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|Title: ||Protection by neuronal growth factors against hyperglycemia induced changes in rat dorsal root ganglion neurons|
|Authors: ||DANIELS, Anneleen|
|Advisors: ||HELLINGS, N.|
DE JONGH, R.
|Issue Date: ||2007|
|Abstract: ||Peripheral neuropathy is a common complication of diabetes that can affect 50% of the
patients. It predisposes the patient to several physiological problems in the lower limbs, which
may lead to gangrene and even amputation. Due to its widespread prevalence and serious
complications it is important to understand the pathogenesis of diabetic neuropathy, so
appropriate therapies can be developed.
In this study the pathogenesis of diabetic peripheral neuropathy was investigated in both an in
vitro and ex vivo model for this disorder. The effect of hyperglycemia on DRG neurons was
investigated by measuring the neuronal stress response, measured by the level of ATF3,
neurite outgrowth and neuronal viability. Both models showed an increase in the ATF3-level
and a decline in neurite outgrowth. There were no significant changes in the number of
apoptotic cells in diabetic rats, compared to control rats. These results indicate that
hyperglycemia is indeed a key player in the development of diabetic neuropathy. In the
second part of the study the beneficial effects of growth factors was documented. Therefore
the effect of Enovin, GDNF and VEGF on the neuronal stress response was investigated. Both
the in vitro and ex vivo model for diabetic neuropathy showed that all three growth factors
can reduce neuronal stress. Furthermore, addition of ENV, GDNF and VEGF increased the
overall neurite outgrowth.
This research indicates that all tested growth factors have a protective effect on
hyperglycemia-induced changes in cultures of DRG neurons. Therefore these compounds can
be considered as possible candidates for the treatment of diabetic peripheral neuropathy.
However, further research must me conducted to test the safety and tolerance of these
compounds before they can be applied for the treatment of this disorder in human patients.|
|Notes: ||Master in de Biomedische wetenschappen - Klinische en moleculaire wetenschappen|
|Type: ||Theses and Dissertations|
|Appears in Collections: ||Master theses|
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