The aim of this study is to evaluate the protective effect of Armillaria mellea polysaccharides (AMP) against ethanol-induced vascular endothelial cell injury in rats. Altogether 40 SD rats were randomly divided into 4 groups: normal control, injury, low- and high-dose AMP. The rats from all groups except the normal control group were gavaged with 40% ethanol at 10 mL/kg mb to induce endothelial cell injury. The rats in the low- and high-dose groups were gavaged with AMP at 100 and 400 mg/kg mb, respectively, while the remaining groups were given an equal volume of physiological saline. The administration period lasted for 4 weeks. The histopathological changes of carotid arteries were observed by hematoxylin-eosin (HE) staining. Serum triglycerides (TG), total cholesterol (T-CHO), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), nitric oxide (NO), endothelin 1 (ET-1), superoxide dismutase (SOD), and malondialdehyde (MDA) levels were detected. In addition, the effects of different doses (100 and 400 μg/mL) of AMP on the levels of reactive oxygen species (ROS), mitochondrial transmembrane potential, apoptosis, and the expression of apoptosis-associated proteins such as B cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax), and caspase-3 in human umbilical vein endothelial cell injured by 600 μmol/mL ethanol were investigated. Results: AMP attenuated ethanol-induced endothelial cell injury, decreased T-CHO, TG, LDL-C, iNOS, NO, ET-1, and MDA levels, and increased HDL-C and SOD activity. In vitro, AMP reduced cellular ROS levels, inhibited the ethanol-induced decrease in mitochondrial transmembrane potential and apoptosis, increased Bcl-2/Bax ratio and down-regulated the expression of cleaved caspase-3. Conclusion: AMP have a protective effect against ethanol-induced endothelial cell injury in rats, and the mechanism may be related to their lipid-lowering, antioxidant, and anti-apoptotic effects.

The protective effect of Lyophyllum ulmarium fibrinolytic enzyme（LUFE） on vascular endothelium injury in hyperlipidemic rats was investigated. The SD rats were randomly divided into normal control group, model group, positive control group, and LUFE group. The normal control group was fed with normal diet, while the rest groups were given high-fat diet, in which the LUFE group was simultaneously gavaged with LUFE(400 mg·kg -1 ·d -1 ). Positive control group started gavage of atorvastatin calcium tablets(5 mg·kg -1 ·d -1 ) at the 5 week of feeding. After 4 weeks and 8 weeks of rearing, the corresponding indexes were tested respectively. Hematoxylin-eosin staining was used to observe the pathological changes of aorta. Oil red O staining was used to observe the distribution of lipid plaques in aortic intima. The levels of plasma total cholesterol（TC）, triglyceride（TG） and low-density lipoprotein cholesterol（LDL-C）, high-density lipoprotein cholesterol（HDL-C）, catalase（CAT）,malondialdehyde（MDA）, superoxide dismutase 2（SOD2）, endothelin-1（ET-1） and 6-keta-PGF1α were measured and the atherogenic index was calculated. Nuclear factor erythroid 2-related factor（Nrf2）, silent information regulator 3（Sirt3）, acetyl-superoxide dismutase 2（Ac-SOD2）, and heme oxygenase 1（HO-1）of aorta were detected by Western blot. LUFE attenuated the pathological injury of aorta in hyperlipidemic rats, reduced the relative area of lipid plaque distribution in aortic intima, decreased the levels of TC, TG, LDL-C, ET-1 and MDA in plasma, and increased the levels of 6-keta-PGF1α, CAT and SOD2. The expression of Nrf2, HO-1 and Sirt3 protein in aortic tissue was up-regulated, and relative protein expression of Ac-SOD2 in aortic tissues was reduced. LUFE attenuated vascular endothelium injury induced by hyperlipidemia in rats, and the mechanism may be related to the reduction of blood lipid and oxidative stress injury.

Objective: To investigate the protective effect and mechanism of Lyophyllum ulmarium fibrinolytic enzyme（LUFE） on rats with hyperlipidemia. Methods: Hyperlipidemia models were established by feeding with a high-fat diet, and the model rats were gavaged with different doses of LUFE. HE stain was used to analyze the morphological changes of liver.The biochemical indexes of rat plasma were detected by colorimetric method.WB analyses the expression level of related proteins. Results: LUFE could alleviate the liver tissue injury of hyperlipidemia rats and reduce the plasma lipid level and IL-6, TNF-α,MCP-1,ALT,AST. LUFE can down regulate TLR4,MyD88,phosphorylated PI3K,phosphorylated Akt and phosphorylated NF-кB protein level. Conclusion: LUFE protects against hyperlipidemia-induced liver injury in rats by regulating PI3K/Akt/NF-кB and TLR4/MyD88/NF-кB signaling pathways.

血小板是血液中除红细胞、白细胞以外的第3种主要细胞，它没有细胞核，由骨髓巨核细胞脱落产生，在血管内以单个的形式循环，维持抗凝与促凝的平衡.血小板可填补血管壁受损时所造成的空隙，为血管壁的完整性提供保障 [1] ,亦具有黏附、聚集、释放等功能，在炎症反应过程中发挥着核心作用.血小板活化后会失去原有的圆盘状形态，呈现不规则形，通过直接或者间接的方式影响周围的细胞及其他血小板.

Objective: To investigate the protective effects of Armillaria mellea polysaccharides on lung injury induced by nicotine in rats. Methods: SD rats were randomly divided into control group, model group and Armillaria mellea polysaccharides low and high dose groups. During modeling, except for the normal group, the other groups were intraperitoneally injected with nicotine 2 mg/kg body weight, and the low and high dose groups were gavaged with Armillaria mellea polysaccharides 200 and 400 mg/kg body weight, respectively. The morphologic changes of lung tissue were observed by HE staining. The levels of TNF-α, IL-6 and IL-1β were detected by ELISA, MDA level was detected by TBA method, SOD activity was detected by WST-1 method. The protein expression levels of Nrf2, HO-1 and p-NF-κB in lung tissues were detected by Western blot assay. Results: Compared with the control group, after intervention of nicotine, the levels of TNF-α, IL-6, IL-1β and MDA were increased, the activity of SOD was decreased in plasma, the phosphorylation expression of NF-κB protein was increased, Nrf2 and HO-1 protein expression were decreased in lung tissue. Compared with the model group, after intervention of Armillaria mellea polysaccharides, the degree of lung tissue injury was alleviated, the levels of TNF-α, IL-6, IL-1β and MDA were significantly decreased, the activity of SOD was increased in plasma, the phosphorylation expression of NF-κB protein was significantly decreased, Nrf2 and HO-1 protein expression were significantly increased in lung tissue. Conclusion: Armillaria mellea polysaccharides can inhibit the lung tissue injury by nicotine induced. The mechanism of action may be related to its regulation of NF-κB and Nrf2/HO-1 signaling pathway.

目的:探讨榆干离褶伞溶栓酶(Lyophyllum ulmarium fibrinolytic enzyme,LUFE)在大鼠动脉血栓形成过程中对血管内膜损伤的保护作用.方法:将50只SD大鼠随机分为假手术组、模型组、阿司匹林组和LUFE低、高剂量组.建立血栓模型前,阿司匹林组和LUFE低、高剂量组分别以10mg/kg mb阿司匹林和100、400mg/kg mb LUFE灌胃7 d.次日,除假手术组以外其余4组以三氯化铁诱导建立大鼠颈动脉血栓模型.苏木精-伊红(hematoxylin-eosin,HE)染色观察颈动脉血管形态学变化;酶联免疫吸附法测定血清C反应蛋白(C-reactive protein,CRP)、白细胞介素(interleukin,IL)-6、IL-8、单核细胞趋化蛋白-1(monocyte chemoattractant protein-1,MCP-1)、细胞间黏附分子-1(intercellular cell adhesion molecule-1,ICAM-1)和血小板-内皮细胞黏附分子-1(platelet endothelial cell adhesion moleculer-1,PEC AM-1)水平;采用流式细胞仪测定血小板-白细胞聚集体(platelet-leukocyte aggregates,PLA)水平.在体外,经LUFE干预后观察血小板在固化胶原上的黏附作用;采用流式细胞仪测定胶原刺激后血小板Ca2+水平;Western blot方法观察血小板T细胞跨膜连接蛋白(linker for activation of T cells,LAT)和磷脂酶Cγ(phospholipase Cγ,PLCy)磷酸化水平.结果:LUFE干预后能明显减轻血管内膜的损伤,不同程度地降低血栓模型大鼠血清CPR、IL-6、IL-8、MCP-1、ICAM-1和PECAM-1水平,降低PLA水平.在体外,LUFE能降低血小板与胶原的黏附,并降低血小板Ca2+水平,下调血小板LAT和PLCγ蛋白的磷酸化水平.结论:LUFE抑制血栓形成过程中的血管炎症反应,这可能与其血管内皮细胞保护作用和抗血小板作用有关.

目的:研究榆干离褶伞溶栓酶(Lyophyllum ulmarium fibrinolytic enzyme,LUFE)对大鼠动脉血栓形成的抑制作用及其机制.方法:将SD大鼠随机分为假手术组、模型组、阳性对照组和LUFE低、高剂量组,除假手术组以外,其余4组均以三氯化铁建立颈动脉血栓模型.造模前阳性对照组和LUFE低、高剂量组分别以10 mg/kg mb阿司匹林以及100、400mg/kg mb LUFE灌胃7d.观察血栓质量和颈动脉血管组织病理变化;酶联免疫吸附测定法检测肿瘤坏死因子α(tumor necrosis factor alpha,TNF-α)、白细胞介素-6(interleukin-6,IL-6)、血小板活化因子(platelet-activating factor,PAF)、可溶性血栓调节蛋白(soluble thrombomodulin,sTM)、E-选择素和组织因子(tissue factor,TF)水平;流式细胞仪检测血小板CD62P表达水平.为观察LUFE对血小板功能的影响,在体外以胶原诱导血小板活化,观察LUFE对大鼠富血小板血浆中P-选择素、β-血小板球蛋白(β-thromboglobulin,β-TG)和血小板膜糖蛋白IIbIIIa(glycoprotein IIbIIIa,GPIIbIIIa)水平的影响;Western blot方法观察LUFE对大鼠血小板磷脂酰肌醇3激酶(phosphatidylinositol 3 kinase,PI3K)、蛋白激酶B(protein kinase B,Akt)和p38丝裂原活化蛋白激酶(p38 mitogen-activated protein kinase,p38 MAPK)表达水平的影响.结果:LUFE能明显减轻血栓质量和血管受损程度,抑制血栓模型大鼠血清sTM、E-选择素、TF、TNF-α、IL-6和PAF水平的上调,下调血小板CD62P的表达.同时,在体外LUFE能够下调胶原诱导的富血小板血浆中P-选择素、β-TG和GPIIbIIIa水平,下调血小板PI3K、Akt和p38MAPK蛋白的磷酸化水平.结论:LUFE具有抗血栓作用,其机制可能与LUFE对血管内皮细胞的保护作用以及对血小板活化的抑制作用有关.

目的:研究榆干离褶伞溶栓酶(Lyophyllum ulmarium fibrinolytic enzyme,LUFE)对酒精诱导大鼠肝损伤的保护作用.方法:将大鼠随机分为4组,即正常对照组,模型组,LUFE低、高剂量组.除正常对照组以外,其余各组每日按10 mL/kg mb灌胃体积分数40％的酒精诱导肝损伤.LUFE低、高剂量组分别以100、400 mg/kg mb的剂量灌胃LUFE,正常对照组和模型组以等量生理盐水灌胃,共28 d.末次给药后次日处死大鼠,苏木精-伊红染色观察大鼠肝组织病理形态学变化,检测血清丙氨酸氨基转移酶(alanine transaminase,ALT)、天冬氨酸氨基转移酶(aspartate aminotransferase,AST)、清蛋白(albumin,Alb)、γ-谷氨酰转移酶(γ-glutamyltranspeptidase,γ-GT)、碱性磷酸酶(alkaline phosphatase,ALP)、总胆红素(total bilirubin,T-BIL)、甘油三酯(triglyceride,TG)、总胆固醇(total cholesterol,T-CHO)、低密度脂蛋白胆固醇(low density lipoprotein cholesterol,LDL-C)和高密度脂蛋白胆固醇(high density lipoprotein cholesterol,HDL-C)水平.蛋白免疫印迹法检测抑制性-κBα(inhibitory kappa B-alpha,I-κBα)蛋白表达水平和核转录因子(nuclear factor,NF)-κB p65磷酸化(p-NF-κB)水平.结果:LUFE干预能减轻肝组织的病理性损伤,抑制酒精所致的血清AST、ALT、γ-GT、ALP活力及TG、T-CHO、LDL-C、T-BIL水平的升高和Alb水平的降低,其中高剂量LUFE能达到显著抑制效果(P<0.05,P<0.01).Western blot结果表明,与模型组相比,LUFE干预能提高I-κBα蛋白表达水平,抑制NF-κB p65蛋白的磷酸化,其中高剂量LUFE能达到显著改善效果(P<0.05,P<0.01).结论:LUFE对酒精所致大鼠肝损伤有保护作用,其机制可能与其抗氧化、抗炎作用有关.

目的:探讨榆干离褶伞溶栓酶对脂多糖(lipopolysaccharide,LPS)诱导的血管内皮细胞炎性损伤的保护作用.方法:以LPS诱导人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVEC)炎性损伤.将HUVEC分为空白对照组、模型组和榆干离褶伞溶栓酶(Lyophyllum ulmarium fibrinolytic enzyme,LUFE)低、中、高剂量组.采用噻唑蓝法测定HUVEC存活率,通过酶联免疫吸附测试法检测细胞上清液乳酸脱氢酶(lactate dehydrogenase,LDH)、肿瘤坏死因子α(tumor necrosis factor α,TNF-α)、白介素6(interleukin 6,IL-6)、E-选择素和单核细胞趋化因子1(monocyte chemoattractant protein 1,MCP-1)水平.流式细胞术检测细胞间黏附分子1 (intercellular cell adhesion molecule 1,ICAM-1)表达水平,采用Hoechst染色法观察HUVEC与人急性单核细胞白血病细胞系(human acute monocytic leukemia cell line-1,THP-1)的黏附作用.用蛋白印迹实验检测HUVEC的Toll样受体4(toll-like receptor 4,TLR4)、丝裂原活化蛋白激酶(mitogen-activated protein kinase,MAPK)以及核因子-KB (nuclear factor κB,NF-κB)通路中主要蛋白(髓样分化因子88(myeloid differentiation factor 88,MyD88)、转化生长因子β激活激酶1(transforming growth factor β activated kinase 1,TAK1)、磷酸化TAK1(phosphorylated TAK1,p-TAK1))的表达和活化情况.结果:LUFE能够抑制LPS所诱导的HUVEC培养上清液LDH、TNF-α、IL-6、E-选择素和MCP-1水平的升高,降低细胞ICAM-1表达水平并减弱HUVEC与THP-1的黏附作用.与模型组比较,LUFE各剂量组TLR4、MyD88、p-TAK1/TAK1、磷酸化c-Jun氨基末端激酶(phosphorylated c-Jun N-terminal kinase,p-JNK) /JNK、p-p38/p38、p-NF-κB/NF-κB水平显著降低(P＜0.05).结论:LUFE对血管内皮细胞的炎性损伤具有保护作用,其作用机制可能是通过抑制TLR4/MyD88/TAK1/NF-κB信号通路及MAPK通路,进而降低炎症因子水平,从而保护血管内皮细胞.

目的:研究榆干离褶伞溶栓酶(fibrinolytic enzyme from Lyophyllum ulmarium,LUFE)对酒精所致人脐静脉内皮细胞(human umbilical vein endothelial cells,HUVECs)损伤的保护作用及其机制.方法:以酒精诱导HUVECs损伤,四甲基偶氮唑蓝法检测细胞活力,检测细胞培养上清液乳酸脱氢酶(lactate dehydrogenase,LDH)活力;比色法检测细胞超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)活力和丙二醛(malondialdehyde,MDA)含量;吖啶橙-溴化乙啶双染法观察细胞凋亡;用荧光染料双氢罗丹明123和罗丹明123分别检测细胞总活性氧(reactive oxygen species,ROS)水平和线粒体跨膜电位;蛋白印迹法检测Bax、Bcl-2、细胞色素c、cleaved半胱氨酸天冬氨酸蛋白水解酶(cysteinyl aspartate specific proteinase,cleaved caspase)-9和cleaved caspase-3的表达水平.结果:LUFE能够提高内皮细胞存活率,降低LDH和MDA水平,提高SOD、GSH-Px活力,减少ROS的生成,并抑制酒精所致的线粒体跨膜电位的下降和细胞凋亡.Western blot结果表明,LUFE提高Bcl-2蛋白表达水平,并减少细胞色素c、cleaved caspase-9和cleaved caspase-3的表达.结论:LUFE对酒精所致血管内皮细胞的损伤有保护作用,其机制可能与其抗氧化、抑制酒精诱导的线粒体途径细胞凋亡有关.

文章以吉林省大学生生物实验技能竞赛为背景,介绍竞赛对学生和指导教师所带来的启示,以充分体现该赛事"以赛促教"的宗旨.

The present study was carried out to investigate the hypoglycemic effect of soy isoflavones from hypocotyl in GK diabetic rats. A single administration and long-term administration tests were conducted in GK diabetic rats to test the hypoglycemic effect of soy isoflavones. At the end of long-term administration trial, blood protein, cholesterol, triglyceride, glycosylated serum protein, C-reactive protein, insulin, aminotransferase, lipid peroxide, interleukin-6, tumor necrosis factor-α were estimated. Inhibition of soy isoflavones against α-amylase and α-glucosidase, as well as on glucose uptake into brush border membrane vesicles or Caco-2 cells were determined in vitro. In single administration experiment, soy isoflavones reduced postprandial blood glucose levels in GK rats. In long-term administration, hypoglycemic effect of soy isoflavones was first observed at week 12 and maintained till week 16. A significant reduction in fasting blood glucose, C-reactive protein, and lipid peroxide was noted at week 16. However, there was no significant treatment effect on blood insulin. Furthermore, soy isoflavone administration resulted in significant decreases in glycosylated serum protein, tumor necrosis factor-α, and interleukin-6. Other biochemical parameters, such as protein, cholesterol, triglyceride and aminotransferases were not modified, however. The results in vitro showed that soy isoflavones showed a potent inhibitory effect on intestinal α-glucosidase, but not on pancreatic α-amylase. Soy isoflavones also decreased glucose transport potency into brush border membrane vesicles or Caco-2 cells. It is concluded that soy isoflavones from hypocotyl, performs hypoglycemic function in GK rats with type 2 diabetes, maybe via suppression of carbohydrate digestion and glucose uptake in small intestine.

[目的]探讨蜜环菌多糖对动脉血栓大鼠炎症反应和细胞凋亡的影响.[方法]蜜环菌多糖低、中、高剂量组分别给予100,200,400 mg/kg蜜环菌多糖,每日1次,连续7d.给予蜜环菌多糖各剂量组及模型对照组三氯化铁诱导大鼠颈动脉血栓模型,假手术组用生理盐水代替三氯化铁.利用流武细胞仪检测血小板膜糖蛋白CD62P水平,采用ELISA法测定组织因子(TF)、C反应蛋白(CRP)、白细胞介素(IL)-6和IL-8含量,Western印记法检测脑组织Caspase-8和Caspase-3蛋白的表达水平,测定超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、谷胱甘肽(GSH)和丙二醛(MDA)水平.[结果]与模型对照组比较,蜜环菌多糖中、高剂量组血小板膜糖蛋白CD62P阳性表达率明显降低(P＜0.05),血清TF,CRP,IL-6,IL-8和脑组织中MDA水平均明显降低(P＜0.01),脑组织中Caspase-8和Caspase-3蛋白表达明显减少(P＜0.05,P＜0.01),SOD,GSH-Px和GSH水平明显升高(P＜0.05,P＜0.01).[结论]蜜环菌多糖具有抗炎、抑制血小板活化及抑制细胞凋亡的作用,其机制认为可能与蜜环菌多糖的抗血栓作用有关系.

本实验研究榆干离褶伞溶栓酶(Lyophyllum ulmarium fibrinolytic enzyme,LUFE)对脂多糖(LPS)诱导的大鼠肝损伤的保护作用,并初步探讨其作用机制.将大鼠随机分为五组,分别为对照组、模型组、阳性对照组、LUFE低剂量组、LUFE高剂量组.LUFE分别以200、400 mg/kg体质量灌胃2周.除对照组以外其余四组均以腹腔注射LPS诱导大鼠肝脏炎性损伤模型.阳性对照组在造模前腹腔注射地塞米松(5 mg/kg).苏木精-伊红(HE)染色观察肝组织病理改变;检测血清肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)、白介素-1β(IL-lβ)、丙氨酸氨基转移酶(ALT)、白蛋白(ALB)和天冬氨酸氨基转移酶(AST)的水平;Western bolt方法观察肝组织Toll样受体4(Toll like receptor4,TLR4)、p-TAK1和p-NF-κB p65蛋白水平.实验结果表明,LUFE可缓解LPS诱导的肝组织的炎性损伤,降低血清TNF-α、IL-6、IL-1β含量和AST、ALT活性,提高ALB水平.Western bolt结果显示,LUFE下调TLR4、p-TAK1、p-NF-κBp65蛋白水平.以上结果表明LUFE抑制肝脏炎性损伤,其机制可能与其下调TLR4-NF-κB通路相关蛋白的表达有关.

[目的]探讨榛蘑多糖对颈动脉血栓模型大鼠血管的保护作用.[方法]取SD大鼠随机分为正常对照组、模型对照组、阳性对照组和榛蘑多糖小、中、大剂量(1,2,4 mg/kg)组.阳性对照组和榛蘑多糖小、中、大剂量组分别利用阿司匹林和不同剂量榛蘑多糖预处理7d,之后利用三氯化铁诱导建立大鼠颈动脉血栓模型.利用光学显微镜观察颈动脉血管组织病理变化,采用酶联免疫吸附方法测定血管性血友病因子(vWF)、p-选择素、血小板膜糖蛋白Ⅱb/Ⅲa(GPⅡb/Ⅲa)、可溶性血栓调节蛋白(sTM)和D-二聚体的含量,同时测定超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、谷胱甘肽(GSH)和丙二醛(MDA)水平.[结果]榛蘑多糖大剂量组血管受损程度明显减轻,血管内膜结构完整,血栓溶解,未见有炎性细胞浸润.榛蘑多糖可明显减少vWF、p-选择素、GPⅡb/Ⅲa,sTM、D-二聚体和MDA水平(P＜0.05,P＜0.01),提高SOD,GSH-Px和GSH水平(P＜0.05,P＜0.01).[结论]榛蘑多糖通过抗氧化作用保护动脉血栓模型大鼠血管内皮细胞.

目的 探讨榆干离褶伞溶栓酶对肾上腺素致血管内皮细胞损伤的保护作用.方法 采用注射肾上腺素结合冰浴的方法制备大鼠血管内皮细胞损伤模型,检测血液循环内皮细胞数(CEC)和血浆血栓素B2 (TXB2)、6-酮-前列腺素E1α(6-keto-PGE1α)、组织纤溶酶原激活物(t-PA)以及抗凝酶Ⅲ(AT-Ⅲ)的含量.结果 模型组的CEC和TXB2水平较正常组明显增高,且t-PA和AT-Ⅲ含量下降.用药组可减少CEC和TXB2水平,提高6-keto-PGE1α、t-PA和AT-Ⅲ含量.结论 榆干离褶伞溶栓酶对血管内皮细胞起保护作用.

[目的]探讨金针菇发酵液对血瘀模型大鼠血管内皮细胞及血小板功能的影响.[方法]采用肾上腺素结合冰浴的方法制作大鼠血瘀模型,灌胃给予金针菇发酵液后观察血管组织形态学改变.采用流式细胞仪检测血小板膜糖蛋白CD62p水平,利用ELISA法测定血浆p-选择素、6-酮-前列腺素E1α (6-keto-PGE1α)、血栓素B2 (TXB2)和血管紧张素Ⅱ(AngⅡ)水平,采用硝酸还原酶法检测血浆一氧化氮含量.[结果]与模型对照组比较,金针菇发酵液低、高剂量组血管组织结构规整,内膜连续,未见炎性细胞浸润;金针菇发酵液高剂量组6-keto-PGE1α水平明显升高,而血小板膜糖蛋白CD62p、血浆p-选择素、TXB2和AngⅡ水平均明显下降(P＜0.05,P＜0.01).[结论]金针菇发酵液具有保护血管内皮细胞及抗血小板活化的作用.

目的:研究榆干离褶伞(Lyophyllum ulmarium,Lu)溶栓酶的抗血栓作用及对血小板活性的影响.方法:三氯化铁诱导大鼠颈动脉血栓模型,检测血栓重量,用流式细胞仪检测CD62P的表达,酶联免疫吸附法测定p-选择素、血管性血友病因子(vWF)、血小板膜糖蛋白Ⅱb/Ⅲa、血栓素B2(TXB2)和6-酮-前列腺素E1α(6-keto-PGE1α)的水平.结果:与模型组相比,Lu溶栓酶处理以后大鼠血栓重量明显减轻,CD62P阳性率、p-选择素、vWF、血小板膜糖蛋白Ⅱb/Ⅲa以及TXB2的含量不同程度地下降,对6-keto-PGE1α的影响不显著.结论:L.u溶栓酶具有抗血栓作用,其机制可能与抑制血小板的活化作用有关.

To study the effect of Flammulina Velutipes fermentation broth on arterial thrombosis in rats and its mechanisms. Animal model was induced by ferric chloride in rats, then the thrombus weight was detected, the morphological changes of vascular tissue were observed, and the levels of 6-keto-PGE1α, TXB2, ET-1, t-PA, PAI-1 and NO in plasma were measured. As compared with the model group, the thrombus weight reduced, the intravascular thrombosis dissolved to some extent, and vascular intimal damage reduced in Flammulina Velutipes fermentation broth group. Flammulina Velutipes fermentation broth increased the levels of NO , 6-keto-PGE1αand t-PA, reduced PAI-1 and TXB2 content. However, there was no significant difference in the ET-1 level. Flammulina Velutipes fermentation broth has the thrombolytic function. The effects may be due to its protective effect on vascular endothelial.

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