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AIM:To investigate the neuroprotective effect of 17β-estradiol(E2)on retina light damage in BALB/c and C57BL/6 mice and provide experimental data for the successful construction of a research model for E2 against retinal light damage.METHODS:Totally 40～45 adult female BALB/c or C57BL/6 mice were divided into six groups, 6 for each group: normal control, ovariectomized control, ovariectomized light(mice were stimulated with continuous white light at 10000 lx for 4, 8, 12, 16, and 24h after 14d of ovariectomy), intravitreal administration sham operation, saline and E2 pre-treatment groups(2μL saline or 10-5mol/L E2 were intravitreal injected respectively after 14d of ovariectomy operation and 24h of dark adaptation). The morphological and functional changes of the retina were detected by paraffin section HE staining, TUNEL staining and electroretinogram.RESULTS:In the ovariectomized light group, the thickness of the inner/outer nuclear layer decreased significantly from the 4h stimulation of 10000 lx white light group. Intravitreal administration of E2 significantly inhibited the apoptosis of retinal cells in the two strains of mice(P<0.01)and the decrease of amplitudes of a- and b-waves in max-ERG of C57BL/6 mice(P<0.05).CONCLUSION:The light loss sensitivity of two strains of mice was different under the same light stimulation. E2 had a protective effect on both morphology and function of the retina in BALB/c mice, and had a significant protective effect on retina function in C57BL/6 mice.
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The retina is a highly specialized tissue with unique structure and adaptability. Maintaining dynamic balance in all different types of retinal cells is essential for maintaining vision. The retina may be exposed to a variety of environmental damage such as light-induced damage, and over the course of evolution, retinal cells have developed adaptive responses to various injuries that together restore dynamic cellular homeostasis and increase the resistance of the tissue to further damage. Howecer, excessive exposure to light can cause a series of pathological changes in photoreceptors, retinal ganglion cells(RGC), retinal glial cells and retinal pigment epithelium(RPE)cells, such as increased expression of reactive oxygen species(ROS)and Ca2+ in mitochondria, apoptosis, endoplasmic reticulum stress, autophagy and inflammation, etc., leading to irreversible damage to the retina. In the present article, the possible pathogenesis and current related research progress of light-induced injury were reviewed, in order to provide research directions for the prevention and treatment of retinal light injury.
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Objective:To explore the potential synergistic protective mechanism of Glycyrrhizae Radix et Rhizoma-Granati Pericarpium formula compound by using the methods and tools of network pharmacology，and provide a basis for the modernization of traditional Chinese medicine（TCM） compounds and the discovery of new drugs. Method:Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP） was used to obtain the active components of Glycyrrhizae Radix et Rhizoma-Granati Pericarpium formula and their corresponding targets. The obtained targets were input to the UniProt database to inquire the gene names corresponding to the targets. By searching the CTD database，Genecards database and OMIM database of disease-related websites，the anti-sunburn targets were obtained. The interaction of the active targets was analyzed with online STRING database to screen the predicted core targets. The gene ontolog（GO） gene function enrichment analysis and Kyoto encyclopedia of genes and genomes（KEGG） pathway enrichment analysis of the predictive targets were performed by using DAVID database. Cytoscape 3.6.1 software was used to make "drug-component-target" network diagram，"protein-protein interaction" network diagram and "component-target-pathway" network diagram. Online website Draw Venn Diagram was used to show the relationship between disease targets and drug predicted targets. R Studio software was used to draw the functional enrichment analysis diagram of GO gene and KEGG pathway. Molecular docking between the active ingredients and the core targets was performed using GOLD software. Result:The 16 active compounds were collected，such as liquiritin，glycyrrhizin，kaempferol and quercetin. The active components mainly acted on 5 core targets：protein kinase B1（AKT1），interleukin（IL）-6，vascular endothelial growth factor（VEGFA），tumor necrosis factor（TNF） and tumor suppressor gene （TP53） and played a role in anti-sunburn effect primarily through these pathways such as hepatitis B，pathways in cancer，toxoplasmosis，chagas disease（American trypanosomiasis），and TNF signaling pathway. Conclusion:Based on the method of network pharmacology，the present study has preliminarily explored the anti-sunburn targets and pathways of Glycyrrhizae Radix et Rhizoma-Granati Pericarpium formula，and further verified the characteristics of multi-component and multi-target treatment of diseases in TCM，so as to provide certain scientific ideas for the modernization research of Chinese herbal compound prescriptions.
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【Objective】 To investigate whether 17β-estradiol (βE2) can activate the NF-E2-related factor 2(Nrf2) pathway to resist the downregulation of retinal function induced by light damage. 【Methods】 Two weeks after female SD rats were castrated, they were divided into the following six groups: control group (control), light-damage group (LD), saline group, saline light-damage group (saline-LD), βE2 group, and βE2 light-damage group (βE2-LD). Rats in the light-damage were exposed to 8000-lux fluorescence for 12 h after 18 h of dark adaptation. Then electroretinogram (ERG), immunofluorescence, Real-time PCR and immunohistochemical detection were performed after one day of dark recovery. 【Results】 The results of ERG showed that ERG was lower in LD group than in control group (P<0.05). After light damage, ROS was increased and the mRNA expressions of antioxidant genes, such as Sod1, Sod2, Cat, Glrx1, Glrx2, Txn1, and Txn2 were decreased (all P<0.05). After βE2 administration, compared with those in saline-LD, ROS level was decreased, the levels of Nrf2 protein and antioxidant genes were increased, and ERG was recovered to a certain extent in βE2-LD (P<0.05). 【Conclusion】 βE2 can restore the function of rat retina, and its mechanism might be related to the upregulation of Nrf2 and antioxidant genes.
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@#AIM: To observe whether exposure to natural light causes damage on corneal tissue in infant rhesus monkeys with monocular hyperopic defocus induced by PRK. <p>METHODS: Twelve infant rhesus monkeys(aged 2mo)were treated monocularly with PRK(-4.0D)and divided into two groups: AL group(<i>n</i>=6)and NL group(<i>n</i>=6). The monkeys in AL were reared under artificial lighting(indoor).The monkeys in NL were exposed to natural lighting(outdoor)for 4h per day(9:00-11:00 and 15:00-17:00), and to indoor lighting for the rest of the light phase. Corneal haziness after PRK was assessed biomicroscopically using the Fantes scale. At 50d post-PRK, tear fluids of both eyes from 8 monkeys in the two groups(4 animals each group)were collected and analyzed for 11 kinds of cytokines using protein microarray analysis. At 180d post-PRK. The corneas were obtained and evaluated by histopathological examination, immunohistochemistry with antibody to TGF-β1 and α-SMA, and TUNEL. The vitality of SOD and the level of MDA in corneas were detected with WST-1 and lipid peroxidation MDA assay kits, respectively.<p>RESULTS: The monkeys in AL group exhibited a lesser degree of haze than those in NL group at 40d following PRK(<i>P</i>=0.015). At 50d post-PRK, EGF and TGF-β1 levels in tears were different in PRK-treated eyes between the two groups(<i>P</i>=0.045, 0.038), and TGF-β1 were significantly different between both eyes in the same group(AL: <i>P</i>=0.003; NL: <i>P</i>=0.036). At 180d post-PRK, there were no differences in histological changes, the expression of TGF-β1 and α-SMA, and apoptosis cell staining of the corneal between the two groups. The vatility of SOD and the levels of MDA in corneal epithelium were not different between the two groups(<i>P</i>>0.05).<p>CONCLUSION: Exposure to natural light in our study could not induce light damage to the normal cornea of the infant rhesus monkeys, but it could aggravate the corneal tissue repair reaction transiently post-PRK.
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Objective@#To investigate the protective effect of human umbilical cord mesenchymal stem cells (UCMSCs) on light-damaged retinal pigment epithelial (RPE) cells in vitro.@*Methods@#Human UCMSCs were cultured, and then identified by flow cytometry.Human RPE cells were isolated and cultured, and then the model of light-damaged RPE cells was prepared.The noncontact co-culture system of light-damaged RPE cells and UCMSCs was established by Transwell chamber.RPE cells were divided into normal control group, model control group and UCMSCs co-culture group.RPE cells in the normal control group were not treated.RPE cells in the model control group were treated with blue light to induce RPE cell damage.Co-culture system of light-damaged RPE cells and UCMSCs was established in the UCMSCs co-culture group.The proliferative ability of RPE cells was measured by methyl thiazolyl tetrazolium (MTT) assay at 24 hours and 48 hours after co-culture.ELISA kits were used to quantitatively measure the levels of pigment epithelium-derived factor (PEDF) and basic fibroblast growth factor (bFGF) in the culture supernatant at 48 hours after co-culture.And the photoreceptor outer segments (POS) phagocytosis assay of RPE cells was also conducted.@*Results@#UCMSCs displayed spindle-shaped morphology, positively expressed CD29, CD44, CD90 and CD105, while negatively expressed CD34 and CD45.RPE cells were polygonal in morphology and positive for the specific marker RPE65 protein.The proliferative ability(A value) of RPE cells in the three groups at different timepoints were significantly different (Fgroup=132.388, P=0.000; Ftime=231.440, P=0.000), the A values of RPE cells in model control group and UCMSCs co-culture group were significantly lower than that in the normal control group, the A value of RPE cells in UCMSCs co-culture group was significantly higher than that in the model control group, and the differences were statistically significant both at 24 hours and 48 hours after co-culture (all at P<0.01). POS phagocytosis test showed that there was a significant difference in the average number of POS particles phagocytized by RPE cells among the three groups(F=28.087, P=0.000). The average number of POS particles phagocytized by RPE cells in model control group was significantly lower than that in normal control group, and the average number of POS particles phagocytized by RPE cells in UCMSCs co-culture group was significantly more than that in model control group (all at P<0.01). ELISA showed that the concentrations of PEDF in RPE cell supernatant of normal control group, model control group and UCMSCs co-culture group were (18.8±1.9), (10.0±1.7) and (20.2±6.0)ng/ml, respectively.The concentrations of bFGF in RPE cell supernatant were (25.2±1.5), (26.3±3.6) and (61.9±14.3)pg/ml, respectively.There were significant differences in PEDF and bFGF concentrations among the three groups (F=8.654, P=0.008; F=23.698, P=0.000). The concentration of PEDF in the model control group was significantly lower than that in the normal control group, and the concentration of PEDF in the UCMSCs co-culture group was significantly higher than that in the model control group (all at P<0.01). The concentration of bFGF in UCMSCs co-culture group was significantly higher than that in the normal control group and model control group (all at P<0.01).@*Conclusions@#Cocultivation with UCMSCs can improve the proliferation ability and phagocytosis function of light-damaged RPE cells, and promote the secretion of PEDF by RPE cells.UCMSCs may protect RPE cells from light damage through paracrine secretion of bFGF.
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Objective To investigate the role of leukemia inhibitory factor (LIF) on retinal photoreceptor cells and the underlying mechanism after light damage.Methods Fifty 5-6 weeks old BALB/c mice were randomly divided into normal control group (10 mice),light damage+LIF group (20 mice) and light damage+PBS group (20 mice).Four days before exposing to light,the right eye of each animal in light damage+LIF group and light damage+PBS group was injected with LIF and PBS,respectively;then the mice in the light damage+LIF group and light damage+PBS group were exposed to 4 000 lx intensity of cool white fluorescent light for 4 hours to establish the experimental model of retinal light damage.The function and morphology of retinal photoreceptor cells were detected by flash electroretinogram (fERG) and histopathological examination.Real-time PCR was used to detect the mRNA expression of Jak3,STAT3,and apoptosis-related factor Bcl-2 and Bax.The use of animals is guided by the State Science and Technology Commission's regulations on the management of experimental animals.Results The amplitudes of scotopic ERG a wave of 0.01,1,100,200,400 cd · s/m2 light in the light damage + PBS group were significantly lower than those in the normal control group and light damage + LIF group (all at P ＜ 0.05).The amplitudes of photopic ERG b wave of different color light in the light damage+PBS group were significantly lower than those in the normal control group and light damage+LIF group (all at P＜0.05).The number of photoreceptor nuclei in the light damage+PBS group was significantly lower than that in the normal control group and light damage+ LIF group (both at P＜0.05).Compared with light damage+PBS group,the relative expression of Jak3,STAT3,Bcl-2 mRNA in light damage+LIF group were significantly increased (all at P＜0.05),and the relative expression of Bax mRNA were significantly decreased (P＜0.05).Conclusions LIF can protect retinal photoreceptor cells from light damage,which may result from the activation of Jak3/STAT3 signaling pathway and inhibition of its downstream Bax/Bcl-2 apoptotic pathway.
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Objective To investigate the protective role of light preconditioning in retinal photoreceptor cells and the underlying mechanisms after light damage.Methods Together 42 BALB/c mice were randomly divided into normal control group,light damage group,light preconditioning + light damage group and light preconditioning group.Mice in the light damage group were exposed to 4000 Lux intensity of cool white fluorescent light for 4 h continually;mice in the light reconditioning + light damage group were maintained in 600 Lux cyclic bright light for preconditioning (12 h ON and 12 h OFF) for 6 days,and then exposed to 4000 Lux bright-light for the induction of the damage;mice in the light reconditioning group were maintained in 600 Lux cyclic bright light for preconditioning (12 h ON and 12 h OFF) for 2 days,4 days,6 days.Then the function and morphology of retinal photoreceptor cells were detected by flash electroretinogram (FERG) and histopathological examination in the normal control group,light damage group and light preconditioning + light damage group,while real-time polymerase chain reaction (PCR) was used to detect the mRNA relative expression of leukemia inhibitory factor (LIF) and Western blot analysis was used to detect the phosphoprotein relative expression of signal transducer and activator of transcription 3(STAT3) in the light preconditioning group.Results FERG results showed the amplitudes of scotopic ERG a wave of the light damage group were decreased when compared with the normal control group,with significant difference (P =0.000).Compared with the light damage group,the amplitudes of scotopic ERG a wave of the light preconditioning + light damage group were increased significantly (P =0.000).Histopathological examination results showed that the number of photoreceptor nuclei in the light damage group was decreased compared with the normal control group,and the difference was statistically significant (P =0.000).Compared with light damage group,the number of photoreceptor nuclei in light preconditioning + light damage group was increased significantly (P =0.000).Real-time PCR results showed light preconditioning enhanced the LIF mRNA relative expression in a time-dependent manner (F=128.776,P =0.000).Western blot results showed light preconditioning up-regulated the phosphoprotein relative expression of STAT3 protein in a time-dependent manner (F =73.493,P =0.000).Conelusion Light preconditioning can protect retinal photoreceptor cells against light damage which may results from the activation of LIF/STAT3 signaling pathway.
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Objective To investigate protective effect of tribulus terrestris L (TTL) on photoreceptor in the model of light-induced retinal degeneration.Methods BALB/c mice were exposed to bright light at the intensity of 10 000 lux for 30 minutes to establish the retinal light damage models.The BALB/c mice were divided into normal control group,model group and treatment group,6 cases in each group.TTL decoction was intraperitoneally administered to mice 30 minutes prior to illumination in the treatment group.Saline vehicle was administered in the normal control group and model group.Photoreceptor protection of TTL was assessed by optical coherence tomography (OCT) at 3 hours and 7 days after illumination.Gross histology and immunohistochemistry approaches were also taken to examine the retinal protection conferred by TTL at 7 days after bright light exposure.Results Compared to normal retinal morphology in the normal control group,prominent photoreceptor loss and diminished rod and cone photoreceptors evidenced by attenuated retinal expression of rhodopsin and M-opsin were observed in the model group.In contrast,TTL treatment resulted in significant protection against bright light-induced photoreceptor degeneration and remarkable preservation of rod and cone photoreceptor cells.The outer retinal nuclear layer in the model group was thinner than that in the normal control group (P ＜ 0.05),but the treatment group was thicker than the model group (P ＜ 0.05).Conclusion Bright light induces obviously degeneration in photoreceptors in BALB/c mice.Moreover,TTL is shown for the first to significantly protect the photoreceptors from bright light-induced degeneration.
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AlM:To discuss the protective effect ofα-mangostin on retinal light damage in mice.METHODS:Totally 30 Balb/c mice, aged 6~8wk, were randomly divided into the control group, light-exposure group and α-mangostin group. Every group contained 10 mice. Mice of α-mangostin group were treated with alpha-mangostin at the dose of 30mg/( kg · d ) body weight by intragastric administration daily for 7d, and then exposed to white light at the 5th d. The light-exposure group and α-mangostin group were exposed to 5 000 ± 200lx white light-emmiting diodes (LEDs) for continuously 1h to establish the mice model of retinal light damage. Flash -electroretinograme was recorded 72h after light exposure. The changes in retinal morphology of mice were observed by light microscopy. Retinas were extracted to detect the malondialdhyde ( MDA ) content change of the retinal homogenate.RESULTS: Flash-electroretinogram ( F-ERG ) showed that retinal dysfunction was less severe in α-mangostin group than in light-exposure group ( P<0. 05 ). Light microscopy test showed that retina structural damage was less severe in α-mangostin group than in light-exposure group (P<0. 05). The level of MDA in retinal tissue of α-mangostin group was significantly lower when compared with light-exposure group (P<0. 05).CONCLUSlON: α-mangostin inhibits lipid peroxidation induced by light damage and protect retina against light damage.
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AIM: To investigate the effect of low intensity white light irradiation on the retinas of mice. METHODS: Thirty C57BL/6J mice were randomly divided into two groups. The number of the mice in each group was 15. The mice in experimental group received dark adaptation from 5:00p. m. to 6:00p. m. , and then exposed to LED white light from 6:00p. m. to 7:00p. m. everyday for a month. At 1, 3, 7, 14 and 30d after the beginning, we examed the histology of mice retinas, calculated the thickness of outer nuclear layer ( ONL ) , inner nuclear layer ( INL ) and analyzed electrophysiology of mice. RESULTS:One month after experiment, compared to the control group, the latency of Rod-R a wave of the mice in experimental group significantly prolonged, the amplitude of Cone-R b wave of the mice in experimental group significantly decreased and the latency of b wave of the mice in experimental group significantly prolonged ( P CONCLUSION: 100lux low intensity white light could give rise to the impairment of the retinal functions in dark-adapted mice.
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Background Investigating the association of blue light-induced damage of retinal pigmenepithelial (RPE) cellwith intracellulaCa2+ conteniimportanfounderstanding the mechanism of retinal disorders.Objective Thistudy wato establish blue light-induced damage model of human RPE celland explore the relationship between the damage of RPE cell and intracellulaCa2+ content.MethodHuman RPE cellwere cultured and passaged.Cell vitality waassayed by trypan blue staining.Fourth-generation cellwere used in these experiments.The cellwere exposed to blue lighwith an intensity of (2000±500)lx fo3,6,9 o12 hours,and the rate of apoptosiwaassayed by TUNEL to assesthe optimal irradiation time focellcultured.The cellwere then randomized into the withouirradiation group,irradiation only group,nifedipine group,ligh+ nifedipine group,(-) BayK8644 group and ligh+ (-) BayK8644 group.The laseconfocal microscope waused to determine the fluorescence intensity of intracellulafree Ca2+ aan excitation wavelength of 488 nm and an emission wavelength of 505 nm.The cell imagewere analyzed using computesoftware.The differenceof fluorescence intensity among the differengroupwere compared by one-way analysiof variance.ResultTrypan blue staining showed thathe viability of RPE cellwamore than 90％ afteculturing and passaging.No apoptoticell waseen aftelighexposure fo3 hours.However,differennumberof apoptoticellappeared aftelighexposure fo6,9 and 12 hours.The fluorescence intensity of intracellulafree Ca2+ in the nifedipine group wasignificantly lowethan thaof the withouirradiation group othe ligh+ nifedipine group(both aP=0.000).Lasescanning confocal microscopy showed thathe fluorescence intensitieof intracellulafree Ca2+ in the irradiation only group,(-) BayK8644 group,ligh+ (-)BayK8644 group were highethan thaof the withouirradiation group,with statistical significancebetween them(all P=0.000).No significandifferencewere found in the fluorescence intensity of intracellulafree Ca2+ between the ligh+ nifedipine group and withouirradiation group awell abetween the (-)BayK8644 group and the ligh+(-) BayK8644 group(P =0.339,P =0.410).ConclusionThe optical conditionfoblue light-induced RPE cell damage were exposure of blue-ligha(2000± 500) lx fo6 hourand culturing the cellfo24 hours.Blue lighexposure can induce damage of human RPE cellprobably by triggering the increase of intracellulafree Ca2+ concentration.
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Background The cryptochrom 2 (Cry2)in mammalian retina is a main influential factor of circadian clock.Objective Purpose of this study was to investigate the effect of light exposure rhythm on expression of Cry2 in retina.Methods Thirty clean healthy Sprague Dawley(SD)rats were collected and divided into two groups randomly.The rats of the control group exposed to natural light with the normal rhythm for 30 days,but rats of the experimental group exposed to the artificial light (light: dark =18 hours:6 hours) for 3 months with the light intensity of(533± 16)lx.The histopathological change and ultrastructural alteration of rat retina in both groups were examined under the light microscope and transmission electron microscope at the end of the experiment.Expressions of Cry2 protein and its mRNA were assayed by immunohistochemistry and quantitative PCR(Q-PCR).Results The rat retinal morphology and ultrastructure were clear and order-arranged under the light microscope and transmission electron microscope in the control group.However,atrophy and disorganization of retina were found under the light microscope,and liquefaction and vacuole of outer segments of photoreceptors were observed.The vacuolar degeneration of mitochondria in the inner segments of photoreceptors,cellular nuclear shrinkage,chromatin margination,nuclear notch and destruction were seen in the outer nuclear layer under the transmission electron microscope.Immunohistochemistry showed that the expression of Cry2 protein located in cytoplasm and nuclei membrane of the retinal ganglion cell layer and inner nuclear layer in both normal rats and experimental rats.The scores of Cry2 protein expression were 0.833±0.197 in the experimental group,and 1.700±0.245 in the control group,with a significant difference between them (P=0.009).The quantities of Cry2 mRNA were 0.962 ± 0.125 in the control group and 0.615±0.100 in the experimental group,showing a significant difference between the two groups (P =0.006).Conclusions Long-term light exposure under the 533 lx leads to retinal structural and functional damage probably by down-regulating Cry2 expression in retina.Whether the regulation of Cry2 expression is helpful for stabilizing the biorhythm or not is a worthy question to explore.
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AIM: To investigate whether the Acrysof Natural has the protective function for retina from blue light in morphology.METHODS: Fresh porcine eye cups were formed in vitro. Blue light beam between 420-450nm spectrum eradiated the porcine retina and cultured RPE cells in 30J/cm2 and 40J/cm2, respectively. The adjacent region in 3mm diameter was eradiated in various ways: exposed directly to light, through AcrySof one piece IOL, PMMA IOL,AcrySof Natural IOL, and without light. Then the eye cups were cultured for 48h. Lastly, tissue and cell structure were observed with light microscope and transmission electron microscope (TEM).RESULTS: In the retinal region without light, the structure of every layer was clear, cells in neuroepithelial layer arrayed in rule, some bubble presented in external granular layer and internal granular layer, RPE cells were compact, and the color of pigment article was coincident. In the region with direct blue light and that with 30J/cm2+Acrysof one-piece/ pMMlA, cells on photoreceptor and external granular layer were lost partially, bubble increased, RPE cells were with different sizes, and cell edema, cell lost and pigment article cluster could be seen.. In region with 30J/cm2+Natural, a little disorganization could be seen comparing to that without light, but more normal than those with Acrysof and direct eradia tion. When the power was 40J/cm2, the situation was similar to that with 30J/cm2 but more severe.CONCLUSION: ① the blue light intensity in 30J/cm2 and 40J/cm2 could both induce the acute retinal light injury, ② AcrySof one piece IOL and other PMMA IOLhave no obvious effect no retina comparing to direct eradiation, ③AcrySof Natural can weaken the injury of blue light to some extent.
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Objective To evaluate the application of optical coherence tomography (OCT) in the rat retinal light damage. Methods Albino Sprague-Dawley (SD) rats (5-8 weeks of age) were exposed to 1 000-1 400 lux of diffuse, cool, white, fluorescent light for 2, 5, and 7 d. OCT image analysis and histological measurements of the retinal thickness were performed. Animals were then sacrificed and the measured results were compared with those by histological examination. Results The sensory retinal thickness of the retina in the rats thinned progressively as the retinal degeneration was in progress. The sensory retinal thickness measured by OCT [the corresponding thickness was (179.11?12.01)?m, (159.27?12.81)?m, and (133.67?11.43)?m, respectively] was well correlated with that measured by histology [the sensory retinal thickness after exposure to the light for 2, 5, and 7 d was (144.26?9.36)?m, (116.16?11.24)?m, and (94.27?10.68)?m, respectively] (r= 0.995, P