生脉注射液对大鼠实验性心肌缺血的保护作用

在大鼠冠脉结扎急性心肌梗死（AMI）模型，生脉注射液5、10ml/kg可明显缩小心肌梗死面积，降低血清CK及LDH活性；在大鼠垂体后叶素诱发急性心肌缺血模型，生脉注射液5、10ml/kg可明显减轻缺血心电图改变，证实生脉注射液具有抗急性心肌缺血作用。     

碟脉灵注射液对急性血瘀模型大鼠血液流变学的影响

采用大鼠皮下注射0.1%肾上腺素加冰水中浸泡5min复制急性血瘀模型,观察碟脉灵注射液对急性血瘀模型大鼠血液流变学的影响。结果表明,碟脉灵注射液2.5、5、10ml/kg可使急性血瘀模型大鼠全血黏度、血浆黏度、血浆纤维蛋白原浓度、血沉、红细胞压积、红细胞电泳时间、红细胞聚集指数及红细胞刚性指数均明显降低。提示其对急性血瘀模型大鼠血液流变学的异常变化有明显改善作用,这有利于防止急性心肌梗死及脑梗死时的高黏状态,预防血栓形成。     

碟脉灵注射液对大鼠实验性心肌缺血的影响

碟脉灵注射液5、10、20g/kg给大鼠舌下iv2次,对脑垂体后叶素引起的大鼠心电图T波和S-T段抬高有明显的拮抗作用,亦能显著缩小冠脉结扎大鼠的心肌梗塞面积,降低血清肌酸激酶(CK)和乳酸脱氢酶(LDH)活性。提示碟脉灵注射液对实验性心肌缺血具有明显的保护作用。     

复方刺五加注射液对大鼠实验性心肌缺血的保护作用

通过异丙肾上腺素及垂体后叶素诱发大鼠急性心肌缺血模型,观察复方刺五加注射液对实验性心肌缺血的保护作用。结果表明,复方刺五加注射液25、50、100mg/kg对皮下注射异丙肾上腺素缩短小鼠在常压缺氧状态下的存活时间均具有明显对抗作用;复方刺五加注射液20、40、80mg/kg可明显减轻静脉注射垂体后叶素诱发的大鼠急性心肌缺血心电图(ST段抬高及T波高耸)变化程度,表明复方刺五加注射液对大鼠实验性心肌缺血具有明显保护作用。     

测定人参水分、总灰分、酸不溶性灰分含量的不确定度评估

通过异丙肾上腺素及垂体后叶素诱发大鼠急性心肌缺血模型,观察复方刺五加注射液对实验性心肌缺血的保护作用。结果表明,复方刺五加注射液25、50、100mg/kg对皮下注射异丙肾上腺素缩短小鼠在常压缺氧状态下的存活时间均具有明显对抗作用;复方刺五加注射液20、40、80mg/kg可明显减轻静脉注射垂体后叶素诱发的大鼠急性心肌缺血心电图(ST段抬高及T波高耸)变化程度,表明复方刺五加注射液对大鼠实验性心肌缺血具有明显保护作用。     

人参皂苷Rb3及Rb2组合物对大鼠实验性心肌梗死的保护作用

目的研究人参皂苷Rb,及Rb,组合物对大鼠急性心肌梗死的保护作用。方法采用大鼠结扎左冠状动脉前降支制备急性心肌梗死模型,计算急性心肌梗死24h后的心肌梗死面积（MIS）,测定血清肌酸磷酸激酶（CK）、乳酸脱氢酶（LDH）、天门冬氨酸氨基转换酶（AST）、超氧物歧化酶（SOD）及谷胱甘肽过氧化物酶（GSH—Px）活力,丙二醛（MAD）及一氧化氮（NO）含量。结果人参皂苷Rb,及Rb：组合物5、10、20mg／kg均可明显缩小急性心肌梗死大鼠的MIS,降低血清CK、LDH、AST活性及MAD含量,提高血清SOD、GSH—Px活性及NO含量。结论人参皂苷Rb,及Rb：组合物对大鼠急性心肌梗死具有明显保护作用,可能与其增强抗氧化酶活性,减少氧自由基对心肌的损伤等机制有关。     

人参果皂苷对实验性心肌缺血的保护作用

通过异丙肾上腺素及垂体后叶素诱发急性心肌缺血模型，观察人参果皂苷(GFS)对实验性心肌缺血的保护作用。结果表明，GFS30、60mg／kg对皮下注射异丙肾上腺素缩短小鼠的常压缺氧状态下的存活时间均具有明显对抗作用，20、40mg／kg均可明显减轻静脉注射垂体后叶素诱发的大鼠急性心肌缺血心电图(ST段抬高及T波高耸)变化程序，表明GFS对实验性心肌缺血具有明显的保护作用。     

山灵参胶囊对大鼠实验性高脂血症的保护作用

目的观察山灵参胶囊对大鼠实验性高脂血症的保护作用。方法雄性Wistar大鼠60只,取10只作为正常组,其余大鼠喂养高脂饲料6周建立实验性高脂血症模型。造模组按体重随机分为模型组,山灵参胶囊250、500、1000 mg/kg组和阳性药辛伐他汀片30 mg/kg组,各组分别灌胃给药,正常组及模型组给予同体积0.5%的羧甲基纤维素钠。给药30天后,各组大鼠水合氯醛麻醉,腹主动脉取血,检测血清TC、TG、LDL-c、HDL-c、FFA、MDA含量及SOD活性;取肝脏制备匀浆,检测肝组织TC、TG、MDA含量及SOD活性。结果与正常组比较,模型组大鼠血清中TC、TG、LDL-c、FFA及MDA含量均明显升高,肝组织TC、TG及MDA含量亦明显升高,SOD活性降低(P0.05或P0.01)。与模型组比较,山灵参胶囊500、1000 mg/kg剂量组能明显降低大鼠血清TC、TG、LDL-c、FFA及MDA含量,升高SOD活性,并能明显降低大鼠肝组织TC、TG及MDA含量,升高SOD活性(P0.05或P0.01)。结论山灵参胶囊对大鼠实验性高脂血症具有明显保护作用,可能通过减轻肝细胞脂质过氧化损伤,增强机体清除氧自由基能力实现的。     

西洋参总皂苷对心肌缺血再灌注损伤大鼠血液流变学的影响

目的探究西洋参总皂苷(AGS)对心肌缺血再灌注损伤大鼠血液流变学的影响;方法正常雌性Wistar大鼠50只随机分为5组,分别为假手术组、模型组、AGS 25 mg/kg剂量组、AGS 50 mg/kg剂量组、AGS100 mg/kg剂量组。各组大鼠连续灌胃7 d后进行缺血再灌注损伤处理,缺血30 min再灌120 min,观察血液流变学相关指标变化。结果与假手术组比较,模型组大鼠血小板粘附率、血小板聚集率及最大聚集率、全血粘度和血浆粘度均显著升高(P0.01);与模型组比较,给药组大鼠血小板粘附率、血小板聚集率及最大聚集率、全血粘度和血浆粘度均均明显降低(P0.05或P0.01)。结论 AGS可显著改善心肌缺血再灌注后的血液流变性,改善大鼠血液循环,对大鼠心肌缺血再灌注损伤具有明显保护作用。     

人参皂苷Rb3对大鼠实验性脑缺血的保护作用

目的观察人参皂苷Rb3对大鼠实验性脑缺血的保护作用。方法建立大鼠结扎双侧颈总动脉伴低血压建立急性不完全性脑缺血模型．计算脑指数及脑含水量,测定血清超氧化物歧化酶（SOD）、一氧化氮合酶（NOS）活力及血清丙二醛（MDA）、一氧化氮（NO）含量,同时测定脑组织SOD、钠-钾-ATP酶（Na^＋-K^＋-ATPase）、钙-镁-ATP酶（Ca^2＋-Mg^2＋-ATPase）活力及MDA含量。结果人参皂苷Rb14、28mg／kg可明显降低脑指数及脑含水量,亦能降低血清和脑组织MDA、NO含量及NOS活性,提高SOD、Na^＋-K^＋-ATPa8e和Ca^2＋-Mg^2＋-ATPase活力。结论人参皂苷Rb3对大鼠实验性脑缺血具有明显保护作用,可能通过抑制脂质过氧化反应,提高抗氧化酶活性,改善细胞能量代谢等环节实现的。     

振源胶囊对急性心肌梗死犬心肌氧代谢的影响

目的研究振源胶囊对急性心肌梗死犬心肌氧代谢的影响。方法采用犬结扎左冠状动脉前降支6小时造成急性心肌梗死模型,同时十二指肠给药进行治疗,以CORNIHG 178型血气分析仪测定动、静脉血氧含量,观察心肌氧代谢变化。结果振源胶囊10、20mg/kg可使急性心肌梗死6小时犬心肌氧利用率及心肌耗氧量明显降低(P<0.05或P<0.01),对心肌耗氧指数无明显影响(P>0.05)。结论振源胶囊可通过降低心肌耗氧及降低心肌氧利用率发挥抗急性心肌缺血作用。     

五杞胶囊对大鼠实验性肝纤维化的保护作用

目的观察五杞胶囊对大鼠实验性肝纤维化的保护作用。方法 Wistar大鼠随机分为对照组、模型组、阳性药物组及五杞胶囊2、4、8g生药/kg组。皮下注射CCL4花生油溶液10周建立大鼠实验性肝纤维化模型,五杞胶囊给药4周后观察大鼠肝脏系数,测定血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、胆碱酯酶(CHE)活力及白蛋白(ALB)、球蛋白(GLO)、总蛋白(TP)含量,肝组织超氧化物歧化酶(SOD)活性及丙二醛(MDA)、羟脯氨酸(Hyp)含量。结果五杞胶囊能明显降低大鼠肝脏系数,升高大鼠血清ALB含量及A/G比值,降低血清AST、ALT、CHE活力及GLO含量,减少肝组织Hyp、MDA含量,升高SOD活性。结论五杞胶囊通过减轻肝细胞脂质过氧化损伤改善肝功能,纠正肝纤维化引起的白蛋白降低。     

参龟保肝升白蛋白丸对实验性肝纤维化大鼠血液生化学的影响

目的建立大鼠实验性肝纤维化模型,观察参龟保肝升白蛋白丸对血液生化学的影响。方法将Wistar大鼠随机分为对照组、模型组、阳性药物组及参龟保肝升白蛋白丸0.5、1.0和2.0g/kg组。皮下注射CCL4花生油溶液10周建立大鼠实验性肝纤维化模型,参龟保肝升白蛋白丸治疗4周后测定血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、胆碱酯酶(CHE)活力及白蛋白(ALB)、球蛋白(GLO)、总蛋白(TP)含量,肝组织超氧化物歧化酶(SOD)及谷胱甘肽-S转移酶(GSH-ST)活性和丙二醛(MDA)、羟脯氨酸(Hyp)含量。结果参龟保肝升白蛋白丸能明显升高大鼠血清ALB含量及A/G比值,降低血清AST、ALT、CHE活力及GLO含量,减少肝组织Hyp、MDA含量,升高SOD及GSH-ST活性。结论参龟保肝升白蛋白丸可改善肝功能,纠正肝纤维化引起的白蛋白低下,减轻肝细胞脂质过氧化损伤。     

Beneficial Effect of S-allylcysteine (SAC) on Blood Glucose and Pancreatic Antioxidant System in Streptozotocin Diabetic Rats

The aim of the present study was to evaluate the possible protective effects of S-allyl cysteine (SAC) on the antioxidant defense system of pancreas in streptozotocin(STZ) induced diabetes in rats. The levels of blood glucose and TBARS in plasma and pancreas were estimated in control and experimental groups of rats. To assess the changes in the cellular antioxidant defense system, the level of reduced glutathione in plasma and pancreas and activities of superoxide dismutase and catalase were assayed in pancreatic tissue homogenate. The levels of glucose, TBARS and enzymatic antioxidants were altered in diabetic rats. These alterations were reverted back to near control levels after the treatment of SAC. The antidiabetic and antioxidant effect of SAC was compared with glyclazide, a well-known hypoglycemic drug. These findings suggest that SAC treatment exerts a therapeutic protective nature in diabetes by decreasing oxidative stress.     

Beta cell protective effects of sodium tungstate in streptozotocin-induced diabetic rats: glycemic control, blockage of oxidative stress and beta cell histochemistry

Background: Diabetes is a major public health problem. The development of new therapies that are able to improve glycemia management and even to cure diabetes is of great interest. In this study, protective effects of sodium tungstate against STZ-induced beta-cell damages were investigated. Methods: Sixty rats were divided into six groups: control, diabetic, sodium tungstate treated diabetic rats from one week before STZ injection (TDB), food-restricted diabetic (FRD), tungstate treated control, sodium tungstate treated diabetic rats from one week after STZ administration (TDA). We evaluated serum insulin, glucose and glucose tolerance; liver glycogen content, glucokinase (GK) activity; blood and pancreas antioxidant power, lipid peroxidation; and fuchsin-aldehyde histochemical staining of beta-cells. Results: Blood glucose levels of TDB group were lower than other diabetic groups (P<0.01). Blood insulin levels of all diabetic groups were lower than controls (P<0.01). Glucose intolerance improved in TDB animals. Blood and pancreas antioxidant power, liver glycogen contents and GK activities and granulated beta cells increased in TDB rats in comparison with other diabetic groups (P<0.01). Likewise, lipid peroxidation decreased significantly in TDB rats (P<0.01). Conclusions: Results suggested that sodium tungstate if administrated before STZ injection improves glycemic state by a direct effect on pancreatic beta-cells and preserves them by reducing the activity of these cells at the time of STZ injection, reducing STZ-induced oxidative stress, reducing insulin secretion, or all of the above mentioned.     

Effects of onion on serum uric acid levels and hepatic xanthine dehydrogenase/xanthine oxidase activities in hyperuricemic rats

The aim of this study was to investigate the effects of onion on serum uric acid levels and hepatic Xanthine Dehydrogenase/Xanthine Oxidase activities in normal and hyperuricemic rats. Hyperuricemia was induced by intraperitoneal injection of 250 mg kg(-1) potassium oxonate in rats. Oral administration of onion at 3.5 and 7.0 mg kg(-1) day(-1) for 7 days was able to reduce serum uric acid levels in hyperuricemic rats with no significant effects on the level of this compound in the normal animals. In addition, onion when tested in vivo on rat liver homogeneities elicited significant inhibitory actions on the Xanthine Dehydrogenase (XDH) and Xanthine Oxidase (XO) activities. This effect resulted less potent than that of allopurinol. However, the hypouricemic effect observed in the experimental animal did not seem to parallel the change in XDH and XO activities, implying that the onion might be acting via other mechanisms apart from simple inhibition of enzyme activities. Such hypouricemic action and enzyme inhibitory activity of onion makes it a possible alternative for allopurinol, or at least in combination therapy to minimize the side-effects of allopurinol, in particular in long-term application.     

Resolvin D1, a Metabolite of Omega-3 Polyunsaturated Fatty Acid,Decreases Post-Myocardial Infarct Depression

We hypothesized that inflammation induced by myocardial ischemia plays a central role in depression-like behavior after myocardial infarction (MI). Several experimental approaches that reduce inflammation also result in attenuation of depressive symptoms. We have demonstrated that Resolvin D1 (RvD1), a metabolite of omega-3 polyunsaturated fatty acids (PUFA) derived from docosahexaenoic acid, diminishes infarct size and neutrophil accumulation in the ischemic myocardium. The aim of this study is to determine if a single RvD1 injection could alleviate depressive symptoms in a rat model of MI. MI was induced in rats by occlusion of the left anterior descending coronary artery for 40 min. Five minutes before ischemia or after reperfusion, 0.1 μg of RvD1 or vehicle was injected in the left ventricle cavity. Fourteen days after MI, behavioral tests (forced swim test and socialization) were conducted to evaluate depression-like symptoms. RvD1 reduced infarct size in the treated vs. the vehicle group. Animals receiving RvD1 also showed better performance in the forced swim and social interaction tests vs. vehicle controls. These results indicate that a single RvD1 dose, given 5 min before occlusion or 5 min after the onset of reperfusion, decreases infarct size and attenuates depression-like symptoms.