Protective effects of Gingko biloba extract EGb 761 on myocardium of experimentally diabetic rats. I: ultrastructural and biochemical investigation on cardiomyocytes.
Chronic diabetes in man and animal models develops cardiomyopathic alterations which cannot be absolutely avoided by insuline therapy. Since diabetic damage is partly attributed to oxidative stress antioxidative treatment could be able to reduce the alterations. Aim of this study was to investigate the cardioprotective effects of EGb 761, known as a radical scavenger, against diabetic alterations in rats. The diabetes was induced by i.p. injection of 60 mg/kg body weight streptozotocin. Duration of diabetes was 4 months, the protected group received 100 mg/kg body weight EGb 761 with the drinking water over 3 months. Electron and light microscopic morphometry of left-ventricular samples revealed typical diabetic alterations consisting in decrease of volume fraction of myofibrils, SR and t-tubules and diminishing of cardiomyocyte diameter, increase of interstitial volume, mitochondrial size and volume fraction, and of vacuoles and of lipid drops. EGb treatment could gradually prevent the loss of myofibrils and reduction of myocyte diameter but has only little influence on interstitial and mitochondria volume. The diabetic-induced increase of lipid and vacuoles and the decrease of SR and t-tubules were not influenced. Biochemical parameters of oxidative stress: malondialdehyde (MDA) was only insignificantly altered by diabetes and EGb. The superoxide dismutase (SOD) activity was increased by diabetes and more increased by EGb treatment. Creatine kinase (CK) activity was diminished by diabetes but slightly increased by EGb. The polymerase chain reaction (PCR) of i-NOS was not different between the diabetic and protected diabetic groups.
Fitzl
G
G
Institute of Anatomy, University Leipzig, Germany.
Martin
R
R
Dettmer
D
D
Hermsdorf
V
V
Drews
H
H
Welt
K
K
D000818:Animals; D009202:Cardiomyopathies / Q000150:complications / Q000201:enzymology / Q000517:prevention & control*; D003402:Creatine Kinase / Q000187:drug effects / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000201:enzymology; D005419:Flavonoids / Q000494:pharmacology*; D016166:Free Radical Scavengers / Q000494:pharmacology*; D015971:Gene Expression Regulation, Enzymologic; D020441:Ginkgo biloba; D008315:Malondialdehyde / Q000378:metabolism; D008854:Microscopy, Electron; D009206:Myocardium / Q000166:cytology / Q000473:pathology / Q000648:ultrastructure; D019001:Nitric Oxide Synthase / Q000235:genetics; D052247:Nitric Oxide Synthase Type II; D010936:Plant Extracts; D012313:RNA / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013482:Superoxide Dismutase / Q000187:drug effects / Q000378:metabolism; D000096983:Ginkgo Extract
D003402:Creatine Kinase; D005419:Flavonoids; D016166:Free Radical Scavengers; D008315:Malondialdehyde; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D010936:Plant Extracts; D012313:RNA; D013482:Superoxide Dismutase; C063170:Ginkgo biloba extract; D000096983:Ginkgo Extract; C496318:Nos2 protein, rat