Objective        To determine the role of transient receptor potential channels 6 (TRPC6) in iron metabolism after traumatic brain injury (TBI) in rats and investigate the underlying mechanism.       Methods       Male Sprague-Dawley rats were randomly divided into 3 groups（n=13 for each group）

that is

sham-operation group

TBI group and deferoxamine (DFO) treatment group. Modified Feeney’s method was used to establish the rat model of experimental TBI with an impact of a weight of 30 g from 15 cm after craniotomy. The rats of DFO treatment group were treated with DFO (100 mg/kg

i.p.

administered 2 h after TBI and then at 12-hour intervals for up to 28 d). Nonhemoglobin iron around the injury site was measured. Immunofluorescence staining was used to detect the expression and location of TRPC6 and NeuN

and Western blotting was also used to detect the expression of TRPC6.       Results       The volumes of nonhemoglobin brain iron was significantly decreased in injured group and DFO treatment group than sham-operation group (P0.05)

but there was no difference between TBI group and DFO treatment group. The expression of TRPC6 was up-regulated significantly after TBI compared with sham-operation group. DFO administration significantly down-regulated the expression of TRPC6. After TBI

there were more neurons positive to TRPC6

but few positive to NeuN around the injury site. However

DFO treatment resulted in more neurons positive to NeuN

which was coexpressed with TRPC6.       Conclusion       Over-loading of iron exerts neurotoxic effect in rats after TBI

which may deteriorate the damage of neurons around injury site. TRPC6 maybe play an important role in the neurotoxicity of the process.