Cidosporin A inhibiting expression of interleukin-1β in rats with diffuse axonal injury / 中华创伤杂志

ABSTRACT

Objective To observe the expression of interleukin-1β (IL-1β) in blood serum after axonal injury in rats and investigate the effects of ciclosporin A (CsA) on it so as to discuss mechanism of CsA protecting neural function. Methods A total of 75 adult male SD rats were randomly divided into control group (Group A with 5 rats), only optic nerve stretch group (Group B with 35 rats) and stretch plus CsA treatment group (Group C with 35 rats). Stretch injury was induced in the right optic nerves of the rats in Group B and C. CsA at 20 mg/L was intraperitonealy injected in Group C immediately after stretch injury. Five animals from both Group B and Group C were killed at 1,3, 6, 12 hours and at days 1,3 and 7 after stretch injury or injection of CsA respectively. Morphological changes of optic nerves and retinal ganglion cells (RGCs) after stretch injury were examined under light microscope. In the mean- time, expression of IL-1β in the blood serum was observed by means of radioimmunoassay. Results (1) Histopathological observation showed lose of R GCs at day 3 and disarranged nerve fiber at day 7 after stretch injury of optic nerve in Group B, but significant amelioration of corresponding changes in Group C. (2) The expression of IL-1β in blood serum in Group B was significantly higher than that in Group A 3, 6, 12 hours and 1 day after injury. The expression of IL-1β reached peak at the 6th hour, then de- creased gradually and returned to the similar level of Group A after 3 days. The expression pattem of IL- 1 β in blood serum of Group C decreased more significantly at 3, 6, 12 hours and 1 day compared with that in Group B but was still higher than that of Group A at 6, 12 hours and 1 day. Conclusions The long-term and excessive expression of IL-1β may be involved in the secondary pathological changes after axonal injury. CsA exerts neuroprotective effect on injured axons mostly by attenuation of inflammation re- action after axonal injury.