Induction of heat shock protein 72 in RGCs of rat acute glaucoma model after heat stress or zinc administration.

PURPOSE

To investigate the dynamics of heat shock protein 72 (HSP72) expression in retinal ganglion cells (RGCs) in rat model of acute glaucoma treated with heat stress or intraperitoneal injection of zinc sulfate.

METHODS

Twenty-seven male Wistar rats were used to make acute glaucoma models. Five others served as normal control. Acute glaucoma models were made by intracameral irrigation in the right eyes with balanced salt saline (BSS) at 102 mmHg for 2 hours. Nine model rats were killed at different intervals after intracameral irrigation without treatment, which served as damage control. Ten were treated with heat stress 40 degrees C-42 degrees C, and 8 were used for zinc sulfate administration 2 days posterior to intracameral irrigation. Treated model rats were sacrificed at designed intervals after treatment. Right eyes were enucleated immediately, and the retinas were dissected for Western blot.

RESULTS

No HSP72 was found in RGCs of normal Wistar rats. In damage control group, slight HSP72 was detected during 6-36 hours posterior to intracameral irrigation. HSP72 was detected significantly expressed in RGCs of both heat shock group and zinc sulfate group. But the dynamics of HSP72 production were quite different in these two treated groups. In heat shock group, HSP72 appeared at the sixth hour after treatment, and increased gradually until its peak production emerged at the 48th hour. HSP72 vanished 8 days later after treatment. In zinc sulfate group, HSP72 expression began 24 hours later after zinc administration, and reached its highest level at the 72th hour posterior to treatment. HSP72 expression then decreased slowly, and disappeared 21 days later after treatment.

CONCLUSION

HSP72 can be induced in RGCs of rat acute glaucoma models with heat stress or zinc sulfate administration. But the dynamics of the HSP72 induction in those two groups were quite different.