Objective To investigate the effect of micropulse di ode laser treatment on the retina in Brown-Norway rats (BN Rats). Methods 130 eyes of BN rats received irradiance of different powers of micr opulse diode laser with 810nm wavelength through a contact lens. Fundus color photography and fundus fluorescein angiography (FFA) were performed on day 1, 3, 7, 14 and 28 days after treatment. Animals were sacrificed on 1, 3, 7, 14 and 28 days separately for historical study. The expression of heat shock protein-70 (HSP-70) in the retina was observed with immunohistochemistry. Cell apoptosis of retina tissue was examined by TdT mediated dUTP nick end labeling (TUNEL). Results (1) No change was found in no visible reaction laser spots by light microscope. High duty cycles with threshold and suprathreshold en ergies can produce severe damage even to the inner nuclear layer. (2) HSP-70 ex pression was markedly increased in the inner nuclear layer at 1d after micropulse diode laser. This increase in HSP-70 expression peaked at day 3 whereafter a decline near to normal at 2 weeks was detected. (3) Apoptosis was detected mainl y in retinal pigment epithelium, outer nuclear layer, inner nuclear layer and ev en choroid by TUNEL after micropulse diode laser treatment. The TUNEL-positive cells increased with the laser power. Maximum TUNEL-positive cells could be seen at day 3 after treatment. Conclusions The retinal injury has positive relationship with laser energy. The thermal damage is confined to the RPE and spare the neurosensory retina when using threshold power (50mW) with 50% duty-cycle and supra-threshold power with high duty-cycle (100mW，5%～15%). The hyper expression of HSP-70 and apoptosis mechanism may play an important role in the tissue repair process. (Chin J Ocul Fundus Dis,2008,24:122-126)
Objective To assess the effects of 670nm LED (lightemitting diode) to protect the photoreceptor from the lightinduced damage in a rat model. Methods 32 SD rats were randomly assigned to one of eight groups: untreated control group, the LEDtreated control group, three groups of lightinduced damage，and three groups of lightinduced damage treated with LED. Lightinduced damage result from exposing to constant light for 3 hours of different illuminations of 900，1800 and 2700 lx, respectively. The LED treatment (50 mW) was delivered for 30 minutes at 3 hours before the light damage and 0，24 and 48 hours after the light damage. Retinal function and morphology were measured by electroretinogram (ERG) and histopathology assay. Results The illumination of 900 lx for 3 hours did not damage the rat retina. The illumination of 1800 lx for 3 hours resulted in thinner ONL and no OS and IS. The ratio of damaged area/total retinal area was 048plusmn;012， the damaged thickness of ONL/normal ONL (L5 ) was 039plusmn;007，and the amplitude of ERG b wave was (431plusmn;120) mu;V. With the LED treatment the ratio of damaged area decreased (M6=017plusmn;0.12, P5/6=0.002), and the ratio of the damaged thickness of ONL also decreased (L6=0.22plusmn;0.09, P5/6lt;0.01), and the amplitude of ERG b wave increased to (1011plusmn;83) mu;V（P5/6lt;0.001）. The illumination of 2700 lx for 3 hours caused severed damage to the rat retina and the LED could not protect them significantly. Conclusions 670 nm LED treatment has an evident protective effect on retinal cells against light-induced damage, which may be a simple and effective therapy to prevent or to delay agerelated macular degeneration.