桑黄预防大鼠肝纤维化作用的实验研究

目的：研究桑黄对肝纤维化的预防作用。方法：采用四氯化碳诱发大鼠肝损伤，辅以高脂，低蛋白复合饲料和一定浓度乙醇饮料，复制肝纤维化模型。用桑黄进行预防，观察其对血清中生化指标的胶原成分的影响。结果：桑黄能提高肝损伤大鼠的蛋白质合成能力，显著降低血清氨基酸转移水平和胶原成分含量，病理组织学观察显示，预防组肝纤维变性减轻，肝脏纤维增生减少。结论：桑黄能减轻肝细胞损伤，预防四氯化碳致大鼠肝纤维化的发生与发展。     

中药金丹肝泰防治大鼠急性肝损伤实验研究

目的:研究金丹肝泰的护肝作用.方法:用D 氨基半乳糖(D GalN)制备大鼠急性肝损伤模型.通过检测血清丙氨酸氨基转移酶(ALT)和天门冬氨酸氨基转移酶(AST)活性并观察光镜下肝组织的病理学改变,探讨中药金丹肝泰对急性肝损伤的保护作用.结果:口服金丹肝泰浸膏可显著降低急性肝损伤大鼠血清ALT和AST水平,减轻肝细胞的变性坏死.结论:金丹肝泰对肝细胞具有一定的保护作用.     

桑黄调节细胞因子及其在抗肝纤维化中的意义

目的 研究桑黄调节细胞因子与抗肝纤维化。方法 以四氯化碳诱导大鼠肝纤维化，观察桑黄对肝纤维化的治疗作用；体外培养人外周血单个核细胞(PMNCs)，考察桑黄对其产生γ-干扰素的增强作用。结果 桑黄能抑制肝纤维化大鼠肝脏内胶原纤维增生，明显降低血清氯基酸转移酶水平和胶原成分含量，降低血清白细胞介素-4水平，而显著提高血清γ-干扰素水平；体外实验表明，桑黄能促进PMNCs生成γ-干扰素，且呈浓度依赖性特征。结论 桑黄具有明显的抗肝纤维化作用，诱生γ-干扰素可能是其作用机理之一。     

肝乐宁粉针剂对实验性肝损伤的保护作用

研究肝乐宁粉针剂对实验性肝损伤的保护作用。方法：采用四氯化碳致小鼠和大鼠肝脏损伤,测定生化指标及观察病理组织学改变。结果：肝乐宁粉针剂能显著降低四氯化碳引起的急性肝损伤小鼠和慢性肝损伤大鼠血清丙氨酸氨基转换酶和天门冬氨酸氨基转换酶增高;亦能明显降低大鼠血清唾液酸和肝羟脯氨酸含量,升高血清总蛋白和白蛋白水平;病理组织学检查肝乐宁粉针剂明显减轻肝细胞的变性和坏死,并抑制慢性肝损伤胶原纤维形成。结论：肝乐宁粉针剂具有肝细胞保护及抗肝纤维化作用。     

鲨肝活性肽对对乙酰氨基酚致小鼠急性肝损伤的保护作用

目的探讨鲨肝活性肽(sHSS)对对乙酰氨基酚(AAP)致小鼠急性肝损伤的保护作用。方法用AAP(200 mg·kg^-1,ip)诱导小鼠急性肝损伤,用改良赖氏法测血清ALT和AST,通过光镜和电镜观察肝细胞显微和亚显微结构的变化,用流式细胞仪分析肝细胞凋亡,同时用RT-PCR方法分析Fas mRNA表达水平。结果sHSS 3.0和1.5 mg·kg^-1可显著降低肝损伤小鼠血清ALT和AST的水平;改善模型鼠肝组织细胞坏死及炎症反应;高剂量sHSS(3 mg·kg^-1)对肝线粒体具有保护作用,下调Fas mRNA的表达水平,并具有抗凋亡作用。结论sHSS对AAP诱导的肝损伤具有明显的保护作用,其机制可能与保护肝线粒体、抑制Fas基因表达及肝细胞凋亡有关。     

玉郎伞多糖对小鼠急性酒精性肝损伤保护作用的研究

目的:研究玉郎伞多糖对小鼠急性酒精性肝损伤的保护作用。方法:小鼠ig10mL·kg-150%酒精,建立急性酒精性肝损伤模型;测定血清转氨酶、肝组织超氧化物歧化酶活性及甘油三酯含量,并进行病理组织学观察。结果:各剂量玉郎伞多糖能显著降低小鼠血清转氨酶活性和甘油三酯含量,显著提高肝组织超氧化物歧化酶活性,减少肝细胞脂滴数量;高、中剂量玉郎伞多糖可显著减轻酒精性肝损伤小鼠肝细胞的脂肪变性。结论:玉郎伞多糖可减轻酒精对脂肪代谢的影响,对急性酒精性肝损伤有保护作用。     

口服1,6-二磷酸果糖对动物肝损伤模型的保护作用

目的研究长期口服1,6-二磷酸果糖(FDP)对不同的肝损伤模型的影响,探索口服FDP作为慢性肝损伤保护药物的可能性。方法用CCl4所致的肝损伤模型来观察FDP对慢性肝损伤的作用;用D-半乳糖(GalN)和脂多糖(LPS)所致的小鼠肝损伤模型来评价FDP对急性肝损伤的作用。结果在CCl4所致的大鼠慢性肝损伤模型中,FDP (1 -4 g·kg-1·d-1ig)连续用药10周,可明显降低血清中病理性升高的ALT、AST、γ-GT、T-BIL和ALP的含量,同时升高病理性降低的TP、ALB和T-CHO的水平;并明显降低肝组织中羟脯氨酸的含量;FDP 4.0 g·kg-1·d-1可明显减少肝硬化发生率和减轻肝组织病理改变。在GalN所致的小鼠急性肝损伤模型中,FDP 1.0 -4.0 g·kg-1·d-1(ig 3 d)显著降低血清中ALT和AST的水平(P<0.01)和肝系数,4.0 g·kg-1·d-1可明显减轻肝细胞超微结构的病理性改变。在LPS所致的小鼠急性肝损伤模型中,FDP最大剂量(4.0 g·kg-1·d-1, ig 12 d)可明显降低血清中的ALT。结论本研究首次证明了长期口服FDP对CCl4所致的慢性肝损伤具有保护作用,同时证实了它对急性肝损伤的保护作用,提示口服FDP对不同原因引起的肝损伤有效,有可能作为口服肝保护药用于临床。     

促肝细胞生长素对异烟肼和利福平诱导大鼠肝损伤的保护作用

目的研究促肝细胞生长素对异烟肼和利福平诱导大鼠肝损伤的保护作用。方法雄性SD大鼠给予异烟肼50mg/kg+利福平100 mg/kg,建立肝损伤模型。促肝细胞生长素组在模型组的基础上给予促肝细胞生长素肠溶胶囊40 mg/kg,给药3周后,称体质量,计算肝系数,同时比较血清肝功能指标丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、碱性磷酸酶(ALP)、总胆红素(TBIL)和直接胆红素(DBIL),肝抗氧化酶系超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、还原型谷胱甘肽(GSH)和丙二醛(MDA)水平,切片观察肝脏病理变化。结果与模型组相比,促肝细胞生长素组ALT、AST显著降低(P0.05),ALP、TBIL和DBIL水平也表现出明显的降低趋势;肝组织SOD、GSH-Px水平显著升高(P0.05),MDA水平显著降低(P0.05),GSH水平有升高趋势。促肝细胞生长素组肝小叶结构清晰,炎症细胞浸润减少。结论促肝细胞生长素对异烟肼和利福平诱导肝损伤具有保护作用,其作用机制可能与其肝再生增强因子提高肝组织抗氧化能力、抑制肝组织炎症反应有关。     

乌丹醒肝颗粒对大鼠急性酒精性肝损伤的影响

目的研究乌丹醒肝颗粒对大鼠急性酒精性肝损伤的影响.方法将大鼠灌胃给予56°红星二锅头,制备急性酒精性肝损伤大鼠模型;末次给药后测定血清ALT、AST、MDA、GSH-PX及肝匀浆中SOD、MDA、GSH-PX等各项指标含量计算肝系数.结果乌丹醒肝颗粒中剂量对造模大鼠血清ALT升高有显著降低作用,对造模大鼠血清GSH-PX活性降低有显著的升高作用;乌丹醒肝颗粒对造模大鼠血清AST升高有降低作用;乌丹醒肝颗粒大剂量对造模大鼠肝组织MDA水平升高有显著且呈剂量依赖性的降低作用;乌丹醒肝颗粒大、中、小剂量可以显著提高造模大鼠肝组织GSH-PX和SOD活性.结论乌丹醒肝颗粒对大鼠急性酒精性肝损伤具有较好的治疗作用,为其临床用药提供了药效学基础.     

二草清肝汤对免疫性肝损伤大鼠细胞因子表达的影响

目的：观察中药二草清肝汤对大鼠免疫性肝损伤的保护作用并探讨其药理学机制。方法：采用卡介苗（BCG）＋脂多糖（LPS）建立大鼠免疫性肝损伤模型。肝组织病理切片观察肝组织损伤情况;采用ELISA法检测血清IL-10及IL-12水平。结果：大鼠免疫性肝损伤时,血清IL-10及IL-12水平显著升高;中药组及西药对照组（环磷酰胺）IL-10及IL-12水平明显低于模型组（P〈0．01）,中药组和西药组肝组织病理改变较模型组明显减轻,中药组一般情况明显好于西药组。结论：二草清肝汤能降低免疫性肝损伤大鼠的血清IL-10及IL-12水平,对实验性免疫肝损伤有明显保护作用。     

桑黄多糖对环磷酰胺所致免疫损伤大鼠生长及外周血的影响

目的：研究桑黄多糖对正常及环磷酰胺所致免疫损伤大鼠的生长及其血常规和生化指标的影响。方法：大鼠随机分成4组,各组大鼠腹腔注射相应药物7d后,连续灌胃给予相应药物28d,大鼠股动脉采血处死后,剥离大鼠的脾脏和胸腺,称脾脏和胸腺湿重,并计算脏器指数,血常规方法测定外周血白细胞(WBC)计数和血红蛋白(Hb)含量、蛋白质含量及AKP,LDH活力测定;结果：桑黄多糖能使大鼠体重、胸腺湿重指数、脾脏湿重指数、外周血WBC数、Hb含量、总蛋白和球蛋白等水平显著提高,并能阻遏由环磷酰胺所致的抑制作用。结论：桑黄多糖能改善并调节大鼠营养状况和造血功能,从而增强机体的免疫功能。     

Immunopharmacological effects and mechanism of dihydroqinghaosu on immunological liver injury mice

AIM: To investigate the immunopharmacological effects and the preliminary mechanism of Dihydroqinghaosu (DQHS) on the Con A-induced liver injury mice. METHODS: Hepatocytes of SD rats were prepared to examine the effect of DQHS on the ALT levels of hepatocytes content in vitro. The Con A-induced liver injury model of ICR mice was made. Dose-dependent and time-dependent difference of serum ALT activity was observed     

基于网络药理学探讨桑黄治疗肝炎的作用机制

目的运用网络药理学方法研究桑黄治疗肝炎的有效成分及作用靶点,为深入探索其药理作用机制提供依据。方法本研究采用TCMSP平台中的CancerHSP软件检索桑黄的化学成分、作用靶点,通过Uniprot数据库及GendCards数据库分别检索各化学成分和肝炎对应的靶基因,找出关键基因;采用Cytoscape 3.7.2软件做出桑黄-肝炎-靶点网络图;通过String数据库构建蛋白质相互作用(PPI)网络图;利用ClueGo软件对关键靶点进行功能富集分析及KEGG通路分析。结果经检索桑黄共有9种化合物,经筛选得到3个化合物、27个靶点、30个基因,与肝炎相关的有MAOB、XDH、ALDH2、SMAD3、ALDH3A1、CYP2A6等22个关键基因。主要通过组氨酸代谢(histidine metabolism)、酪氨酸代谢(tyrosine metabolism)等7条通路发挥作用。结论本研究初步验证了桑黄治疗肝炎的作用靶点及作用通路,为进一步揭示其肝脏保护机制奠定基础。     

药用真菌桑黄的研究现状

文章综述了药用真菌桑黄的来源分布及其化学成分、药理作用、人工发酵培养方面的研究现状。     

齐墩果酸钠盐对大鼠化学性肝损伤的保护作用

目的 观察齐墩果酸钠盐对化学性损伤的肝细胞保护作用。方法 采用CCl4亚急性染毒建立化学性肝损伤大鼠模型,用齐墩果酸钠盐每天按三个剂量(3mg／kg、15mg／kg、30mg／kg)喂食大白鼠30天,测其血液生化指标并作组织病理学检查。结果 与对照组比较,齐墩果酸钠盐能显著降低大鼠血清的ALT和AST活性．肝脏组织结构病理损伤明显改善。结论 齐墩果酸钠盐对亚急性OCl4损伤的肝细胞具有保护作用。     

Augmenter of liver regeneration improves therapeutic effect of hepatocyte homotransplantation in acute liver failure rats

Hepatocyte transplantation (HCT) is an available option on treatment for acute liver failure (ALF). However, short-term survival of engraftment and immunological rejections of recipient are major obstacles. Augmenter of liver regeneration (ALR) has cytoprotective and immunoregulatory effects in liver injury, and has been used in many experimental applications. In the present study, we investigated the potential effect and mechanism of recombinant human ALR (rhALR) on ALF rats treated with intraperitoneal HCT. ALF rats induced by d-galactosamine (GalN) were studied in vivo, and were intraperitoneal injected with or without hepatocytes and rhALR 24 h after the induction. Animal survival, serum and ascites liver enzymes, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were assessed. Histological examination was performed, and liver regeneration, apoptosis and immunological responses were identified by immunohistochemistry assay. Our results showed that rhALR promoted hepatocytes regeneration, attenuated liver injury and suppressed immunological responses. The ascites liver enzyme, serum and ascites pro-inflammatory cytokines (TNF-α, IL-1β), liver histological injury, apoptotic hepatocytes and activated immunocytes were significantly reduced in ALF rats treated with rhALR and HCT compared with those without rhALR. The proliferative and mitotic hepatocytes were markedly increased, and overall survival improved with rhALR. The administration of rhALR improved survival and promoted liver recovery in HCT treatment for ALF, which was associated with the role of proliferative promoter and immunosuppressor. This study suggests that co-treated with rhALR and HCT can provide a promising strategy for the treatment of ALF.     

Protection against D-galactosamine-induced acute liver injury by oral administration of extracts from Lentinus edodes mycelia

The development of oral medications to help prevent liver injury is desirable, and some mushrooms contain chemicals that show promise as such a treatment. Here, we tested whether a hot-water extract (L.E.M.) of the cultured mycelia of an edible mushroom, Lentinus edodes, could protect primary cultured hepatocytes from D-galactosamine (GalN)-induced injury. GalN induced cell death in the hepatocytes, and this effect was completely suppressed by the addition of 0.5 mg/ml L.E.M. Polyphenolic compounds contained in the L.E.M. seemed to be responsible for the protective effect. We next examined the protective effect of L.E.M. in a GalN-induced liver injury model in rats. In rats that had been treated with L.E.M. given orally or intraperitoneally, GalN caused less leakage of aspartate aminotransferase and alanine aminotransferase, markers for liver injury, and a lower decrease in serum protein content, than in non-L.E.M.-treated rats. Histological analysis of the liver also showed a protective effect of L.E.M. Our findings indicate that L.E.M. administration is a promising treatment for protecting the liver from acute injury.     

桑黄发酵多糖胶囊急性毒性和遗传毒性研究

本文通过急性毒性试验、小鼠精子畸形试验和骨髓微核试验,研究桑黄发酵多糖胶囊的急性毒性和遗传毒性的影响。试验结果表明,小鼠对桑黄发酵多糖胶囊的最大耐受量大于20g/kg,与空白组相比,胶囊组小鼠的精子畸形率和骨髓细胞微核率无显著性差异。结果表明,桑黄发酵多糖胶囊属实际无毒物质,无遗传毒性。     

鲨鱼肝再生因子对大鼠慢性肝损伤的治疗作用

目的:探讨鲨鱼肝再生因子(sHRF)对大鼠慢性肝损伤的治疗作用。方法:CCl4致大鼠慢性肝损伤模型,给药后取血清及肝组织测定各项肝指标。结果:当用药8周时,对CCl4引起的肝损伤大鼠血清中AST、ALT活性的升高和羟脯氨酸含量的升高均有抑制作用,且0.8、1.6mg/kg剂量组的作用差异均有统计学意义。此外,sHRF能在一定程度上增加白蛋白含量,并使白蛋白/球蛋白比值有一定程度的升高。肝组织病理切片亦显示sHRF能减轻CCl4所致大鼠肝细胞脂肪变性及纤维组织增生。结论:sHRF对CCl4所致大鼠慢性肝损伤有一定的治疗作用。     

Comparison of the Prophylactic Effect of Silymarin and Deferoxamine on Iron Overload-Induced Hepatotoxicity in Rat

In pathologic conditions or poisoning states, iron overload can affect different tissues including liver. In this study, the prophylactic effect of deferoxamine and silymarin was compared in decreasing experimental iron-overload-induced hepatotoxicity in rats. The study was done in six groups of rats, which received drugs q2 days for 2 weeks. The rats in groups 1 to 6 received drugs, respectively: normal saline, iron dextran, iron dextran?+?deferoxamine (intraperitoneally), iron dextran?+?silymarin (orally), iron dextran?+?silymarin (intraperitoneally), and iron dextran?+?deferoxamine (intraperitoneally)?+?silymarin (intraperitoneally). At the end of the study, blood was collected, and serum was separated for laboratory tests. The liver of rats was separated for iron measuring and tissue processing. The serum iron concentration and the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity were determined. The numbers of necrotic hepatocytes were counted as quantity index tissue injury in light microscopic examination. The mean of serum and liver iron in group 2 was significantly greater than group 1. Liver iron was significantly decreased in other groups except group 4. Also serum iron was decreased in groups 3 to 6 compared to group 2 (nearly 400%). ALT activity in group 3 and AST activity in group 5 were significantly lesser than in other groups. The mean of necrotic hepatocytes in group 2 was significantly increased in comparison to group 1. This elevation was significantly prevented by deferoxamine and silymarin. The result of the present study shows that silymarin has a protective effect similar to deferoxamine on iron overload-induced hepatotoxicity.