川芎嗪抗剪切应力诱导血小板聚集的实验研究

目的：观测川芎嗪对剪切应力诱导血小板聚集（ＳＩＰＡ）的影响。方法：采用新研制的激光散射剪切装置观测川芎嗪及对照药Ａｓｐｉｒｉｎ在体内外对抗ＳＩＰＡ的作用。结果与结论：Ａｓｐｉｒｉｎ能抑制ＡＤＰ诱导的血小板聚集，但不能抑制ＳＩＰＡ。川芎嗪在体内（２５～５０ｍｇ·ｋｇ－１）体外（９．２～７３．４ｍｍｏｌ·Ｌ－１）均有显著抗ＳＩＰＡ作用（Ｐ＜０．０１），其机制待进一步研究。     

川芎嗪联用左旋精氨酸对缺血-再灌注损伤兔肝脏能量代谢的影响

目的:探讨川芎嗪(LGT)、左旋精氨酸(L-Arg)联合使用对肝缺血-再灌注损伤(HIRI)时肝细胞能量代谢的影响及其机制。方法:实验兔40只,建立肝缺血-再灌注模型后随机分4组:模型组,LGT组,L-Arg组和LGT+L-Arg组,每组10只。再灌注45 min时,分别检测肝组织内三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、一磷酸腺苷(AMP)含量、总腺苷酸量(TAN)、能荷(EC)、丙二醛浓度(MDA)、超氧化物歧化酶活性(SOD)、一氧化氮代谢产物(NO2-／NO3-)水平、血栓素B2(TXB2)、6-酮基-前列腺素F1α(6-keto-PGF1α)含量和TXB2／6-keto-PGF1α比值。结果:与模型组比较,LGT组、L-Arg组、LGT+L-Arg组肝组织内ATP、EC、NO2-／NO3-、6-keto-PGF1α含量及SOD活性均明显增高(P<0.05和P<0.01),MDA、TXB2含量及TXB2／6-keto-PGF1α比值均显著减少(P<0.05和P<0.01)。结论:LGT联用L-Arg可通过降低体内氧自由基水平、提高一氧化氮水平、纠正TXA2与PGI2的平衡,而改善缺血-再灌注损伤肝脏的能量代谢。     

川芎嗪注射液对正常家兔体感诱发电位的影响

目的　探讨川芎嗪注射液对正常家兔脑神经功能的影响。方法　动态观测了静脉注射川芎嗪注射液后 ,正常家兔不同时点的后肢体感诱发电位变化。结果　注射 2 0 %川芎嗪后除 1 2 0min外各个时点的体感诱发电位P波潜伏期均明显延迟 ,其中在 1 5min延迟最明显 ,分别与用药前比较 ,均有显著性差异 (P均 <0 .0 5～ 0 .0 1 )。而使用川芎嗪注射液后的各个时点的体感诱发电位P波波幅无明显变化 ,但与用药前比较均显著降低 (P均 <0 .0 5～ 0 .0 1 )。结论　川芎嗪注射液对正常家兔的脑神经功能有明显的抑制作用。     

An experimental and clinical study on TXA_2 and PGI_2 content after head injury

The correlation of secondary brain injury with thromboxane A_2(TXA_2) and prostacy-clin (PGI_2) levels following head injury was studied in rats and patients.Thromboxane B_2(TXB_2) and 6-keto-PGF_(1α) in rat brain homogenate and TXB_2 in cerebral spinal fluid (CSF) ofpatients with severe head injury were determined by RIA.The effects of ligustrazini hydrochlo-rioi were also tested.The results showed that the concentration of TXB_2 and 6-keto-PGF_(1α) inrat brain was progressively increased within 3h after injury (P<0.01),and the ratio betweenTXB_2 and 6-keto-PGF_(1α)(T/K value) increased during the early stage after injury,along withthe tissue damage aggravation.After the use of ligustrazini hydrochlorioi,TXB_2 content inbrain decreased sharply accompanied with a drop in T/K value.Moreover,TXB_2 content inCSF increased within 7 d after injury (P<0.01),and it reached its peak value on the 3rd day.This could indicate that the metabolic imbalance between TXA_2 and PGI_2 might be one of theimportant factors in the development of secondary brain injury,and ligustrazini hydrochlorioiproved to have a protective effect on the brain tissue by normalizing the metabolism of TXA_2and PGI_2.In addition,the metabolic disorders of TXA_2 in the brain tissue of head injured pa-tients have much to do with the outcome of the patients.     

川芎嗪对缺血-再灌注损伤兔心肌线粒体结构及功能的影响

为了探讨川芎嗪对心肌缺血一再灌注损伤(MIRI)时心肌细胞线粒体功能及结构的影响。本实验选用日本大耳白兔30只,随机分为正常对照组(A组)、心肌缺血一再灌注损伤组(B组)和心肌缺血-再灌注损伤 川芎嗪治疗组(C组)。复制MIRI模型,分别观察心肌线粒体呼吸功能、Ca^2 浓度([Ca^2 ]m)、丙二醛浓度(MDA)、超氧化物歧化酶活性(SOD)及超微结构的改变和心肌组织三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、一磷酸腺苷(AMP)含量、总腺苷酸量(TAN)、能荷(EC)的变化。结果发现,C组与B组比较,线粒体呼吸控制率(RCR)、Ⅲ态呼吸速率(ST3)、SOD、面密度(Sv)、比表面(δ)明显升高,Ⅳ态呼吸速率(ST4)、[Ca^2 ]m、MDA、体密度(Vv)、横径(Hd)显著降低,心肌组织ATP、ADP、TNA及EC均明显增高;且与A组比较,ST3、ST4、SOD、Vv、Sv、δ、数密度(Nv)、纵径(Vd)及ADP、AMP、TNA无明显差异。可见,川芎嗪可通过降低氧自由基水平和减轻钙超载,而改善缺血一再灌注损伤心肌的线粒体功能及结构。     

川芎嗪联用异丙酚对实验性缺血一再灌注损伤肝脏能量代谢的干预

目的 探讨川芎嗪（LGT）、异丙酚（PRO）联合使用对肝缺血-再灌注损伤（HIRI）时肝细胞能量代谢的影响及其机制。方法 实验兔40只，随机分为肝缺血-再灌注组（A组）和肝缺血-再灌注＋LGT治疗组（B组）、肝缺血-再灌注＋PRO治疗组（C组）和肝缺血-再灌注＋LGT＋PRO治疗组（D组）。在再灌注45min时，分别检测肝组织内三磷酸腺苷（ATP）、二磷酸腺苷（ADP）、一磷酸腺苷（AMP）含量及总腺苷酸量（TAN）、能荷（EC）、丙二醛浓度（MDA）、超氧化物歧化酶活性（SOD）、一氧化氮代谢产物（NO2^-／NO3^-）水平。结果 与A组比较，B、C、D组肝组织内ATP、EC、NO2^-/NO3^-及SOD活性均明显增高（P〈0．05和P〈0．01），MDA含量显著减少（P〈0．01）。结论 LGT联用PRO可通过降低体内氧自由基水平、提高一氧化氮（NO）水平，而改善缺血-再灌注损伤肝脏的能量代谢。     

川芎嗪预处理对体外培养乳鼠心肌细胞低氧再给氧损伤的保护作用

用体外培养乳鼠心肌细胞观察了川芎嗪预处理对低氧／再给氧损伤的保护作用。结果表明：川芎嗪20μg/ml能明显提高低氧3小时／再给氧0、30、60、120分钟时细胞搏动和细胞生存率,使乳酸脱氢酶（LDH）、丙二醇（MDA）释放减少,超氧化物歧化酶（SOD）释放增多。这种保护作用与低氧预处理（HP）产生的结果一致。上述结果表明川芎嗪预处理对体外培养乳鼠心肌细胞低氧／再给氧所致损伤具有保护作用,其机制可能与提高心肌细胞抗氧化酶活性,清除氧自由基有关。     

川芎嗪对肝缺血—再灌注损伤家兔血浆TXA2／PGI2水平的影响

目的:探讨川芎嗪对肝缺血-再灌注损伤家兔血浆TXA_2/PGI_2水平的影响.方法:制作家兔肝缺血-再注损伤模型,30只家兔平均分为川芎组、盐水组和对照组,应用放免法测定血浆TXB_z,6-酮基-PGF_(1(?))及其比值.结果:家兔肝缺血45min及再灌注45min血浆TXB_2.水平明显上升,6-酮基-PGF_(1(?))水平缺血45min时无明显变化,再灌注45min时显著下降,TXB_2/6-酮基-PGF_(1(?))水平增加;应用川芎嗪治疗能降低TXB_2水平,升高6-酮基-PGF_(1(?))水平,使TXB_2/6-酮基-PGF_(1(?))比值保持在正常水平.结论:川芎嗪可纠正肝缺血-再灌注后循环血中TXA_2/PGI_2的平衡失调,对肝缺血-再灌注损伤具有积极的防治作用.     

Mechanism of ligustrazini against thrombosis

Objective To investigate the mechanism of Chinese medicine ligustrazini against thrombosis, and the effects of ligustrazini on plasminogen activator inhibitor (PAI-1) expression in normal endothelial cells and lipopolysaccharide (LPS) stimulated endothelial cells. Methods Human umbilical vein endothelial cells (HUVECs) were cultured by trypsin digestion method. PAI-1 protein in HUVEC conditioned medium was measured by Sandwich enzyme-linked immunosorbent assay (ELISA), and PAI-1 mRNA expression was determined by Northern blot analysis. Using electrophoretic mobility shift assay (EMSA), we observed HUVEC nuclear factor-kappa B (NF-κB) nuclear translocation. Results LPS treatment of cultured HUVECs resulted in a significant increase in PAI-1 protein and mRNA expression by these cells. However, when HUVECs were incubated with LPS plus ligustrazini, the upregulation of PAI-1 by LPS was abated. Moreover, ligustrazini could decrease the basal level of PAI-1 protein and mRNA in HUVECs as compared with control. Nuclear extracts prepared from HUVECs stimulated by LPS demonstrated that binding to the NF-kB oligo nucleotide increased as compared with the unstimulated cells, but ligustrazini did not change those binding in the absence or presence of LPS. Conclusions Ligustrazini inhibited both basal and LPS-induced PAI-1 protein and mRNA expression in endothelial cells, and the modulation of PAI-1 in HUVECs by ligustrazini might have other mechanisms rather than NF-kB