Changes in peripheral nerves of rats four months after induction of streptozotocin diabetes

Bestetti, G; Rossi, G. L.; Zemp, C.

doi:10.1007/bf00689405

Cited by 35 publications

(9 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Under HG condition, the SCs' injury was earlier than ongoing myelinic denaturation and axonal atrophy 39-41. Because of the similar characteristics on primary SCs, the cultured rat Schwann cell line-RSC 96 cells in 30 mM high-glucose (HG) medium were able to mimic metabolic changes of diabetic patients with DPN.…”

Section: Discussionmentioning

confidence: 99%

Dual Delivery of NGF and bFGF Coacervater Ameliorates Diabetic Peripheral Neuropathy via Inhibiting Schwann Cells Apoptosis

Wu³

et al. 2017

Int. J. Biol. Sci.

View full text Add to dashboard Cite

Diabetic neuropathy is a kind of insidious complications that impairs neural and vascular function and ultimately leads to somatic and visceral denervation. Basic fibroblast growth factor (bFGF) and nerve growth factor (NGF) are important neurotrophic factors for stimulating angiogenesis and improving peripheral nerve function. Administrating a single factor has good therapeutic effect on diabetic peripheral neuropathy (DPN). However, the short half-life and rapid diffusion of growth factors under physiological conditions limits its clinical applications. Here, we used a biodegradable coacervate, composed of heparin and polycation, to dominate the combined release of bFGF and NGF in a steady fashion. We found this combined growth factors (GFs) coacervate, administered as a single injection, improved motor and sensory functions, restored morphometric structure and decreased apoptosis of Schwann cells in a rat model of prolonged DPN. Similarly the GFs coacervate, as compared with free bFGF and NGF combination, markedly reduced the apoptosis level of a rat Schwann cell line, RSC 96 cells in vitro. We also demonstrated that neuroprotective effects of the GFs coacervate in both rat DPN model and hyperglycemia-induced RSC 96 cell model is likely due to suppression of endocytoplasmic reticulum stress (ERS).

show abstract

Section: Discussionmentioning

confidence: 99%

Dual Delivery of NGF and bFGF Coacervater Ameliorates Diabetic Peripheral Neuropathy via Inhibiting Schwann Cells Apoptosis

Wu³

et al. 2017

Int. J. Biol. Sci.

View full text Add to dashboard Cite

show abstract

“…Also, a reduced axon diameter represents a characteristic common in diabetes caused by persistent hyperglycemia. In fact, axonal atrophy is a common finding in diabetic peripheral nerves after short- (15 days)26 and long-term (12 weeks and 12 months) diabetes 2,27. …”

Section: Discussionmentioning

confidence: 99%

Beneficial effects of treadmill training in experimental diabetic nerve regeneration

Malysz

Ilha

Nascimento

et al. 2010

Clinics

View full text Add to dashboard Cite

OBJECTIVES:We investigated the effects of treadmill training (10 weeks) on hindlimb motor function and nerve morphometric parameters in diabetic rats submitted to sciatic nerve crush.MATERIALS AND METHOD:Wistar rats (n = 64) were divided into the following groups: non-diabetic; trained non-diabetic; non-diabetic with sciatic nerve crush; trained non-diabetic with sciatic nerve crush; diabetic; trained diabetic; diabetic with sciatic nerve crush or trained diabetic with sciatic nerve crush. Diabetes was induced by streptozotocin injection (50 mg/kg, iv). Hindlimb motor function was evaluated weekly by assessing sciatic functional indices, and the proximal and distal portions of the sciatic nerve were used for morphometric analysis.RESULTS:At 13 weeks post-injury, the distal nerve portion of all injured groups and the proximal nerve portion of the diabetic with sciatic nerve crush group presented altered morphometric parameters such as decreased myelinated fiber diameter (∼7.4±0.3µm vs ∼4.8±0.2µm), axonal diameter (∼5±0.2µm vs ∼3.5±0.1µm) and myelin sheath thickness (∼1.2±0.07µm vs ∼0.65±0.07µm) and an increase in the percentage of area occupied by endoneurium (∼28±3% vs ∼60±3%). In addition, in the non-diabetic with sciatic nerve crush group the proximal nerve portion showed a decreased myelinated fiber diameter (7.4±0.3µm vs 5.8±0.3µm) and myelin sheath thickness (1.29±0.08µm vs 0.92±0.08µm). The non-diabetic with sciatic nerve crush, trained non-diabetic with sciatic nerve crush, diabetic with sciatic nerve crush and trained diabetic with sciatic nerve crush groups showed normal sciatic functional index from the 4th, 4th, 9th and 7th week post-injury, respectively. Morphometric alterations in the proximal nerve portion of the diabetic with sciatic nerve crush and non-diabetic with sciatic nerve crush groups were either prevented or reverted to values similar to the non-diabetic group by treadmill training.CONCLUSION:Diabetic condition promoted delay in sciatic nerve regeneration. Treadmill training is able to accelerate hindlimb motor function recovery in diabetic injured rats and prevent or revert morphometric alterations in proximal nerve portions in non-diabetic and diabetic injured rats.

show abstract

“…1982;Rodrigues et al 1986). Since the vascular {Reinilrt and Akerblom 1984) and nervous (Bestetti 1981) systems are also affected, it would be reasonable to refer to these rats as a model of poorly controlled type 1 diabetics.…”

Section: Discussionmentioning

confidence: 99%

Hypertriglyceridemia in experimental diabetes: relationship to cardiac dysfunction

Rodrigues

Grassby²,

Battell³

et al. 1994

Can. J. Physiol. Pharmacol.

View full text Add to dashboard Cite

The incidence of mortality from cardiovascular disease is higher in diabetic patients. The objective of the present investigation was to test the hypothesis that the diabetes-induced depression in cardiac function may be due to hypertriglyceridemia. Hyperlipidemia and a depressed left ventricular developed pressure and rate of increase and decrease of ventricular pressure (+/- dP/dt) were produced in isolated hearts from rats made diabetic with streptozotocin compared with hearts from control animals. This depressed cardiac performance was successfully prevented by hydralazine treatment (for 3 weeks), which also lowered plasma triglyceride levels and suggested that hyperlipidemia may be important in altering cardiac function in experimental diabetic rats. The beneficial effects of clofibrate, verapamil, prazosin, enalapril, and benazepril administration were then studied in diabetic rats. The treatments (with the exception of enalapril) significantly reduced plasma triglyceride levels but did not prevent the onset of heart dysfunction in chronically diabetic rats. These studies suggest that in the chronically diabetic rat, hypertriglyceridemia may not be as important as previously suggested, in the development of cardiac dysfunction. Since acute dichloroacetate perfusion improves cardiac function in 6 week (but not 24 week) diabetic rats, it appears more likely that improving myocardial glycose utilization is more critical than triglyceride lowering, in preventing cardiac dysfunction in the diabetic rat at this time point.

show abstract

Changes in peripheral nerves of rats four months after induction of streptozotocin diabetes

Cited by 35 publications

References 6 publications

Dual Delivery of NGF and bFGF Coacervater Ameliorates Diabetic Peripheral Neuropathy via Inhibiting Schwann Cells Apoptosis

Dual Delivery of NGF and bFGF Coacervater Ameliorates Diabetic Peripheral Neuropathy via Inhibiting Schwann Cells Apoptosis

Beneficial effects of treadmill training in experimental diabetic nerve regeneration

Hypertriglyceridemia in experimental diabetes: relationship to cardiac dysfunction

Contact Info

Product

Resources

About