Background
Diabetes can result in pathological changes to enteric nervous system. Our
Methods
A single injection of streptozotocin (STZ) was used to establish diabetic rats. Animals were randomly distributed into diabetic 1-, 4-, 8-, and 16-week groups, as well as age-matched control groups. The PGP9.5- and glial fibrillary acidic protein (GFAP)-immunopositive cells were quantified by immunohistochemistry. The protein levels of PGP9.5, ChAT, nNOS, S-100β, and c-fos were determined by western blotting. The levels of nerve growth factor (NGF), neurotrophin 3 (NT-3), and glial cell-derived neurotrophic factor (GDNF) were tested by ELISA. Key
Results
An increase in blood glucose and a decrease in body weight were observed following STZ administration. PGP9.5 expression did not change in the diabetic ileum. However, ChAT increased after 16 weeks, and nNOS decreased after 8 and 16 weeks in the ilea of diabetic rats. The absence of degeneration of enteric neurons during the acute stage of the disease could be the consequence of the up-regulation of GFAP, S-100β, and c-fos. Moreover, the content of NGF, NT-3, and GDNF in the ileum increased by varying degrees after 1 and/or 4 weeks of diabetes. Using 2 co-culture models of EGCs and SH-SY5Y cells in a high glucose condition, the supportive role of EGCs was further confirmed. Conclusions & inferences: Enteric glial cell activation can protect enteric neurons from damage due to diabetes in the acute stage of the disease, in part via the promotion of neurotrophin release.