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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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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.