1: Ann N Y Acad Sci.  2002 Nov;973:359-62.  

Inhibition of p38 MAP kinase corrects biochemical and neurological deficits in
experimental diabetic neuropathy.

Agthong S, Tomlinson DR.

Division of Neuroscience, School of Biological Sciences, University of
Manchester, Oxford Road, Manchester M13 9PT, UK.

Diabetes is known to activate MAP kinase p38 in sensory neurons in both rats and
patients. In vitro, activation of p38 in sensory neurons by combined glucose and
oxidant stress causes cell damage or death. Consequently we tested the
hypothesis that inhibition of MAP kinase p38 might prevent neuronal dysfunction
in rats with experimental diabetes, such as the classical defect of slowed nerve
conduction. Thus, treatment of streptozotocin-diabetic rats with the p38
inhibitor SB239063 for the second half of a 12-week diabetes protocol
selectively prevented the nerve conduction deficit in sensory neurons. This
implicates activation of MAP kinase p38 as an early step in the signal pathway
to dysfunction in experimental diabetic neuropathy.

PMID: 12485893 [PubMed - indexed for MEDLINE]