Visual evoked potentials and optic nerve histopathology in normal and diabetic rats and effect of ginkgo biloba extract.

In: Acta Ophthalmol (Copenh) (1993 Oct) 71(5):623-8

The purpose of this study was to test the possible therapeutic role of ginkgo biloba extract on the impairment of visual function and pathological histology of the optic nerve caused by early diabetes. Ginkgo biloba extract entraps oxygenated free radicals and is also a strong inhibitor of the platelet activation factor (PAF). For this purpose, VEP recordings and optic nerve histopathology were studied on alloxan diabetic and normal Swiss albino rats in four experimental groups. The VEP recordings showed no statistical significance between diabetic and normal rats. However, the amplitudes were significantly increased in diabetic animals with ginkgo biloba extract compared with the diabetics, supposing an impression of axonal protection. But the amplitude values were decreased in normal rats treated with the same extract compared with normal animals, assuming a toxic activity. Optic nerve ultrastructural findings also confirmed these VEP changes. It was concluded that this extract could be encouraging for human clinical trials of diabetes.

Atzori C Bruno A Chichino G Bombardelli E Scaglia M Ghione M

Activity of bilobalide, a sesquiterpene from Ginkgo biloba, on Pneumocystis carinii.

In: Antimicrob Agents Chemother (1993 Jul) 37(7):1492-6

The sesquiterpene bilobalide, extracted from Ginkgo biloba leaves, was tested in vitro and in vivo for the ability to inhibit Pneumocystis carinii growth. Bilobalide was inhibitory to trophozoites cultured on human embryonic lung fibroblasts (HEL 299) at approximately the same concentration as trimethoprim plus sulfamethoxazole (lowest effective concentration, 50 micrograms of bilobalide per ml versus 9/45 microgram of trimethoprim- sulfamethoxazole per ml), inducing microscopically detectable morphological changes in the cytoplasm of the parasite. In pharmacologically immunosuppressed Sprague-Dawley rats transtracheally infected with a suspension of about 5 x 10(6) P. carinii trophozoites per ml, the daily intraperitoneal administration of bilobalide (10 mg/kg of body weight for 8 days) lowered the number of organisms by approximately 2 logs (that is, about 99%). There was no apparent toxicity either in uninfected HEL 299 feeder cells or in infected and uninfected animals. These studies suggest that the sesquiterpene bilobalide might be useful for therapy of and prophylaxis against P. carinii infections in humans.

Bauer U.,

Six months double-blind randomised clinical trial of Ginkgo biloba extract versus placebo in two parallel groups in patients suffering from peripheral arterial insufficiency.

In: Arzneimittel - ForsehlDru: Res, 1984, 34, 716-720.

Boismare F.:

Etude de l'action hemodynamique de l'extrait concentre de Ginkgo biloba comparee a celle du gaz carbonique chez le sujet jeune et chez le sujet senile.

In: Ouesl Medical, 1976, 29, 747-749.

Bono Y., Mouren P.:

L'insuffisance circulatoire cerebrale et son traitement par l'extrait de Ginkgo biloba.

In: Med. Med., 1975, 3, 59-62.

Boudouresques G., Vigouroux R., Boudouresques J.:

Interet et place de l'extrait de Ginkgo biloba en pathologie vasculaire cerebrale.

In: Medecine Pralicienne, 1975, 59:, 75-78.

Bourgain RH Maes L Andries R Braquet P

Thrombus induction by endogenic paf-acether and its inhibition by Ginkgo Biloba extracts in the guinea pig.

In: PROSTAGLANDINS (1986 Jul) 32(1):142-4

The anti-thrombotic effects of specific paf-acether antagonist BN 52021 were compared to the effects of Ginkgo Biloba extracts A, B, (A+ B), and C. Local superfusion of BN 52021 over an experimentally injured arterial segment embolizes an existent paf-acether induced platelet thrombus. When applied before paf-acether, BN 52021 prevents local thromboformation in this model. Applied intravenously, BN 52021 reduces local thromboformation in a significant way. As compared to this BN 52021 standard, only Ginkgo Biloba B and the (A + B)-mixture present major thromboreductive activity.

Braquet P

Cedemin, a Ginkgo biloba extract, should not be considered as a PAF antagonist [letter; comment]

In: Am J Gastroenterol (1993 Dec) 88(12):2138

Chabrier PE Roubert P

[Effect of Ginkgo biloba extract on the hemato-encephalic barrier]

Effet de l'extrait de Ginkgo biloba sur la barriere hemo-encephalique.

In: Presse Med (1986 Sep 25) 15(31):1498-501

The different methods used to explore the blood-brain barrier (made up of cerebral capillary vessels), and notably, at molecular level, isolated microvessel preparations, have greatly improved our knowledge in this particular field. Some of these methods could be used to evaluate the protective effects of therapeutic substances, such as Ginkgo biloba extract, on the blood-brain barrier.

Chaterjee G.:

Effects of Ginkgo biloba extract on cerebral metabolic processes.

In: Effects of GBE and Organic Cerebral Impairment, Paris, London, John Lilley, 1985.

Clostre F

[From the body to the cell membrane: the different levels of pharmacological action of Ginkgo biloba extract]

In: PRESSE MED 1986 Sep 25; 15(31):1529-38 (Published in FRENCH)

The pharmacological study of Ginkgo biloba extract has required numerous experiments over several years: diffe rent pathological models of cerebral ischaemia to evaluate its effects, and experiments at both cellular and molecular levels to determine its mechanisms of action. In experimental models of ischaemia, oedema and hypoxia, Ginkgo biloba extract reduced vascular, tissular and metabolic disturbances as well as their neurological and behavioural consequences. The pharmacological effects of Ginkgo biloba extract concern vascular, rheological and metabolic processes. Several membrane mechanisms seem to be involved: protection of the membrane ultrastructure against free radicals, modulation of some enzymatic systems and ionic pumps. The originality of the pharmacological properties of Ginkgo biloba extract lies in preferential focusing of its effects on ischaemic areas.

Creutzig A

[Is Ginkgo biloba extract EGb 761 clinically effective in intermittent claudication? (letter)]

In: Vasa (1993) 22(2):189-90 (Published in German)

Diwok M Kuklinski B Ernst B

[Superoxide dismutase activity of Ginkgo biloba extract]

In: Z Gesamte Inn Med (1992 Jul) 47(7):308-11 (Published in German)

The Ginkgo biloba extract is obtained from green leaves of the Ginkgo biloba tree. Preparations with this active substance are among others used for the treatment of disturbances of the cerebral function and arteriosclerotic diseases. In in-vitro and in-vivo studies antagonistic effects of radical scavenger and PAF (platelet activating factor) were described. In this study a concentration- depending superoxide dismutase activity of the Ginkgo biloba extract rokan liquid could be made evident.

Droy-Lefaix-M-T; Szabo-M-E; Doly-M

Ischaemia and reperfusion-induced injury in rat retina obtained from normotensive and spontaneously hypertensive rats: Effects of free radical scavengers.

In: International Journal of Tissue Reactions (1993)15(2): 85-91

The authors have studied the effects of free radical scavengers, superoxide dismutase (SOD) and extract of Ginkgo biloba (EGb 761, flavone-rich extract) on ion shifts (Na, K and Ca) induced by ischaemia and reperfusion in rat retina obtained from normotensive and spontaneously hypertensive rats. Eyes were subjected to 90 min of ischaemia by occlusion of the retinal artery, followed by 4 and 24 hours of reperfusion. SOD (15, 000 U/kg, i.v.) or EGb 761 (50 mg/kg, per os) was administered in a daily dose for 10 days. In the drug-free control groups, 90 min of ischaemia significantly increased tissue Na gains from their pre-ischaemic control values of 63 +- 7 mu-M/g dry weight (in retina obtained from normotensive rats) and 76 mu-M/g dry weight (in retina obtained from hypertensive rats) to 89 +- 9 mu-M/g dry weight and 101 +- 7 mu-M/g dry weight, respectively. During reperfusion, a further elevation was found in retinal Na in both the normotensive and hypertensive groups. Probably, because of the ischaemia-induced inhibition of Na-K-ATPase, retinal K loss was detected after ischaemia and reperfusion, respectively. An accumulation of retinal Ca was measured after ischaemia and reperfusion in the normotensive and spontaneously hypertensive groups. Both free radical scavengers significantly reduced the maldistribution of ions induced by ischaemia and reperfusion, but the effectiveness of drugs was more evident in normotensive than hypertensive groups. The present results indicate that the elimination of free radicals by free radical scavengers may reduce, probably via an indirect mode, the reperfusion-induced ionic imbalance and improve the ionic homeostasis in injured retinal cells obtained from normotensive and spontaneously hypertensive rats.

Dumont E Petit E Tarrade T Nouvelot A

UV-C irradiation-induced peroxidative degradation of microsomal fatty acids and proteins: protection by an extract of Ginkgo biloba (EGb761).

In: Free Radic Biol Med (1992 Sep) 13(3):197-203

After exposure of rat liver microsomes to UV-C irradiation, analysis of membrane fatty acids by gas chromatography confirmed that EGb 761, a drug containing a dosed and standardized extract of Ginkgo biloba, provides effective protection against free radical attack in vitro. This analysis, coupled with thiobarbituric acid (TBA) reaction, permitted qualitative and overall quantitative evaluation of radical- induced damage to polyunsaturated fatty acids (PUFA), as well as evidence of the antioxidant properties of the Ginkgo biloba extract. Assay of thiobarbituric acid reactive substances (TBARS) showed a correlation between TBARS concentration and the state of degradation of the polyunsaturated fatty acids. Mannitol (5.5 mM) did not prevent degradation of microsomal PUFA or malondialdehyde (MDA) production, nor did it prevent polymerization of membrane proteins. Low doses of EGb 761 were found to provide efficient protection of membrane PUFA regardless of individual susceptibility to peroxidation. This protection was accompanied by a decrease in the production of TBARS. EGb 761 also protected membrane proteins from the irreversible polymerization induced by these degradation products, but did not appear to prevent thiols oxidation into disulfide bonds.

Eckmann F., Schlag H.:

Etude controlee, a double insu, de l'activite de l'Extrait de Ginkgo biloba chez des malades atteints d'insuffisance cerebrale chronique.

In: Fortschritte der Medizin, 1982, 31132, 1474-1478.

Etienne A Hecquet F Clostre F

[Mechanism of action of Ginkgo biloba extract in experimental cerebral edema]

Mecanismes d'action de l'extrait de Ginkgo biloba sur l'oedeme cerebral experimental.

In: Presse Med (1986 Sep 25) 15(31):1506-10

Oedema is one of the major complication of cerebral ischaemia being at the same time a consequence and an aggravating factor. Its first phase is intracellular and cytotoxic, with breakdown of ionic pumps through loss of energy, resulting in a whole sequence of ionic perturbations characterized by loss of intracellular K+ and accumulation of water and Na+, Cl-, and Ca2+ ions in the cells of the ischaemic zone. The second phase, termed vasogenic, applies to the accumulation of lactates, inorganic phosphates and free polyunsaturated fatty acids and in particular, arachidonic acid. This last compound is responsible for the production of membrane "aggressors", amongst which free radicals play an important role. Ginkgo biloba extract limits the formation of cerebral oedema and suppresses its neurological consequences, whether the oedema is of cytotoxic (triethyltin) or vasogenic (unilateral traumatic oedema) origin. Several membrane mechanisms could be implicated in the protective action manifested by Ginkgo biloba extract against cerebral oedema.