A new prostaglandin E1 analogue (TFC-612) prevents a decrease in motor nerve conduction velocity in streptozocin-diabetic rats

Yasuda, Hitoshi; Sonobe, Masanobu; Hatanaka, I; Yamashita, Makio; Miyamoto, Yukio; Terada, Masahiko; Amenomori, Masanori; Kikkawa, Ryuichi; Shigeta, Yukio; Motoyama, Yukio; Saito, Noriyuki

doi:10.1016/0006-291x(88)90509-8

Cited by 28 publications

(9 citation statements)

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“…Unlike ONO 2235, the effect of TFC 612 was independent of the sorbitol and myo-inositol contents of the nerve. The ability of TFC 612 to prevent a decrease in MNCV immediately after the induction of diabetes has previously been reported (29), and our study reconfirmed the therapeutic effect in more chronically diabetic rats. Furthermore, the effect of TFC 612 was greater and more persistent than that of ONO 2235.…”

Section: Discussionsupporting

confidence: 86%

“…Intravenous infusion of this compound stabilized with cyclodextrin and in the form of a lipid emulsion has been reported to be effective for symptoms and nerve dysfunction in diabetic neuropathy (28). We have already reported the preventive effect of PGE, analogue TFC 612 on nerve dysfunction in experimental an-imals (29). The effect was not due to the correction of either sorbitol or myo-inositol metabolism (29).…”

mentioning

confidence: 89%

“…We have already reported the preventive effect of PGE, analogue TFC 612 on nerve dysfunction in experimental an-imals (29). The effect was not due to the correction of either sorbitol or myo-inositol metabolism (29).…”

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confidence: 89%

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Effect of Prostaglandin E1 Analogue TFC 612 on Diabetic Neuropathy in Streptozocin-Induced Diabetic Rats Comparison With Aldose Reductase Inhibitor ONO 2235

et al. 1989

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The effect of a newly developed oral agent, prostaglandin E1 (PGE1) analogue TFC 612, on diabetic neuropathy was studied by giving it for 6 wk to streptozocin-induced diabetic rats that had been diabetic for 3 mo and was compared with the effects of aldose reductase inhibitor ONO 2235. Although both compounds improved decreased motor nerve conduction velocity, the effect of TFC 612 continued during the 6 wk of treatment, whereas that of ONO 2235 became weaker from wk 4. The abnormality in sciatic nerve sorbitol and myo-inositol levels was reversed with ONO 2235, whereas it was unchanged with TFC 612. With the laser Doppler flowmetry technique, a decrease in the sciatic nerve blood flow in diabetic rats was shown to improve with both compounds, but TFC 612 had a greater effect than ONO 2235, and the increased lactate level of the diabetic nerve was corrected with both compounds, suggesting that both may be associated with the amelioration of ischemia in the diabetic endoneurium. Both TFC 612 and ONO 2235 partially but significantly normalized decreased fiber size in diabetic rats. On the other hand, TFC 612 completely normalized the dilated lumen area in diabetic rats, whereas ONO 2235 did not. These results suggest that the PGE1 analogue TFC 612 has a significant effect on diabetic neuropathy, possibly via vasotropic action, and may be a potent compound for the treatment of diabetic neuropathy.

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Section: Discussionsupporting

confidence: 86%

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confidence: 89%

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Effect of Prostaglandin E1 Analogue TFC 612 on Diabetic Neuropathy in Streptozocin-Induced Diabetic Rats Comparison With Aldose Reductase Inhibitor ONO 2235

et al. 1989

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“…Recent studies have shown that a structural analogue of prostaglandin E1 can prevent the acute deficit in MNCV when administered to streptozotocin diabetic rats (Yasuda et al, 1988;1989). Prostaglandin El and/or derived secondary mediators, might directly modulate the biochemical events increasing nerve conduction or might improve the endoneurial microcirculation by dilating arterioles and inhibiting platelet aggregation (Gorman, 1978) hence preventing the development of any MNCV deficit related to ischaemic endoneurial hypoxia (Tuck et al, 1984;Dyck, 1989).…”

Section: Discussionmentioning

confidence: 99%

The effects of dietary treatment with essential fatty acids on sciatic nerve conduction and activity of the Na⁺/K⁺ pump in streptozotocin‐diabetic rats

Lockett

Tomlinson

1992

British J Pharmacology

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1 This study examined the effects of dietary essential fatty acid supplementation (5% (w/w) evening primrose oil) upon sciatic motor nerve conduction velocity and 86Rb+ pumping in sciatic nerve endoneurial preparations in rats with 4 to 5 weeks of streptozotocin-induced diabetes. 2 Control diabetic rats (dietary supplementation with 5% (w/w) hydrogenated coconut oil) exhibited a reduction in motor nerve conduction velocity (16%; P < 0.05) compared to similarly-fed non-diabetic controls, but there was no significant alteration in ouabain-sensitive 86Rb+ pumping, a parameter reflecting activity of the Na+/K+ pump.3 Treatment of diabetic rats with evening primrose oil prevented completely the development of the motor nerve conduction velocity deficit without affecting the severity of diabetes. Evening primrose oil treatment did not significantly affect motor nerve conduction velocity of non-diabetic animals. 4 Evening primrose oil treatment caused a significant reduction in activity of the Na+/K+ pump in sciatic nerves of diabetic animals (45%; P < 0.05). 5 These results suggest that the acute conduction velocity defect arising in streptozotocin-diabetic rats, and the actions of evening primrose oil upon this, are independent of any effect on activity of the Na+/K+ pump. Other putative mechanisms are discussed.

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“…Na + /K + -ATPase activity in diabetic rats can be affected through several perturbed metabolic pathways some of which are associated with activation of the polyol pathway such as nitric oxide synthesis [6], pseudohypoxia [75] or prostacyclin deficiency [76,77]. This explains not only the effects of aldose reductase inhibition and myo-inositol supplementation on Na + /K + -ATPase and NCV in experimental diabetic neuropathy but also those of prostacyclin analogues or their precursors [77], acetyl-l-carnitine [8,78] or C peptide [15].…”

Section: Pathogenetic Mechanismsmentioning

confidence: 99%

Experimental diabetic neuropathy: an update

1999

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Diabetic neuropathy consists of several clinical syndromes affecting motor, sensory and autonomic nerves. Of these the most common is distal symmetric sensory polyneuropathy usually referred to as diabetic neuropathy. Animal studies, mainly in diabetic rodents, have contributed tremendously to our understanding of this disease. From these it is clear that the pathogenesis of diabetic neuropathy is multifactorial involving sequentially occurring and often closely interrelated metabolic aberrations. Major pathogenetic mechanisms include increased activity of the polyol pathway, abnormalities in vasoactive substances, non-enzymatic glycation, increased presence of free radicals, and perturbed neurotrophism. Traditionally the neuropathies accompanying Type I (insulin-dependent) and Type II (non-insulin-dependent) diabetes mellitus have been regarded as identical. Recent investigations have, however, clearly delineated distinct differences in the functional and structural expressions of the neuropathies in the two types of diabetes. Major future challenges are the identification of the differences in underlying pathogenetic mechanisms in the two types of neuropathy and in gaining a better understanding of the hierarchy of the multifactorial mechanisms underlying the disease. This will be important for designing meaningful therapies which to date have failed miserably in diabetic neuropathy.

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A new prostaglandin E1 analogue (TFC-612) prevents a decrease in motor nerve conduction velocity in streptozocin-diabetic rats

Cited by 28 publications

References 19 publications

Effect of Prostaglandin E1 Analogue TFC 612 on Diabetic Neuropathy in Streptozocin-Induced Diabetic Rats Comparison With Aldose Reductase Inhibitor ONO 2235

Effect of Prostaglandin E1 Analogue TFC 612 on Diabetic Neuropathy in Streptozocin-Induced Diabetic Rats Comparison With Aldose Reductase Inhibitor ONO 2235

The effects of dietary treatment with essential fatty acids on sciatic nerve conduction and activity of the Na⁺/K⁺ pump in streptozotocin‐diabetic rats

Experimental diabetic neuropathy: an update

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A new prostaglandin E1 analogue (TFC-612) prevents a decrease in motor nerve conduction velocity in streptozocin-diabetic rats

Cited by 28 publications

References 19 publications

Effect of Prostaglandin E1 Analogue TFC 612 on Diabetic Neuropathy in Streptozocin-Induced Diabetic Rats Comparison With Aldose Reductase Inhibitor ONO 2235

Effect of Prostaglandin E1 Analogue TFC 612 on Diabetic Neuropathy in Streptozocin-Induced Diabetic Rats Comparison With Aldose Reductase Inhibitor ONO 2235

The effects of dietary treatment with essential fatty acids on sciatic nerve conduction and activity of the Na+/K+ pump in streptozotocin‐diabetic rats

Experimental diabetic neuropathy: an update

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The effects of dietary treatment with essential fatty acids on sciatic nerve conduction and activity of the Na⁺/K⁺ pump in streptozotocin‐diabetic rats