The Effects of Ginkgo Biloba Extract(GBe)on Axonal Transport, Microvasculature and Morphology of Sciatic Nerve in Streptozotocin-induced Diabetic Rats
10.1265/ehpm.5.53
- Author:
JinMan KIM
;
Kazuhiro YOKOYAMA
;
Shunichi ARAKI
- Publication Type:Journal Article
- Keywords:
Ginkgo alkaloides;
neuropathy;
tublin;
actin;
neurofilament
- MeSH:
Rattus norvegicus;
lower case pea;
Streptozocin;
Science of Morphology;
slow axonal transport
- From:Environmental Health and Preventive Medicine
2000;5(2):53-59
- CountryJapan
- Language:Japanese
-
Abstract:
To evaluate the protective effects of Ginkgo biloba extract (GBe) which has antioxidant activity against peripheral neuropathy due to diabetes mellitus, slow axonal transport and morphology of sciatic nerve including endoneurial microvessels were examined in 12 rats with diabetes mellitus induced by streptozotocin (STZ, 60mg/kg, b.w., i.p.). Six of the diabetic rats were treated with 0.1% of GBe for 6 weeks from one week after the STZ injection. Serum glucose and lipid peroxide levels in GBe−treated diabetic rats were significantly lower than those in untreated diabetic rats (p<0.01, respectively), though the serum glucose level was higher than that in the control rats. L−[35S] methionine pulse radiolabeling with subsequent gel fluorography demonstrated that mean velocities (Vmean) of actin and β−tubulin, i.e. slow component b(SCb) transport in untreated diabetic rats were significantly lower than those in control rats (p<0.05, respectively); mean diameter of axons in the former rats was significantly smaller than that in the latter (p<0.01). Vmean of actin transport in GBe−treated diabetic rats was significantly faster than that in untreated diabetic rats (p<0.05). Vmean of slow axonal transport was significantly correlated with mean diameter of axons in the three groups of rats combined (p<0.01). On electron microscopy, severe altered endoneurial microvessels decreasing in luminal area together with endothelial cell degeneration or hypertrophy, pericyte debris and basement membrane thickening were observed in untreated diabetic rats; on the other hand these findings were less prominent in the diabetic rats treated with GBe. It is suggested that GBe treatment may protect disturbed slow axonal transport and pathological alterations of peripheral nerve with abnormal endoneurial microvasculature from diabetes mellitus by antioxidant activity.
