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1.
目的研究升麻葛根汤对CCl4致小鼠急性肝损伤的保护作用。方法用CCl4诱导化学性急性肝损伤模型,测定小鼠血清中谷丙转氨酶(ALT)和谷草转氨酶(AST)活力;肝组织中总超氧化物歧化酶(TSOD)、总抗氧化能力(T-AOC)和谷胱甘肽过氧化物酶(GSH-Px)的活性及脂质过氧化产物丙二醛(MDA)含量。结果在CCl4诱导小鼠急性肝损伤模型中,升麻葛根汤可明显降低血清ALT和AST水平,降低肝组织中MDA的含量,明显增加T-SOD,GSH-PX,T-AOC的活性。结论升麻葛根汤对CCl4诱导小鼠急性肝损伤具有保护作用,该作用可能与提高小鼠肝脏抗氧化损伤能力、降低脂质过氧化水平有关。  相似文献   

2.
为研究大豆水提物(SWEs)对四氯化碳(CCl4)所致急性肝损伤小鼠的保护作用以及对肝脏抗氧化活力的影响。将60只试验小鼠随机分为正常对照组、模型组、SWEs低(50 mg·kg-1),中(100 mg·kg-1),高(150 mg·kg-1)剂量组及阳性对照组(联苯双脂,100 mg·kg-1)。每天灌胃给药1次,连续7 d。末次给药1 h后,除正常对照组外的其余5组采用10%CCl42.0 m L·kg-1剂量一次性腹腔注射,建立小鼠急性肝损伤模型。6 h后摘眼球取血及肝脏,计算各组小鼠的肝指数,比色法测定血清谷丙转氨酶(ALT)和谷草转氨酶(AST)活性,及总胆红素(TBIL)和白蛋白(ALB)水平,检测肝组织中丙二醛(MDA)和还原型谷胱甘肽(GSH)水平及一氧化氮合酶(NOS)活性。结果表明:模型组小鼠肝重和肝指数、血清ALT和AST活性及TBIL水平、肝组织MDA水平及NOS活性均显著高于对照组;而血清ALB及肝组织GSH水平显著低于对照组。与模型组相比,中、高剂量的SWEs及联苯双脂显著降低CCl4所致急性肝损伤小鼠的肝重和肝指数、血清ALT和AST活性及TBIL水平、肝组织NOS活性和MDA水平,并显著提高血清ALB及肝组织GSH水平。大豆水提物对CCl4所致小鼠急性肝损伤具有保护作用,其机制可能与抗氧化作用有关。  相似文献   

3.
目的观察人参及灵芝超微粉对四氯化碳(CCl4)所致小鼠急性肝损伤的保护作用。方法将80只小鼠随机分为正常组,模型组,人参超微粉低、高剂量(0.25、0.5g/kg)组,灵芝超微粉低、高剂量(0.25、0.5g/kg)组及人参超微粉联合灵芝超微粉低、高剂量(0.25+0.25 g/kg、0.5+0.5g/kg)组,每组10只。各给药组每天灌胃相应受试物1次,连续给药30天,对照组及模型组灌胃0.5%羧甲基纤维素钠,灌胃体积均为20ml/kg。末次药后1小时,除对照组外,各组均腹腔注射0.1%CCl4橄榄油溶液10ml/kg诱导小鼠急性肝损伤。24小时后,各组小鼠眼球内眦静脉丛取血,分离血清,测定核因子-κB(NF-κB)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、丙二醛(MDA)含量及丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、超氧化物歧化酶(SOD)活性。取部分肝脏制备匀浆,检测肝组织MDA含量及SOD活性。结果与正常组比较,模型组大鼠血清NF-κB、TNF-α、IL-6含量及AST、ALT活性均明显升高,血清及肝组织MDA含量明显升高,SOD活性明显降低(P0.05或P0.01)。与模型组比较,人参、芝超微粉高剂量组及人参联合灵芝超微粉低、高剂量组均能明显降低小鼠血清NF-κB、TNF-α、IL-6含量及AST、ALT活性,并能明显降低血清及肝组织MDA含量,升高SOD活性(P0.05或P0.01)。结论人参及灵芝超微粉对CCl4所致小鼠急性肝损伤均具有明显的保护作用,二者联合应用具有协同作用。  相似文献   

4.
目的研究细柱五加果实乙醇提取物对四氯化碳致小鼠急性肝损伤的保护作用。方法将60只小鼠随机分成细柱五加果实的高、中、低剂量组以及阳性对照组、模型对照组、空白对照组共6组。6组小鼠ig给药20 mL/(kg.d)。连续14 d。第14 d给药1 h后,除空白对照组外,其余各组均ip 0.1%CCl4 0.2 mL/20g。所有小鼠在ip CCl4 16 h后采用眼球取血并脱颈椎处死。然后离心取血清,剖腹取肝。分别将各组肝脏取出0.1 g,加0.9 mL生理盐水进行匀浆。检测血清中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转氨酶(AST)活性及肝匀浆中丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性的变化。结果与模型对照组相比,不同剂量的细柱五加果实乙醇提取物均能显著降低血清中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转氨酶(AST)的活性及肝组织中丙二醛(MDA)的含量,提高超氧化物歧化酶(SOD)的活性。结论细柱五加果实乙醇提取物对四氯化碳致小鼠的急性肝损伤有保护作用。  相似文献   

5.
目的研究环翠楼高丽红参复方制剂对小鼠酒精性肝损伤的保护作用。方法通过测定小鼠眼球血清谷丙转氨酶(ALT)、谷草转氨酶(AST)活性和小鼠肝脏的MDA活性。结果高剂量药物组可降低由酒精性肝损伤引起的血清中ALT活性(P0.01,P0.05),作用相当于阳性药物;各剂量药物组均可降低小鼠血清中的ALT活性,并呈现了一定的量效关系;各剂量药物组和阳性对照组对小鼠酒精性肝损伤引起的AST升高,均有降低作用,且呈现了量效关系;随着药物剂量的增加,酒精性肝损伤小鼠肝组织MDA含量较模型组有下降趋势,其中高剂量组差异显著(P0.01,P0.05)。结论环翠楼高丽红参复方制剂具有较强的对小鼠酒精性肝损伤的保护作用。  相似文献   

6.
萎凋适度的一芽二叶福安大白茶,一组用30℃烘干,另一组用120℃烘干.分剐制成白茶茶剂喂饲小鼠,研究其对CCl4致急性肝损小鼠的肝保护作用.肝组织病理切片结果表明,两种茶剂都能显著减轻CCl4对肝脏细胞的病理损伤(p<0.01),但两茶剂处理间的差异不大.30℃烘干白茶高剂量处理的小鼠CSH、ALT、MDA分别是模型组的116.4%、71.2%(P<0.01)和61.5%(P<0.01);120℃烘干白茶高剂量处理的小鼠GSH、ALT/CPT、MDA分别是模型组的118.5%(9<0.05)、85.1%(P<0.01)和68.1%(P<0.01).研究结果表明,烘干温度对白茶减轻Ccl4肝损伤的影响差异不显著,可见长时间萎凋是白茶具有护肝作用的关键加工工艺.  相似文献   

7.
研究狭叶茶(Camellia angustifolia Chang)提取物对拘束负荷诱发小鼠应激性肝损伤的保护作用。采用拘束负荷小鼠应激性肝损伤模型,18h拘束负荷诱发小鼠应激性肝损伤,分别用赖氏法测定小鼠血浆和肝组织丙氨酸转移酶(ALT)活性、硫代巴比妥酸法测定丙二醛(MDA)含量、HPLC法测定谷胱甘肽(GSH)水平、比色法测定黄嘌呤氧化酶(XOD)、谷胱甘肽过氧化物酶(GPX)和谷胱甘肽S转移酶(GST)活性,荧光酶标仪测定血浆、肝组织及狭叶茶提取物体外抗氧化能力指数(ORAC)。与拘束模型组相比,狭叶茶提取物可以明显提高拘束负荷小鼠血浆与肝组织匀浆的ALT活性和抗氧化能力指数,提高GSH水平,增强GPX和GST活性,有效降低肝组织中MDA含量和XOD活性,并在体外显示出较强的抗氧化能力。说明狭叶茶提取物对拘束应激引起的小鼠肝损伤具有一定的保护作用,其作用机制可能部分来自于减少拘束负荷小鼠氧化应激水平,清除自由基和抑制脂质过氧化过程。  相似文献   

8.
目的建立HPLC同时测定柳蒿(Artemisia integrifolia Linn.)中绿原酸、芦丁、木犀草苷、槲皮素含量的方法,并研究柳蒿提取液对肝脏的保护作用,探讨其可能机理。方法采用高效液相色谱法。色谱柱为Inertsil ODS-3柱,流动相为乙腈-0.2%磷酸水溶液(梯度洗脱),流速为1.0 mL·min~(-1),检测波长270 nm,柱温25℃,进样量为10μL;60只雄性小鼠随机分为6组,每组10只,除正常组外,其余各组均腹腔注射0.1%的CCl_4橄榄油溶液致小鼠急性肝损伤,测定小鼠血清中谷丙转氨酶(ALT)和谷草转氨酶(AST)活力;肝组织中丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)、总抗氧化能力(T-AOC)和总超氧化物歧化酶(T-SOD)。结果绿原酸、芦丁、木犀草苷、槲皮素检测进样量线性范围分别为1.015 2~16.243 2μg(r=0.999 9),0.257 1~4.113 6μg(r=0.999 9),0.081 6~1.305 6μg(r=0.999 8),0.027 3~0.436 8μg(r=0.999 9);精密度、稳定性、重复性试验的RSD2.0%;加样回收率分别为98.73%~100.42%(RSD=0.52%,n=5),95.64%~102.07%(RSD=1.52%,n=5),94.05%~99.79%(RSD=1.73%,n=5),96.22%~101.89%(RSD=2.45%,n=5)。柳蒿提取液可明显抑制CCl_4致小鼠肝损伤后血清中ALT和AST升高,肝组织中MDA含量升高,提高肝组织中T-SOD、GSH-PX、T-AOC活性。结论建立的HPLC方法,简便、精确、灵敏度高,可用于柳蒿药材中4种成分含量的同时测定。柳蒿对CCl_4所致小鼠急性肝损伤具有保护作用。该结果可为今后柳蒿的开发利用和深入研究提供一定的参考。  相似文献   

9.
目的探究肝纤胶囊对(GC)小鼠肝损伤的初步影响。方法取昆明小鼠120只,将其随机均分为Ⅰ组:四氯化碳造模;Ⅱ组:D-氨基半乳糖造模。对Ⅰ、Ⅱ两组分别进行造模后,Ⅰ组小鼠取肝组织制作病理切片、测量血清中的谷丙转氨酶(ALT)和谷草转氨酶(AST)含量、肝组织中SOD及GSH-Px的活性和MDA的含量,以及Ⅱ组小鼠血清中ALT和AST的含量及肝组织中SOD的活性和MDA的含量。结果肝纤胶囊大、中剂量组能够显著抑制四氯化碳组小鼠的肝组织病变程度并增强肝组织中GSH-Px与SOD活性,同时能够降低两种模型小鼠血清中ALT和AST的含量及肝组织中MDA水平。结论肝纤胶囊对四氯化碳及D-氨基半乳糖诱导的小鼠肝损伤起到保护作用。  相似文献   

10.
本文对复合人参素及其所含人参多糖的药理作用进行了对比研究。结果表明,复合人参素200、400mg/kg和人参多糖100、200mg/kg给小鼠多次灌胃,均能明显提高小鼠耐缺氧和抗疲劳能力,可使正常小鼠免疫器官的重量增加,并增强网状内皮系统的吞噬功能,亦能明显降低CCl、肝损伤小鼠肝组织中丙二醛含量。提示复合人参素药理作用的发挥是其所含人参皂甙人参多糖和人参多肽等多种活性成分综合作用的结果。  相似文献   

11.
Liver Protective Effects of Morinda citrifolia (Noni)   总被引:1,自引:0,他引:1  
This study evaluated the protective effects of Noni fruit juice on acute liver injury induced by carbon tetrachloride (CCl(4)) in female Sprague-Dawley (SD) rats. Liver damage (micro-centrilobular necrosis) was observed in animals pretreated with 20% placebo (drinking water) + CCl(4). However, pretreatment with 20% Noni juice in drinking water + CCl(4) resulted in markedly decreased hepatotoxic lesions. Furthermore, serum alanine aminotransferase and aspartate aminotransferase levels were significantly lower in the Noni group than the placebo group. In a correlative time-dependent study, one dose of CCl(4) (0.25 mL/kg in corn oil, p.o.) in female SD rats, pretreated with 10% placebo for 12 days, caused sequential progressive hepatotoxic lesions over a 24 h period, while a protective effect from 10% Noni juice pretreatment was observed. These results suggest that Noni juice is effective in protecting the liver from extrinsic toxin exposure.  相似文献   

12.
Fucoidan is an l-fucose-enriched sulfated polysaccharide isolated from brown algae and marine invertebrates. In this study, we investigated the protective effect of fucoidan from Fucus vesiculosus on alcohol-induced murine liver damage. Liver injury was induced by oral administration of 25% alcohol with or without fucoidan (30 mg/kg or 60 mg/kg) for seven days. Alcohol administration increased serum aspartate aminotransferase and alanine aminotransferase levels, but these increases were suppressed by the treatment of fucoidan. Transforming growth factor beta 1 (TGF-β1), a liver fibrosis-inducing factor, was highly expressed in the alcohol-fed group and human hepatoma HepG2 cell; however, the increase in TGF-β1 expression was reduced following fucoidan administration. Treatment with fucoidan was also found to significantly reduce the production of inflammation-promoting cyclooygenase-2 and nitric oxide, while markedly increasing the expression of the hepatoprotective enzyme, hemeoxygenase-1, on murine liver and HepG2 cells. Taken together, the antifibrotic and anti-inflammatory effects of fucoidan on alcohol-induced liver damage may provide valuable insights into developing new therapeutics or interventions.  相似文献   

13.
为了解油酸在黄曲霉毒素B1(aflatoxin B1,AFB1)诱发的肝损伤中所起的保护作用,以体外培养的肝细胞(L-02)作为靶细胞,研究油酸的保护机制。设置3组实验:对照组(无处理)、AFB1组(只有AFB1)、油酸组(AFB1和油酸共同处理),药物处理24h后显微镜观察细胞形态,细胞增殖-毒性检测试剂盒(Cell Counting Kit-8, CCK-8)检测细胞活力,荧光法检测活性氧(reactive oxygen species,ROS)水平,Annexin V-FITC/PI检测细胞凋亡率,蛋白质免疫印迹检测血红素加氧酶-1(heme oxygenase 1,HO-1)、Caspase-3以及Survivin蛋白的表达。采用t检验或单因素方差分析进行统计分析。结果发现:与对照组相比,AFB1暴露能够明显抑制细胞活力(P<0.05),促进细胞凋亡(P<0.001),升高ROS水平(P<0.001);与AFB1组相比,油酸作用后细胞活力显著增加(P<0.01),细胞凋亡减少(P<0.01),ROS水平降低(P<0.001)。与AFB1组相比,油酸作用后可显著提高 HO-1(P<0.05)和抑凋亡蛋白Survivin的表达(P<0.05),降低凋亡蛋白Caspase-3(P<0.01)表达。因此认为油酸对AFB1引发的肝细胞损伤具有保护作用,其机制可能与其通过促进抗氧化酶蛋白HO-1的表达,从而降低氧化应激水平,降低细胞凋亡有关。  相似文献   

14.
为探讨茯砖茶对高脂诱导的非酒精性脂肪肝病(Non-alcoholic fatty liver disease,NAFLD)大鼠肠黏膜屏障及肝损伤的保护作用,将SD雄性大鼠随机分为正常组、NAFLD组、茯砖茶低、高剂量组,每组8只。通过分析大鼠的采食量、体重变化、血脂指标、肝脏指标及病理切片来评估NAFLD大鼠模型的构建情况及茯砖茶的干预作用。通过分析空肠与结肠病理及PAS染色切片、绒毛高度/隐窝深度值(V/C值)、血清二胺氧化酶(DAO)和脂多糖(LPS)活力评估肠道完整性和通透性;通过分析空肠上皮间淋巴细胞(JIL)数量和血清肿瘤坏死因子(TNF-α)活力评估肠道相关炎症。结果表明,茯砖茶能减少NAFLD大鼠的采食量和体重,降低血脂水平,减少血清中谷草转氨酶(AST)和谷丙转氨酶(ALT)活力,并抑制肝脏的脂质聚集和炎细胞浸润。茯砖茶还降低了血清炎症因子TNF-α和血清LPS的水平,并使血清DAO活力上升。同时,茯砖茶抑制了NAFLD大鼠空肠和结肠绒毛中发生的炎细胞浸润现象,减少了空肠绒毛脱落、断裂、稀疏和紊乱现象,增加了空肠绒毛V/C值,降低了空肠上皮间淋巴细胞数量,增加了空肠和结肠的杯状细胞数量。这些结果说明,茯砖茶能够有效的改善高脂饮食诱导的肠道黏膜屏障及肝损伤,起到防治NAFLD的作用。  相似文献   

15.
Peptides from oyster hydrolysate (OPs) have a variety of biological activities. However, its protective effect and exact mechanism on testicular injury remain poorly understood. This study aimed to evaluate the protective effect of OPs on triptolide (TP)-induced testis damage and spermatogenesis dysfunction and investigate its underlying mechanism. In this work, the TP-induced testis injury model was created while OPs were gavaged in mice for 4 weeks. The results showed that OPs significantly improved the sperm count and motility of mice, and alleviated the seminiferous tubule injury. Further study showed that OPs decreased malonaldehyde (MDA) level and increased antioxidant enzyme (SOD and GPH-Px) activities, attenuating oxidative stress and thereby reducing the number of apoptotic cells in the testis. In addition, OPs improved the activities of enzymes (LDH, ALP and ACP) related to energy metabolism in the testis and restored the serum hormone level of mice to normal. Furthermore, OPs promoted the expression of Nrf2 protein, and then increased the expression of antioxidant enzyme regulatory protein (HO-1 and NQO1) in the testis. OPs inhibited JNK phosphorylation and Bcl-2/Bax-mediated apoptosis. In conclusion, OPs have a protective effect on testicular injury and spermatogenesis disorders caused by TP, suggesting the potential protection of OPs on male reproduction.  相似文献   

16.
The Active Peptide from Shark Liver (APSL) was expressed in E. coli BL21 cells. The cDNA encoding APSL protein was obtained from shark regenerated hepatic tissue by RT-PCR, then it was cloned in the pET-28a expression vector. The expressed fusion protein was purified by Ni-IDA affinity chromatography. SDS-PAGE and HPLC analysis showed the purity of the purified fusion protein was more than 98%. The recombinant APSL (rAPSL) was tested for its biological activity both in vitro, by its ability to improve the proliferation of SMMC7721 cells, and in vivo, by its significant protective effects against acute hepatic injury induced by CCl4 and AAP (acetaminophen) in mice. In addition, the rAPSL could decrease the blood glucose concentration of mice with diabetes mellitus induced by alloxan. Paraffin sections of mouse pancreas tissues showed that rAPSL (3 mg/kg) could effectively protect mouse islets from lesions induced by alloxan, which indicated its potential application in theoretical research and industry.  相似文献   

17.
Background: Hepatic ischemia reperfusion (IR) is an important issue in complex liver resection and liver transplantation. The aim of the present study was to determine the protective effect of astaxanthin (ASX), an antioxidant, on hepatic IR injury via the reactive oxygen species/mitogen-activated protein kinase (ROS/MAPK) pathway. Methods: Mice were randomized into a sham, IR, ASX or IR + ASX group. The mice received ASX at different doses (30 mg/kg or 60 mg/kg) for 14 days. Serum and tissue samples at 2 h, 8 h and 24 h after abdominal surgery were collected to assess alanine aminotransferase (ALT), aspartate aminotransferase (AST), inflammation factors, ROS, and key proteins in the MAPK family. Results: ASX reduced the release of ROS and cytokines leading to inhibition of apoptosis and autophagy via down-regulation of the activated phosphorylation of related proteins in the MAPK family, such as P38 MAPK, JNK and ERK in this model of hepatic IR injury. Conclusion: Apoptosis and autophagy caused by hepatic IR injury were inhibited by ASX following a reduction in the release of ROS and inflammatory cytokines, and the relationship between the two may be associated with the inactivation of the MAPK family.  相似文献   

18.
Reactive oxygen species (ROS) are the key factors that cause many diseases in the human body. Polysaccharides from seaweed have been shown to have significant antioxidant activity both in vivo and in vitro. The ameliorative effect of Ulva lactuca polysaccharide extract (UPE) on renal injury induced by oxidative stress was analyzed. As shown by hematoxylin–eosin staining results, UPE can significantly improve the kidney injury induced by D-galactose (D-gal). Additionally, the protective mechanism of UPE on the kidney was explored. The results showed that UPE could decrease the levels of serum creatinine (Scr), blood urea nitrogen (BUN), serum cystatin C (Cys-C), lipid peroxidation, protein carbonylation, and DNA oxidative damage (8-OHdG) and improve kidney glutathione content. Moreover, UPE significantly increased the activities of superoxide dismutase and glutathione peroxidase and total antioxidant activity in mice. UPE also decreased the levels of inflammatory cytokines TNF-α and IL-6. Further investigation into the expression of apoptotic protein caspase-3 showed that UPE decreased the expression of apoptotic protein caspase-3. These results indicate that UPE has a potential therapeutic effect on renal injury caused by oxidative stress, providing a new theoretical basis for the treatment of oxidative damage diseases in the future.  相似文献   

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