示,IFNα2b和丹参粉针剂显著下调了转化生长因子β1和血小板源性生长因子(PDGF)。总之,丹参粉针剂对二甲基亚硝胺导致的大鼠肝纤维化具有一定的保护作用,其机制可能与下调TGF-β1和PDGF有关。     

仁青芒觉胶囊对二甲基亚硝胺诱导的大鼠肝纤维化的治疗作用

目的 观察仁青芒觉胶囊对二甲基亚硝胺（DMN）诱导的肝纤维化模型大鼠的治疗作用。方法 大鼠ip DMN制备肝纤维化模型,治疗给予低、中、高剂量（0.05、0.10、0.20 g/kg）的仁青芒觉胶囊,1.5 g/kg扶正化瘀胶囊作为阳性药,对照组及模型组给予同体积的蒸馏水,每天给药1次,连续4周。观察大鼠血清生化及胶原水平,肝脏组织蛋白、羟脯氨酸（Hyp）及超氧化物歧化酶（SOD）水平的变化;取肝脏,测定肝脏指数;肝组织固定,HE及Masson染色,镜下观察肝脏组织结构和纤维化程度变化。结果 ①与模型组比较,仁青芒觉胶囊各剂量组动物体质量,高、低剂量组肝质量显著增加（P<0.05、0.01）,高剂量组动物肝脏系数明显增加（P<0.05）。②与模型组比较,仁青芒觉胶囊各剂量组血清总蛋白（TP）和白蛋白（ALB）含量显著升高,血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）活性和总胆红素（TBIL）、透明质酸（HA）、IV型胶原（IV-C）、Ⅲ型前胶原（PC-Ⅲ）含量显著降低（P<0.05、0.01、0.001）;层粘蛋白（LN）也有不同程度的降低,低剂量组差异显著（P<0.05）。③与模型组比较,低、中剂量的仁青芒觉胶囊可以显著增加肝组织中蛋白含量（P<0.01、0.001）,各剂量SOD水平均显著升高（P<0.05、0.001）。④肝组织病理学显示,0.2 g/kg剂量的仁青芒觉胶囊能够显著改善弥漫性肝细胞水肿变性、坏死及减轻纤维增生程度,中、低剂量可以改善肝纤维化程度。结论 仁青芒觉胶囊对DMN诱导的肝纤维化模型大鼠具有一定程度的治疗作用。     

Inhibition of methylation of DNA by dimethylnitrosamine (DMN) in dehydroepiandrosterone-fed rats

The influence of the anticarcinogen dehydroepiandrosterone (DHEA) on the metabolism and macromolecular interactions of the potent hepatocarcinogen dimethylnitrosamine (NDMA) was investigated. Male Sprague-Dawley rats (2-3 mo old) were fed DHEA for 14 d at a dietary level of 0.8%. Compared with pair-fed controls, the liver weights of the DHEA-treated animals increased significantly (11.7 vs. 7.1 g) with increases, per total liver, in proteins including those of cytosol and microsomes as well as cytochromes P-450 and b5. DNA content of the liver, however, remained constant. Five hours after a single ip dose of [14C]NDMA (30 mg/kg body wt, 42 microCi/rat) DNA methylation was reduced in the DHEA-fed animals as measured by 7-methyl- and O6-methylguanine per mole of guanine, by 39 and 31%, respectively. The rate of NDMA metabolism was slightly higher in the DHEA-fed rats as determined in vivo by the exhalation of 14CO2 and by the declining concentrations of NDMA in the blood. The incorporation of radioactivity from [14C]NDMA into hepatic proteins in vivo was greater (2.1-fold) in the DHEA-fed rats. Our results suggest that feeding rats with the adrenal steroid DHEA enhances the metabolic activation of NDMA in vivo, and that the increased association of NDMA-derived metabolites with increased hepatic cellular proteins may be partially responsible for protection of hepatic DNA from NDMA-induced damage.     

The protective effect of resveratrol on dimethylnitrosamine-induced liver fibrosis in rats

Oxidative stress in liver injury is a major pathogenetic factor in progress of liver fibrosis. Resveratrol, a representative antioxidant derived from grapes, has been reported to show widespread pharmacological properties. In this study, we investigated the protective effects of resveratrol on dimethylnitrosamine (DMN)-induced liver fibrosis in rats. Rats were treated with resveratrol daily by oral gavage for seven days after a single intraperitoneal injection of DMN (40 mg/kg). Resveratrol remarkably recovered body and liver weight loss due to DMNinduced liver fibrosis. Liver histology showed that resveratrol alleviated the infiltration of inflammatory cells and fibrosis of liver tissue. Resveratrol decreased the level of malondialdehyde and increased the levels of glutathione peroxidase and superoxide dismutase. Also, resveratrol significantly inhibited the mRNA expression of inflammatory mediators including inducible nitric oxide, tumor necrosis factor-alpha and interleukin-1beta. In addition, resveratrol showed not only reduced mRNA expression of fibrosis-related genes such as transforming growth factor beta 1, collagen type I, and alpha-smooth muscle actin, but also a significant decrease of hydroxyproline in rats with DMN-induced liver fibrosis. Our results suggest that resveratrol could be used to treat liver injury and fibrosis and be useful in preventing the development of liver fibrosis and cirrhosis.     

The protective effects of Hibiscus sabdariffa extract on CCl4-induced liver fibrosis in rats.

Dried flower Hibiscus sabdariffa L. (HSE) extracts, a local soft drink material and medicinal herb, were studied for their protective effects against liver fibrosis induced using carbon tetrachloride (CCl(4)) in rats. Male Wistar rats were administered CCl(4) by intraperitoneal injection for 7weeks and received a normal diet or normal diet with various HSE doses (1-5%) for 9weeks. HSE significantly reduced the liver damage including steatosis and fibrosis in a dose dependent manner. Moreover, HSE significantly decreased the elevation in plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT). It also restored the decrease in glutathione content and inhibited the formation of lipid peroxidative products during CCl(4) treatment. In the primary culture, HSE also significantly inhibited the activation of the hepatic stellate cells. These results suggested that HSE may protect the liver against CCl(4)-induced fibrosis. This protective effect appears due to HSEs antioxidant properties.     

Effect of Sho-saiko-to extract on hepatic inflammation and fibrosis in dimethylnitrosamine induced liver injury rats

Sho-saiko-to extract, a Chinese herbal medicine, is widely used for treatment of chronic hepatitis in Japan. However, it is not clear what conditions Sho-saiko-to extract improves hepatic inflammation and fibrosis. We therefore induced various stages of liver injury in model rats and administered Sho-saiko-to extract. We then evaluated the liver inflammation and liver fibrosis-improving effects of Sho-saiko-to extract. The liver injury model rats were produced by administration of various doses of dimethylnitrosamine (DMN) and Sho-saiko-to extract was administered to these rats. Then the liver inflammation and fibrosis-improving effects of Sho-saiko-to extract were evaluated according to L-asparate aminotransferase (AST), L-alanine aminotransferase (ALT), liver retinoid levels, levels of hydroxyproline, Transforming Growth Factor-beta (TGF-beta), and the liver fibrosis area. These indicators depended on the total doses of DMN. The ability of Sho-saiko-to extract to improve liver inflammation and fibrosis was limited to the following levels of the respective parameters: AST levels (234-264 U/l), ALT levels (208-232 U/l), TGF-beta levels (1102-1265 pg/g liver tissue), hydroxyproline levels (633-719 nmol/g liver tissue), and liver fibrosis area (9.7-10.6 times for normal rat). These findings suggested that Sho-saiko-to extract is effective in the treatment of liver inflammation and fibrosis up to a certain degree of severity, but it produces no improvement in more severe cases.     

糖尿病高糖高脂对四氯化碳诱导的大鼠肝纤维化的作用研究

目的探讨糖尿病高糖高脂状态对四氯化碳(CCl_4)诱导的化学性肝纤维化进展的影响。方法采用高脂饲料及链脲佐菌素(STZ)建立糖尿病模型,四氯化碳诱导肝纤维化模型,高脂饲料、STZ及CCl_4诱导糖尿病合并肝纤维化模型,动态监测各组大鼠体重、血糖及相关血清学指标;HE染色观察各组大鼠的肝脏病理学变化;Western blot、q-PCR检测各组大鼠肝组织中α-SMA和Collagen Ⅰ的表达。结果与对照组大鼠相比,糖尿病组和糖尿病合并肝纤维化组大鼠体重明显下降,血糖血脂均升高,肝纤维化组无明显差异;HE染色及血清AST/ALT检测表明,与对照组大鼠肝组织相比,糖尿病大鼠、肝纤维化大鼠及糖尿病合并肝纤维化大鼠肝组织均有不同程度的肝损伤,以糖尿病合并肝纤维化组大鼠最为严重;3组大鼠肝组织α-SMA和Collagen Ⅰ表达较对照组也不同程度增加,以糖尿病合并肝纤维化组大鼠最为明显,与单纯糖尿病组和肝纤维化组比较,差异有显著性。结论糖尿病可诱发肝损伤,加剧CCl_4诱导的大鼠肝纤维化病变。     

软肝片抗肝纤维化作用的实验研究

目的探讨软肝片对四氯化碳中毒性肝纤维化的防治作用。方法用四氯化碳皮下注射造成大鼠肝纤维化模型 ,以联苯双酯作为阳性对照 ,测定血清丙氨酸氨基转移酶 (ALT)、天冬氨酸氨基转移酶 (AST)、玻璃酸(HA)、唾液酸及肝组织羟脯氨酸 (Hyp)、丙二醛 (MDA)、超氧化物歧化酶 (SOD)含量 ,以反映肝细胞损伤及肝纤维化程度。结果软肝片可明显降低肝纤维化大鼠血清ALT、AST、HA、唾液酸水平及肝组织Hyp和MDA水平 ,提高肝组织中SOD活力。结论软肝片具有一定的抗肝纤维化及抗脂质过氧化作用。     

Metabonomics study of the protective effects of Lonicera japonica extract on acute liver injury in dimethylnitrosamine treated rats

A metabonomics approach, consisting of gas chromatography coupled to mass spectrometry (GC/MS) and a multivariate statistical technique, was developed to estimate the protective effects of Lonicera japonica extract (LJE) on acute liver injury. A high dose of dimethylnitrosamine (DMN) was used to induce an acute stage of hepatic injury in 21 male Wistar rats. The rats were divided into three groups: normal, model and treatment. Pathological changes, particularly fibrosis, were also examined by Azan staining. The results indicate that clear and consistent biochemical changes occur. Nine candidate biomarkers for DMN treatment and LJE intervention under controlled conditions were identified using chemometric analysis. Pathological analysis suggests that LJE has a protective effect to the liver. This work suggests that a metabonomics approach can be used to estimate pharmacodynamic action of naturally occurring drugs in a dynamic and non-invasive way.     

Methyl palmitate prevents CCl(4)-induced liver fibrosis

Liver fibrosis is characterized by an excess of collagen fiber deposition, and it is known that Kupffer cells play an important role by immunomodulation of the toxic response. Methyl palmitate (MP) is an effective Kupffer cell inhibitor. The aim of this work was to evaluate the effect of MP on experimental liver fibrosis. Four groups were formed: the control group, which received the vehicles only; CCl(4) group (0.4 g kg(-1), i.p., three times a week, for eight weeks); CCl(4) plus MP (300 mg kg(-1), i.p., daily); and MP alone. Alanine aminotransferase was increased by CCl(4), and MP did not prevent this increase. Lipid peroxidation was increased markedly by CCl(4); again, MP was not able to prevent this effect. Fibrosis increased nearly 6-fold (measured as liver hydroxyproline content) in the CCl(4) group; MP preserved the normal content of collagen. These results were corroborated by histopathology. To elucidate the antifibrogenic mechanism of MP, we measured the production of TGF-beta; CCl(4) increased this cytokine several-fold, and MP abolished this increase. Collectively the present results indicate that MP possesses a strong antifibrogenic effect at least in the CCl(4) model of fibrosis. The antifibrotic effect of MP is probably associated with its ability to reduce TGF-beta content, maybe by immunomodulation of Kupffer cells functioning.     

灯盏花素对糖尿病大鼠肝脏保护作用的实验研究

目的　探讨灯盏花素对糖尿病大鼠肝脏保护作用。方法　建立STZ诱导的糖尿病模型 ,随机分 4组 :对照组、模型组、灯盏花素给药组、维生素E给药组 ,每组 10只 ,观察8wk。应用分光光度法检测肝组织MDA含量及SOD、CAT与GSH PX活性 ;HE染色对肝组织作病理检查 ;油红O染色观察肝组织脂肪浸润 ;肝组织ED1(单核 巨噬细胞表面标志 )免疫组织化学采用SABC技术。结果　灯盏花素给药组对糖尿病大鼠血糖、体重无明显影响 ,维生素E给药组可降低血糖 ,延缓体重下降。HE染色模型组部分肝细胞脂肪变性 ;各给药组对肝细胞保护效果较好。模型组肝细胞油红O染色评分为 2 11± 0 82 ,对照组为 0 35± 0 15 ,相比差异有显著性 (P <0 0 1) ;灯盏花素给药组评分为 0 75± 0 6 6 ,维生素E给药组评分为 1 13± 0 78,与模型组相比差异均有显著性 (P均 <0 0 1)。模型组肝组织MDA含量明显升高 ,SOD、CAT、GSH PX活性明显降低 ,各给药组均可降低肝组织MDA含量 ,提高SOD、CAT与GSH PX活性。免疫组织化学显示各给药组均能抑制糖尿病肝组织单核 巨噬细胞浸润的增加。结论　灯盏花素对糖尿病大鼠肝脏保护作用机制部分与抑制肝内脂肪浸润、氧化应激及巨噬细胞浸润有关。