Objective To investigate the mechanism of retinal injury in rats caused by light-emitting diodes(LEDs)with different color rendering indexes(CRIs).Methods Totally 20 Sprague-Dawley rats were randomly divided into nor-mal control(NC)group(sunlight),low CRI(CRI-L)group(blue light),medium CRI(CRI-M)group(conventional LED),and high CRI(CRI-H)group(full-spectrum LED),with 5 rats in each group,exposed to light for 12 hours daily for 4 consecutive weeks.Hematoxylin & eosin staining was used to assess morphological changes in the retina.Dihydroethidi-um staining was employed to detect the levels of reactive oxygen species(ROS)in retinal tissues.The messenger ribonu-cleic acid(mRNA)expressions of NOD-like receptor family pyrin domain containing protein 3(NLRP3),Gasdermin D(GSDMD)and Caspase-1 were analyzed by real-time quantitative polymerase chain reaction(RT-qPCR),and their protein expressions were measured through immunohistochemical staining.Environmental light spectra were measured using a spectroradiometer.Results Rats in the CRI-L group showed the thinnest retina,followed by the CRI-M group and CRI-H group.The fluorescence intensity of ROS in the NC group,CRI-L group,CRI-M group and CRI-H group was 1.000±0.046,25.060±1.732,14.530±3.776 and 1.821±0.587,respectively.The ROS level in the CRI-H group was significantly lower than that in the CRI-L group and CRI-M group(both P＜0.05).RT-qPCR showed that the relative mRNA expression of NL-RP3 in the NC group,CRI-L group,CRI-M group and CRI-H group was 1.004±0.005,4.004±0.716,2.027±0.303 and 0.741±0.069,respectively;the relative mRNA expression of Caspase-1 was 1.010±0.006,4.337±0.345,2.268±0.058 and 0.713±0.021,respectively;the relative mRNA expression of GSDMD was 1.000±0.000,2.938±0.559,1.955±0.166 and 1.213±0.051,respectively.Compared with the NC group,the relative expressions of NLRP3,Caspase-1 and GSDMD in the CRI-L group and CRI-M group significantly increased(all P＜0.05).The immunohistochemical staining results showed that the fluorescence intensity of NLRP3 in the retina of rats in the NC group,CRI-L group,CRI-M group and CRI-H group was 0.379 4±0.002 2,0.400 7±0.011 4,0.379 0±0.006 9 and 0.377 0±0.007 5,respectively;the fluorescence intensity of Caspase-1 was 0.367 2±0.005 8,0.442 6±0.041 1,0.382 4±0.011 9 and 0.380 6±0.006 5,respectively;the fluorescence intensity of GSDMD was 0.159 5±0.013 4,0.167 5±0.011 9,0.397 6±0.014 3 and 0.377 2±0.022 8,respec-tively.Compared with the NC group,rats in the CRI-L group showed increased fluorescence intensity of NLRP3 and Caspase-1,and rats in the CRI-M and CRI-H showed increased fluorescence intensity of GSDMD(all P＜0.05).The spec-tral comparison revealed that the CRI-H group had a broader spectral coverage and a distribution closer to natural light spectra.Conclusion Conventional LED exposure can induce a decrease in retinal thickness,upregulate the ROS expres-sion in retinal tissues,and increase the expression levels of NLRP3,Caspase-1 and GSDMD.High CRI full-spectrum LEDs can mitigate pyroptosis through the ROS/NLRP3 pathway by optimizing their spectral distribution,offering better biosafety.

Objective To establish an animal model of dampness-syndrome in mice (single model) and evaluate its characteristics of dampness-syndrome. The above-mentioned mice with dampness syndrome were used to construct mice model of ischemic stroke (double model) and observe the effect of dampness-pathogenic on the outcome of stroke. Methods Healthy C57BL/6J male mice were randomly divided into dampness-syndrome (including sham-surgery group and ischemic stroke group,with 10 mice in each group) and non dampness-syndrome groups (including sham-surgery group and ischemic stroke group,with 10 mice in each group). The dampness-syndrome group was fed with high-fat diet and the non dampness-syndrome group was fed with normal diet for 12 weeks. After the mice model of dampness-syndrome was successfully established,transient middle cerebral artery occlusion/reperfusion (tMCAO/R) surgery was used to replicate an ischemic stroke mice model. Evaluation indicators for dampness-syndrome mice model:the general status including body weight,morphology,posture,activity status,and physical characteristics,the histopathological observation of the aorta (oil red O staining,Masson-trichrome staining) and liver (HE staining,oil red O staining),electron microscopic observation of the tongue tissue (scanning electron microscopy,electron microscopy),blood lipid levels[total cholesterol(TC),triglycerides(TG)]and liver coefficient. Evaluation indicators for ischemic stroke mice model:neurological function score and the cerebral infarction volume ratio. Results Compared with the non dampness-syndrome group,the mice in the dampness-syndrome group showed an increased in body weight,poor hair color,sparse hair,fatigue and laziness,mental atrophy,anorexia and lethargy. It was observed that the aortic lumen was narrowed,the intima was significantly thickened,lipid plaque deposition was increased,and foam cells were visible. A large amount of red lipid droplets appeared in liver cells. There were obvious lipid infiltration and diffuse steatosis. Increased keratosis of the mucosal layer of tongue tissue,the thicker stratum corneum,lipofuscin,and bacteria on the tongue surface were found. Serum TG and TC levels significantly increased(P<0.01),and the liver coefficient significantly decreased (P<0.001). Compared with non dampness-syndrome group (sham-surgery group),neurological function score and the cerebral infarction volume ratio in dampness-syndrome ischemic stroke group obviously increased (P<0.001). Conclusion High-fat feeding for 12 weeks combined with tMCAO/R modeling can successfully establish a mice model with dampness-syndrome ischemic stroke,and the neurological function score and cerebral infarction volume in the dampness-syndrome ischemic stroke group was more severe than that in the non dampness-syndrome ischemic stroke group.