Objective  To observe the expressions of heat shock protein 70 (HSP70) and Tau in retinal ganglion cells (RGCs) after stretch injury to right optic nerve in rats and the effect of heat stress on HSP 70 and Tau expressions in order to explore the mechanism of neuroprotective role of HSP70.    Methods  Fifty-seven male Wistar rats were randomly divided into 4 groups

that is

control group (Group A

3 rats)

stretch-only group (Group B

18 rats)

heat stress group (Group C

18 rats) and heat stress pretreatment plus stretch group (Group D

18 rats). Stretch injury was induced in the right optic nerves of rats according to Gennarelli’s model stimulating diffuse axonal injury. Heat stress was applied to animals by keeping their rectal temperature up to 42 ℃ in water bath. Animals in Group D inflicted the stretch injury 24 h after heat stress. Three rats respectively from Group B

Group C and Group D were killed at 4

8 and 16 h

1

3 and 5 d after injury respectively. Morphological changes of optic nerves and RGCs after stretch injury were examined under light microscope. The expressions of HSP70 and Tau in RGCs were observed using immunohistochemistry.   Results  Obvious pathological changes of axons and RGCs after stretch injury were identified morphologically or quantitatively

and significantly ameliorated through pretreatment with heat stress before stretch injury. The increased expressions of HSP70 and Tau in RGCs occurred Group B. The increased expression of HSP70 and no change of expression of Tau were observed in Group C. A much more enhanced expression of HSP 70 with an earlier peak and longer maintenance period and a significantly decreased expression of Tau were found in Group D.   Conclusion  The increased expression of Tau is associated to delayed axotomy and neuron apoptosis. The neuroprotection of HSP70 is likely based its effect on reducing aggregation of Tau. A new approach to treatment of diffuse axonal injury(DAI) may be developed through the enhancement of intrinsic neuroprotective functions.