银杏叶提取物(EGb761)对大鼠急性创伤性脑水肿的影响

目的探讨银杏叶提取物(EGb761)对大鼠急性创伤性脑水肿的疗效及其潜在机制。方法将60只SD大鼠随机分至假手术(A)组、创伤+等剂量生理盐水(B)组、创伤+低剂量EGb761(C)组、创伤+高剂量EGb761(D)组。采用Feeney自由落体致伤法制作大鼠顶叶局灶皮质挫裂伤模型,其中C组和D组,在创伤1 h后,分别给予EGb761 25 mg/kg和50 mg/kg治疗。采用干湿重法检测脑组织含水量,苏木素-伊红(HE)染色观察脑组织形态学变化,二氢乙锭(DHE)染色观察氧自由基表达水平,Western印迹检测AQP4蛋白表达水平。结果与A组相比,B、C、D组均出现脑水肿,氧自由基和AQP4表达水平上升,其中B组与A组有显著差异(P0.05);C组和D组脑水肿程度较B组有明显改善,脑组织中氧自由基,AQP4表达水平较B组显著降低(P0.05),且C组和D组之间无显著差异(P0.05)。结论 EGb761对创伤性脑水肿有保护作用,其机制可能与清除氧自由基,降低AQP4的表达有关。     

EGb761对AD大鼠大脑神经生长因子(NGF)及其受体p75的影响

目的 研究EGb761（达纳康）对Aβ25-35所致阿尔茨海默病（AD）模型大鼠脑组织神经生长因子（NGF）及其受体p75的调节机制。方法 采用双侧杏仁核注射Aβ25-35造成AD大鼠模型，观察大鼠Morris水迷宫空间记忆能力，并分别通过免疫组化和RT-PCR方法研究AD大鼠神经元NGF及其受体p5和APPmRNA变化以及EGb761对其影响。结果 AD模型大鼠Morris水迷宫测试出现空间记忆能力下降，APPmRNA表达提高，NGF减少，神经系统失去了营养保护。EGb761能有效控制以上病理变化。结论 EGb761提高模型大鼠定向学习记忆能力。可能通过降低皮层、海马部位APPmRNA的表达，增加NGF阳性样细胞、减少p75受体阳阳样细胞调节神经营养而发挥作用。提示通过有效调节NGF及其受体是EGh761的重要作用机制之一。     

银杏叶提取物EGb761对慢性乙型肝炎患者肝纤维化的影响

目的:探讨银杏叶提取物(EGb761)对慢性乙型肝炎患者肝组织纤维化的影响.方法:将60例慢性乙型肝炎患者分为EGb761治疗组(n=32)及对照组(n=28),治疗前后分别检测肝功能、Ⅲ型前胶原(PCⅢ)、Ⅳ型胶原(CⅣ)、透明质酸(HA)、层黏蛋白(LN)、血小板活化因子(PAF)、内皮素(ET-1)和转化生长因子-β_1(TGF-β_1)水平.两组中分别有26例和21例患者于治疗前后进行肝活检术,肝组织行HE、胶原纤维、网织纤维染色观察组织学变化.结果:治疗后两组的肝功能水平均较治疗前显著好转,但两组比较无差异.EGb761组治疗后ALT (621.8±271.7 nkat/L vs 1258.6±308.4 nkat/L,P<0.05),TBIL(17.1±9.5μmol/L vs 39.3±21.2μmol/L,P<0.01),PT(13.2±2.1 s vs 15.2±3.4 s,P<0.05),PCⅢ(168±48μg/L vs 307±93μg/L,P<0.95),CⅣ(102±35μg/L vs 191±35μg/L,P<0.01),HA(94±39μg/L vs 178±57μg/L,P<0.05),LN(101±31μg/L vs 193±21μg/L,P<0.05),PAF(7.62±6.54μg/L vs 13.23±9.79μg/L,P<0.05),ET-1(47.61±15.34μg/L vs 68.13±21.71μg/L,P<0.01)及TGF-β_1(17.61±5.06μg/L vs 58.43±11.04μg/L,P<0.05)水平与治疗前相比均显著下降,而ALB水平显著升高(38.2±5.9g/L vs 34.9±4.4g/L,P<0.05).与对照组相比,EGb761组治疗后血清TGF-β_1(17.61±5.06μg/L vs 61.17±11.45μg/L,P<0.05),PAF(7.62±6.54μg/L vs 11.65±8.96μg/L,P<0.05),ET-1(47.61±15.34μg/L vs 61.17±16.45μg/L,P<0.01),PCⅢ(168±48μg/L vs 298±86 ug/L,P<0.05),CⅣ(102±35μg/L vs 178±61 ug/L,P<0.05),HA(94±39μg/L vs 179±82μg/L,P<0.05)及LN(101±31μg/L vs 190±39 ug/L,P<0.01)指标改善更为明显.治疗组肝活检证实,治疗后肝脏细胞损伤减轻,纤维化程度减轻,而对照组治疗前后均无明显变化.结论:银杏叶提取物EGb761对慢性乙肝有明显的抗肝纤维化作用.     

尼群地平对食饵性家兔动脉粥样硬化的影响Ⅰ．对血浆总胆固醇和主动脉病变的作用

用新西兰白兔观察了尼群地平对实验性动脉粥样硬化的影响。结果发现，尼群地平时食饵性高脂血症影响不大，但可明显抑制其主动脉壁病变，降低主动脉组织胆固醇含量，表明尼群地平具有显著抗动脉粥样硬化作用。     

Egb 761对NO供体SNP诱导的海马神经元凋亡的保护作用

目的　探讨银杏叶提取物 (EGb761 )对 NO供体硝普钠 (SNP)引起的大鼠海马神经元凋亡的影响。方法　采用 MTT比色分析测细胞存活率、 Hoechst 332 58荧光染色及 DNA琼脂糖凝胶电泳分析等方法检测凋亡。结果　不同剂量 EGb 761预处理海马神经元 6 h可剂量依赖地对抗 SNP引起的神经元凋亡 ,提高神经元的存活率 ;减少 SNP引起的核固缩、凝聚和碎裂现象 ;DNA凝胶电泳图谱未见典型的“梯子状”改变。结论　 EGb 761对 NO供体 SNP诱导的海马神经元凋亡具有明显的保护作用     

尼群地平对食饵性家兔动脉粥样硬化的影响Ⅰ.对血浆总胆固醇和主动脉病变的作用

用新西兰白兔观察了尼群地平对实验性动脉粥样硬化的影响。结果发现,尼群地平时食饵性高脂血症影响不大,但可明显抑制其主动脉壁病变,降低主动脉组织胆固醇含量,表明尼群地平具有显著抗动脉粥样硬化作用。     

银杏叶提取物对饲高胆固醇兔动脉粥样硬化和低密度脂蛋白体外氧化的作用

目的 :观察银杏叶提取物对饲高胆固醇兔动脉粥样硬化斑块形成和低密度脂蛋白体外氧化的拮抗作用。方法 :采用饲高胆固醇兔动脉粥样硬化模型 ,观察银杏叶提取物对兔主动脉动脉粥样硬化斑块形成的影响 ;采用铜离子 (10× 10 -6mol/L)体外氧化低密度脂蛋白模型 ,观察银杏叶提取物对低密度脂蛋白脂质过氧化产物丙二醛 (MDA)含量和维生素E水平的影响。结果 :银杏叶提取物 (0 5 g/kg/天 )明显减少饲高胆固醇兔主动脉动脉粥样硬化斑块面积百分比 (19 0 %± 8 2 %vs 44 9%±17 6 % ,P <0 0 1) ;银杏叶提取物明显抑制铜离子氧化低密度脂蛋白致MDA增加和维生素E减少 (P<0 0 5 ) ,且呈剂量依赖性和时间依赖性。结论 :银杏叶提取物有延缓饲高胆固醇兔动脉粥样硬化斑块形成的作用和抗低密度脂蛋白体外氧化修饰的作用。     

银杏叶提取物及其合剂对饲胆固醇兔动脉粥样硬化的作用

目的：研究银杏叶提取物和银杏叶提取物合剂（银杏叶提取物＋维生素Ｅ＋Ｌ－精氨酸＋牛磺酸,２：１：２：２．５）对饲胆固醇兔动脉粥样硬化的防治作用。方法采用饲１％胆固醇兔形成动脉粥样硬化为模型,观察银杏叶提取物和银杏叶提取物合剂对饲胆固醇兔胸主动脉动脉粥样硬化斑块面积百分比及对血浆丙二醛和一氧化氮含量的影响。结果银杏叶提取物合剂（１－３ｍｇ／ｋｇｐｅｒｄａｙ）和银杏叶提取物（０．５ｍｇ／ｋｇｐｅｒｄａｙ     

实验性高胆固醇血症与家兔腹主动脉粥样硬化的关系研究

目的　研究实验性高胆固醇血症与家兔腹主动脉粥样硬化的关系 ,评价胆固醇在家兔腹主动脉粥样硬化形成中的作用。方法　对 16只雄性家兔分别于高脂饲料喂饲前及 12周后进行腹主动脉超声检查 ,测量腹主动脉内膜 -中层厚度的最大值 (IMTm) ,测定血清总胆固醇 (TC)、高密度脂蛋白胆固醇 (HDL- c)、低密度脂蛋白胆固醇(L DL- c) ,计算 TC与 HDL- c之比 (C/ H) ,取腹主动脉做病理切片测量动脉 IMTm。结果　 12周后家兔腹主动脉IMTm值明显增高 ,TC、L DL - c、C/ H明显升高。 IMTm与 L DL - c及 C/ H呈正相关。 IMTm的超声与病理测值之间无显著性差异 ,并高度一致。结论　高胆固醇是动脉粥样硬化的重要危险因素 ,其中的 HDL- c及 L DL- c在总胆固醇中所占比例的变化与动脉粥样硬化病变的形成密切相关 ,超声方法检测活体家兔腹主动脉 IMT准确可行。     

银杏叶提取物EGb761对局灶性脑缺血再灌注大鼠XIAP和Smac表达的影响

目的 探讨银杏叶提取物EGb761对局灶性脑缺血大鼠脑组织X-连锁凋亡蛋白抑制剂(X-linked inhibitor of apoptosis protein,XIAP)和Smac蛋白表达的影响.方法 40只雄性Wistar大鼠随机分为假手术组、脑缺血再灌注组、EGb761小剂量组和EGb761大剂量组,每组10只.制作大鼠大脑中动脉闭塞1.5 h再灌注24 h模型.EGb761小剂量组和EGb761大剂量绀于模型制作前1 h分别腹腔注射ECY0761 50 mg/kg和100 mg/kg.大鼠脑组织XIAP和Smac表达用免疫组化方法 检测.结果 EGb761小剂量绀和EGb761大剂量组脑组织XIAP表达分别为18.33±4.01和26.7±3.27,显著高于脑缺血再灌注绀的12.13±3.44(P均<0.01),且EGb761大剂量组高于EGb761小剂量组(P<0.01);EGb761小剂量组和EGb761大剂量组脑组织Smac表达分别为21.33±3.15和11.33±2.10,显著低于脑缺血再灌注组的28.93±4.96(P均<0.05),EGb761大剂最组显著低于EGb761小剂量组(P<0.01).结论 脑缺血再灌注可诱导XIAP和Smae表达,EGn761干预在上调XIAP表达的同时能抑制Smac蛋白表达,提高XIAP/Smac比值,可能是EGb761干预的保护机制之一.     

Ginkgo biloba extract EGb 761 attenuates myocardial stunning in the pig heart

Myocardial stunning, a transient contractile dysfunction that appears following a brief period of ischemia, is at least partly due to the production of oxygen-derived free radicals. The objective of the present study was to determine whether the Ginkgo biloba extract EGb761, which has antioxidant properties in vitro, can attenuate myocardial stunning in vivo. Forty-seven anesthetized open-chest farm pigs underwent 10 min of occlusion of the left anterior descending coronary artery (LAD), followed by 3 hours of reperfusion. They were pretreated with either physiological saline, 100 mg or 300 mg of EGb 761 (Protocol I) or 3 mg or 9 mg of ginkgolide B (GkB) (Protocol II). Contractile function was assessed by sonomicrometry. Both doses of EGb 761 significantly improved recovery of contractile function in the reperfused myocardium with segment shortening averaging 23 +/- 5 % of baseline values at 3 hours post-reflow in controls versus 81 +/- 10 % and 57 +/- 12 % in the EGb100 and EGb300 groups, respectively (p < 0.05 vs control in both cases). In contrast, neither dose of GkB improved functional recovery during reperfusion. ESR experiments revealed that EGb761 resulted in a 59 % decrease in myocardial spin-adduct release during reperfusion (p < 0.05 versus control and GkB groups). A significant 28 % decrease (p < 0.05 vs control group) was also obtained in GkB-treated animals. These results indicate that EGb 761 can attenuate myocardial stunning following a brief ischemic insult in the in situ pig heart by an effect that involves a decrease in the formation of free radicals. As the effect of EGb 761 on functional recovery cannot be explained by the presence of GkB, the beneficial action of the extract on myocardial stunning likely involves complementary effects of both its non-ginkgolide and ginkgolide constituents.     

EGb761诱导血红素加氧酶-1在肺缺血再灌注损伤中的抗凋亡作用

目的 探讨银杏叶提取物EGb761诱导血红素加氧酶-1(HO-1)在肺缺血再灌注损伤中的抗凋亡作用.方法 40只健康SD大鼠随机分为4组:对照组(Sham组,不阻断右肺门)、缺血/再灌注组(I/R组,阻断右肺门30 min再灌注2 h),EGb761组(术前给予EGb761腹腔注射)、锌原卟啉组(Znppix组,术前给予EGb761及术中给予HO-1抑制剂Znppix干预).采用蛋白免疫印迹法(Western blot)检测肺组织HO-1蛋白、磷酸化JNK蛋白及Bcl-2蛋白表达;DNA原位末端标记(TUNEL)法测定肺组织细胞凋亡指数.结果 EGb761组HO-1表达灰度比值较I/R组与Sham组均升高(3.257±0.432 vs 1.329±0.310、0.187±0.101,P<0.05).磷酸化JNK1、磷酸化JNK2、Bcl-2蛋白表达灰度比值与细胞凋亡指数在I/R组、EGb761组、Znppix组分别为1.897±0.354、1.674±0.273、0.420±0.093与(14.91±0.49)%,0.681±0.131、0.715±0.116、1.384±0.190与(7.48±0.72)%,1.031±0.201、0.965±0.167、0.621±0.114与(9.01 =0.65)%.与I/R组比较,EGb761组磷酸化JNK蛋白表达下降,Bcl-2蛋白表达增加,细胞凋亡指数下降(P值均<0.05).与EGb761组比较,Znppix组磷酸化JNK蛋白表达增高,Bcl-2蛋白表达下降,细胞凋亡指数增高(P值均<0.05).结论 银杏叶提取物EGb761可诱导HO-1表达,进一步通过抑制JNK蛋白激酶活性及促进Bcl-2表达而在肺缺血再灌注损伤中发挥抗凋亡作用.     

Ginkgo biloba Extract (EGb 761) Pretreatment Limits Free Radical Oxidative Stress in Patients Undergoing Coronary Bypass Surgery

A growing body of evidence supports the trigger role of free radicals in the delayed functional and metabolic myocardial recovery following cardiopulmonary bypass (CPB) in humans, thus opening the field to specific therapies. This clinical study was designed to evaluate, in 15 patients undergoing aortic valve replacement, whether the extent of CPB- and reperfusion-induced lipid peroxidation, ascorbate depletion, tissue necrosis, and cardiac dysfunction is reduced by orally administered EGb 761, a Ginkgo biloba extract withpotent in vitro antiradical properties. Patients received either EGb 761 (Tanakan, 320 mg/day, n = 8) or a matching placebo (n = 7) for 5 days before surgical intervention. Plasma samples were obtained from the peripheral circulation and the coronary sinus at crucial stages of the operation (i.e., before incision, during ischemia, and within the first 30 minutes post-unclamping), and up to 8 days postoperatively. Upon aortic unclamping, EGb 761 inhibited the transcardiac release of thiobarbituric acid species (p ` 0.05), as assessed by high-performance liquid chromatography, and attenuated the early (5–10 minute) decrease in dimethylsulfoxide/ascorbyl free radical levels, an electron spin resonance index of the plasma ascorbate pool (p ` 0.05). EGb 761 also significantly reduced the more delayed leakage of myoglobin (p = 0.007) and had an almost significant effect on ventricular myosin leakage (p = 0.053, 6 days postoperatively). The clinical outcome of recovery of treated patients was improved, but not significantly, compared with untreated patients. Our results demonstrate the usefulness of adjuvant EGb 761 therapy in limiting oxidative stress in cardiovascular surgery and suggest the possible role of highly bioavailable terpene constituents of the drug.     

Complementary cardioprotective effects of flavonoid metabolites and terpenoid constituents of Ginkgo biloba extract (EGb 761) during ischemia and reperfusion

Hemodynamic and electron spin resonance (ESR) analyses were performed on isolated ischemic and reperfused rat hearts to assess the cardioprotective and antioxidant effects of therapeutically relevant concentrations of Gingko biloba extract (EGb 761; 5, 50 or 200 μg/ml), its terpenoid constituents (ginkgolide A; 0.05 μg/ml and ginkgolide B; 0.05, 0.25 or 0.50 μg/ml), and a terpene-free fraction of EGb 761 (CP 205; 5 or 50 μg/ml). Hearts underwent 10 min of low-flow ischemia, 30 min of no-flow global ischemia, and 60 min of reperfusion. Test substances were added to the perfusion fluid during the last 10 min of control perfusion, low-flow ischemia and the first 10 min of reperfusion. A separate group of rats were treated with CP 205 (60 mg/kg/day; p.o.) for 15 days, after which the hearts were perfused with plain buffer. In ESR experiments, the spin-trap 5,5-dimethyl-1-pyrroline N-oxide (DMPO) was added to the perfusate to determine the effects of treatment on post-ischemic myocardial free radical generation. Results showed that in vitro exposure of hearts to EGb 761 (5 or 50 μg/ml) or to ginkgolides A and B (both at 0.05 μg/ml), or in vivo pretreatment of the rats with CP 205 delayed the onset of contracture during ischemia. The strong reperfusion-induced elevation of left ventricular end-diastolic pressure observed in untreated hearts was significantly reduced by in vitro exposure to the lowest concentrations of EGb 761, by ginkgolide A, and to a lesser extent by ginkgolide B, or by prior oral treatment with CP 205. Post-ischemic functional recovery was significantly improved by in vivo administration of CP 205, by perfusion with 5 μg/ml of EGb 761 or with both terpenoids as compared to untreated group but in vitro CP 205 was not effective. ESR analyses revealed that DMPO-OH (the DMPO / hydroxyl radical spin-adduct) concentrations in coronary effluents were markedly decreased by all treatments, except for the lowest concentration of gingkolide B. Perfusing 5 μg/ml EGb 761 resulted in a better inhibition of baseline DMPO-OH concentration than 5 μg/ml CP 205 (−70% and −48% vs. control, respectively), indicating that both terpenoid and flavonoid constituents of EGb 761 are required to produce this effect. CP 205 was significantly more efficient in reducing DMPO-OH concentration when administered in vivo than when applied in vitro, indicating that the antioxidant effect of flavonoid metabolites (formed in vivo) is superior to that of intact flavonol glycosides (present in vitro). Collectively, these findings provide the first evidence that part of the cardioprotection afforded by EGb 761 is due to a specific action of its terpenoid constituents and that this effect involves a mechanism independent of direct free radical-scavenging. Thus, the terpenoid constituents of EGb 761 and the flavonoid metabolites that are formed after in vivo administration of the extract act in a complementary manner to protect against myocardial ischemia-reperfusion injury. Received: 30 September 1999 Returned for revision: 1 December 1999 Revision received: 14 January 2000 Accepted: 8 February 2000     

Ginkgo biloba extract EGb 761 and Wisconsin Ginseng delay sarcopenia in Caenorhabditis elegans

Previously we reported that the standardized Ginkgo biloba extract EGb 761 extended life span and increased stress resistance in Caenorhabditis elegans. In this study, pharmacological modulation of age-dependent muscle degeneration, or sarcopenia, was determined. Transgenic C. elegans strain (PD4251) expressing green fluorescent protein (GFP)-MYO-3, localized in body wall muscles and vulval muscle nuclei, were fed with EGb 761 or Wisconsin Ginseng, and muscle integrity was analyzed by quantification of GFP fluorescence. Both EGb 761 and Wisconsin Ginseng significantly delayed sarcopenia. Ginseng was more effective in worms of more advanced age, which is consistent with the ultrastructural changes observed by transmission electron microscopy. Furthermore, both agents ameliorated age-associated decline of locomotive behaviors including locomotion, body bend, and pharyngeal pumping. These results suggest that pharmacological extension of life span is a consequence of maintaining functional capacity of the tissue, and that C. elegans is a valid model system for testing therapeutic intervention for delaying the progress of sarcopenia.     

Inhibition of amyloid-beta aggregation and caspase-3 activation by the Ginkgo biloba extract EGb761

Standardized extract from the leaves of the Ginkgo biloba tree, labeled EGb761, has been used in clinical trials for its beneficial effects on brain functions, particularly in connection with age-related dementias and Alzheimer's disease (AD). Substantial experimental evidence indicates that EGb761 protects against neuronal damage from a variety of insults, but its cellular and molecular mechanisms remain unknown. Using a neuroblastoma cell line stably expressing an AD-associated double mutation, we report that EGb761 inhibits formation of amyloid-beta (Abeta) fibrils, which are the diagnostic, and possibly causative, feature of AD. The decreased Abeta fibrillogenesis in the presence of EGb761 was observed both in the conditioned medium of this Abeta-secreting cell line and in solution in vitro. In the cells, EGb761 significantly attenuated mitochondrion-initiated apoptosis and decreased the activity of caspase 3, a key enzyme in the apoptosis cell-signaling cascade. These results suggest that (i) neuronal damage in AD might be due to two factors: a direct Abeta toxicity and the apoptosis initiated by the mitochondria; and (ii) multiple cellular and molecular neuroprotective mechanisms, including attenuation of apoptosis and direct inhibition of Abeta aggregation, underlie the neuroprotective effects of EGb761.     

Effect of the antioxidant action of Ginkgo biloba extract (EGb 761) on aging and oxidative stress

Aging is responsible for oxidative damage to DNA, protein, lipid, and other macromolecules linked to tissue alterations. The resultant damage contributes significantly to degenerative diseases, to include those of the brain, sensorial tissues, and cardiovascular system. To protect cellular components from oxyradical attack, especially lipoperoxidation, a substantial interest in the use of antioxidants has evolved. A free radical scavenger, Ginkgo biloba extract (EGb 761) may be effective in fighting the oxidative stress related to aging. Many data support the efficacy of EGb 761 in biological model systems. In aging processes, EGb 761 may ameliorate the mitochondria respiratory chain function by quenching the superoxide anion, and the hydroxyl and peroxyl radicals. It protects the brain by facilitating the uptake of neurotransmitters and by reducing ischemia-reperfusion episodes and level of apoptosis. Moreover, in sensorial tissues, EGb 761 reduces apoptosis in the olfactive bulb and in the retinal pigmented epithelium of the eye, and protects against the lipoperoxidation alteration of the retina that results in a decrease of the electroretinogram response. In the cardiovascular system, by a direct effect on oxidative low density lipoproteins, EGb 761 may decrease atherosclerosis evolution, and is shown to accelerate cardiac mechanical recovery after ischemia-reperfusion. In conclusion, the antioxidant effects of EGb 761 noted in many experimental data, may explain the therapeutic efficacy observed in clinical trials of the elderly. These beneficial properties seem in part to come from the activity of EGb 761 constituents, such as flavonoids and terpens.     

Interventional effect of Ginkgo biloba extract on the progression of gastric precancerous lesions in rats

OBJECTIVE: To investigate the effect of Ginkgo biloba extract on gastric precancerous lesions in rats. METHODS: 80 4‐week‐old Wistar rats were randomly divided into four groups: a control group, a model group, a low and a high dose Ginkgo biloba extract intervention group; 20 in each group. Gastric precancerous lesions were induced by giving them 100 mg/L N‐methyl‐N′‐nitro‐N‐nitrosoguanidine (MNNG) solution to drink ad libitum for 20 weeks. In addition to the MNNG, the intervention groups were lavaged with Ginkgo biloba extract (0.5 mg/kg/d in the low dose group, 1.5 mg/kg/d in the high dose group) for 20 weeks. Starting from week 21 all the rats were fed with normal rat chow and tap water. At the end of week 30 the rats were killed. The histopathological changes of their gastric mucosa, ISA, NGI, the serum and gastric mucosal SOD/MDA and the expressions of oncogenes were studied. RESULTS: The incidence of mild to severe intestinal metaplasia and dysplasia were significantly lower in the intervention groups than those in the model group (P < 0.01). The ISA and NGI in the intervention groups were significantly lower than those in the model group (P < 0.01). In the intervention groups the activity of SOD was increased and the concentration of MDA was decreased (P < 0.01). Expressions of Bcl‐2, c‐myc and FasL decreased in the intevention groups, whereas the expression of Fas increased. When compared with the model group, the differences were statistically significant (P < 0.01, P < 0.05, respectively). CONCLUSION: Ginkgo biloba extract can increase anti‐oxidative activity and inhibit the progression of gastric precancerous lesions via the regulation of cell proliferation and apoptosis.     

Protective effect of the standardized leaf extract of Ginkgo biloba (EGb761) against hypertension-induced renal injury in rats

ABSTRACT

Background: Ginkgo biloba leaves extract has been widely used worldwide to protect against oxidative stress-induced cell damage and improves blood circulation. Methods: The potential protective role of the standardized leaf extract of Ginkgo biloba (EGb761) on hypertension-induced renal injury was investigated in rats. Hypertension was induced in rats by L-NAME. Result: Repeated treatment with EGb761 produced progressive reductions in the systolic, diastolic and mean arterial blood pressure. Also, EGb761 increased the progressive reductions in blood pressure induced by losartan. Hypertension-induced marked elevation of renal malondialdehyde (MDA) and nitrite levels and reduction of reduced glutathione (GSH) level were inhibited by EGb761. In addition, hypertension-induced increases in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β)) levels in renal tissues were inhibited by EGb761. Also, treatment with EGb761 inhibited hypertension-induced decrease in endothelial nitric oxide synthase (eNOS) protein expression and increase in the protein expressions of inducible NO synthase (iNOS), TNF-α, IL-6 and IL-1B in the kidney tissues. EGb761 enhanced losartan effects on renal tissues oxidative stress, nitrite, and inflammatory markers levels and on protein expressions of eNOS, iNOS, TNF-α, IL-6 and IL-1B. effects. Conclusions:These results indicate that EGb761 has the ability to protect against hypertension-induced renal injury.