Blue Light Exposure Research Articles

Blue light-driven cell cycle arrest in thyroid cancer via Retinal-OPN3 complex

BackgroundPapillary thyroid carcinoma (PTC) is the most common type of thyroid malignancy, with a rising incidence. Traditional treatments, such as thyroidectomy and radiotherapy, often lead to significant side effects, including impaired thyroid function. Therefore, there is an urgent need for non-invasive therapeutic approaches. This study aims to explore the potential of photobiomodulation therapy (PBMT), a non-invasive treatment using specific wavelengths of light, in the management of PTC.MethodsWe investigated the effects of blue light PBMT on PTC cells, focusing on the Retinal-OPSIN 3 (OPN3) complex’s role in mediating cellular responses. Blue light exposure was applied to PTC cells, and subsequent changes in cellular proliferation, cell cycle progression, and protein expression were analyzed. Statistical tests, including one-way ANOVA and t-tests, were used to evaluate the significance of the findings.ResultsBlue light exposure led to the dissociation of 11-cis-retinal from OPN3, resulting in the accumulation of all-trans retinal. This accumulation disrupted cellular proliferation pathways and induced G0/G1 cell cycle arrest in PTC cells. The Retinal-OPN3 complex was found to be a key mediator in these processes, demonstrating that thyroid cells can respond to specific light wavelengths and utilize their photoreceptive potential for therapeutic purposes.ConclusionsOur findings suggest that PBMT, through the modulation of the Retinal-OPN3 complex, offers a promising non-invasive approach for treating PTC. This study highlights the therapeutic potential of light signal transduction in non-ocular tissues and opens new avenues for non-invasive cancer therapies.

The ameliorating effects of adipose-derived stromal vascular fraction cells on blue light-induced rat retinal injury via modulation of TLR4 signaling, apoptosis, and glial cell activity.

Blue light (BL)-induced retinal injury has become a very common problem due to over exposure to blue light-emitting sources. This study aimed to investigate the possible ameliorating impact of stromal vascular fraction cells (SVFCs) on BL-induced retinal injury. Forty male albino rats were randomly allocated into four groups. The control group rats were kept in 12-h light/12-h dark. Rats of SVFC-control as the control group, but rats were intravenously injected once by SVFCs. Rats of both the BL-group and BL-SVFC group were exposed to BL for 2 weeks; then rats of the BL-SVFC group were intravenously injected once by SVFCs. Following the BL exposure, rats were kept for 8 weeks. Physical and physiological studies were performed; then retinal tissues were collected for biochemical and histological studies. The BL-group showed physical and physiological changes indicating affection of the visual function. Biochemical marker assessment showed a significant increase in MDA, TLR4 and MYD88 tissue levels with a significant decrease in TAC levels. Histological and ultrastructural assessment showed disruption of the normal histological architecture with retinal pigment epithelium, photoreceptors, and ganglion cell deterioration. A significant increase in NF-κB, caspase-3, and GFAP immunoreactivity was also detected. BL-SVFC group showed a significant improvement in physical, physiological, and biochemical parameters. Retinal tissues revealed amelioration of retinal structural and ultrastructural deterioration and a significant decrease in NF-κB and caspase-3 immunoreactivity with a significant increase in GFAP immunoreaction. This study concluded that SVFCs could ameliorate the BL-induced retinal injury through TLR-4/MYD-88/NF-κB signaling inhibition, regenerative, anti-oxidative, and anti-apoptotic effects.

Thioflavin-T: application as a neuronal body and nucleolar stain and the blue light photo enhancement effect

Thioflavin-T (THT) is a common and indispensable tool for the study of amyloid pathologies and protein aggregation, both in vitro and for histological samples. In this study we expand the use of THT beyond its canonical usage for staining amyloid plaques and demonstrate its novel use as an easy and rapid stain comparable to fluorescent Nissl staining, allowing for clear discernment of neuronal cell bodies and also nucleoli in fixed tissue and live cells. We believe that this is of value for any lab that studies central nervous system (CNS) tissues. Furthermore, we show that THT could potentially be used as a an alternative to the use of fluorescent reporters or other more costly RNA binding compounds in the study of nucleolar dynamics owing to its ability to clearly stain nucleoli in live cells. We also discovered the previously unreported effect of blue light exposure on the photo enhancement of THT excited by a 488 nm laser in stained tissue sample and how to avoid complications arising from this effect. Finally, we provide a simple protocol that can be easily adjusted either for using THT as a neuronal cell body and nucleoli stain, compatible with antibody based staining methods tested up to 4 fluorophores, or alternatively by using an additional washing step the protocol may be used for amyloid plaque detection in fixed brain tissue.

Effects of light quality on agronomic traits, antioxidant capacity and nutritional composition of Sarcomyxa Edulis

Sarcomyxa edulis, a notable edible and medicinal mushroom indigenous to northeast China, is celebrated for its high nutritional value and delightful taste. In this study, white light as a control and examined the effects of red, green, and blue light on the agronomic traits, antioxidant capabilities, and nutritional composition of S. edulis. The results showed that different monochromatic light qualities affected the color of S. edulis pileus, with blue light demonstrating particular efficacy. Furthermore, blue light also regulated pileus length, whereas red light was instrumental in significantly increasing stalk length. Regarding antioxidant capacity, compared with red and green light, the activities of POD, SOD, and CAT were significantly improved by blue light irradiation, decreased MDA levels, and improved free radical scavenging potential. Additionally, blue light exposure led to an increase in the contents of 15 amino acids. Green light treatment reduced the crude fat content. For the first time, we found that light quality is a key factor in controlling the color of S. edulis. Blue light is an effective way to regulate the color and pileus size of S. edulis, and improve the antioxidant properties. The photobiological characteristics and the response of nutritional quality to light environment of S. edulis were clarified.

A Selective Melatonin 2 Receptor Agonist, IIK7, Relieves Blue Light-Induced Corneal Damage by Modulating the Process of Autophagy and Apoptosis

This study aims to investigate the effect of the selective MT2 receptor agonist, IIK7, on corneal autophagy and apoptosis, aiming to reduce corneal epithelial damage and inflammation from blue light exposure in mice. Eight-week-old C57BL/6 mice were divided into BL-exposed (BL) and BL-exposed with IIK7 treatment (BL + IIK7 group). Mice underwent blue light exposure (410 nm, 100 J) twice daily with assessments at baseline and on days 3, 7, and 14. Corneal samples were analyzed for MT2 receptor expression, autophagy markers (LC3-II and p62), and apoptosis indicators (BAX expression and TUNEL assay). Then, mice were assigned to normal control, BL, and BL + IIK7. Ocular surface parameters, including corneal fluorescein staining scores, tear volume, and tear film break-up time, were evaluated on days 7 and 14. On day 14, reactive oxygen species (ROS) levels and CD4+ IFN-γ+ T cells percentages were measured. The BL group exhibited higher LC3-II and p62 expression, while the BL + IIK7 group showed reduced expression (p < 0.05). The TUNEL assay showed reduced apoptosis in the BL + IIK7 group compared to the BL group. ROS levels were lower in the BL + IIK7 group. The BL + IIK7 group showed improved ocular surface parameters, including decreased corneal fluorescein staining and increased tear volume. The percentages of CD4+ IFN-γ+ T cells indicated reduced inflammatory responses in the BL + IIK7 group. The MT2 receptor agonist IIK7 regulates corneal autophagy and apoptosis, reducing corneal epithelial damage and inflammation from blue light exposure.

Effect of stress mitigation measures on the aggressive behaviour and body weight loss of Large White Yorkshire crossbred pigs during transportation

This study examined the impact of stress mitigation measures on the live body weight loss and skin lesion scores of Large White Yorkshire pigs after a 200 km transportation by road. Twenty-four LWY pigs were randomly allotted into four groups of six each: control group (T1 ), pigs injected with vitamin E and selenium (T2 ), pigs administered hydrogen rich water (T3 ), and pigs exposed to monochromatic blue light (T4 ). Hydrogen-rich water administration (T3 ) resulted in the highest live body weight loss, while exposure to monochromatic blue light (T4 ) induced the lowest. Shrinkage during transport mirrored the live body weight loss trend. Significant differences emerged in skin lesion scores, notably in the hindquarter and tail regions. Monochromatic blue light exposure (T4 ) correlated with reduced aggressive behaviour, evidenced by lower hindquarter skin lesion scores. Conversely, hydrogen-rich water administration (T3 ) resulted in higher tail region skin lesion scores. The findings suggest that exposure to monochromatic blue light may have a calming effect during transport and can be recommended as a stress mitigation strategy to enhance overall animal welfare during transportation Keywords: Transportation stress, body weight loss, shrinkage, aggressive behaviour

An Invisible Dermal Nanotattoo-Based Smart Wearable Sensor for eDiagnostics of Jaundice.

Despite substantial progress in the diagnosis of jaundice/hyperbilirubinemia as the most common disease and cause of hospitalization of newborns, on the eve of Industry/Healthcare 5.0, the development of accurate and reliable wearable diagnostic sensors for noninvasive smart monitoring of bilirubin (BIL) is still in high demand. Aiming to fabricate a smart wearable sensor for early diagnosis of neonatal jaundice and its therapeutic monitoring, we here report a fluorescent dermal nanotattoo that further coupled with an IoT-integrated wearable optoelectronic reader for minimally invasive, continuous, and real-time monitoring of BIL in interstitial fluid. Selective recovery of quenched fluorescence of the dermal tattoo sensor, composed of biocompatible dissolving/hydrogel microneedles loaded with fluorescent carbon quantum dots, upon blue light exposure used for jaundice phototherapy was utilized for highly selective BIL sensing. The fascinating features of our developed smart wearable tattoo sensor and its successful results with high correlation with blood BIL results make it a highly promising sensor for easy, minimally invasive, reliable, and smart eDiagnostics and continuous therapeutic eMonitoring of jaundice and other BIL-induced diseases at the point of care. We envision that the developed nanotattoo sensing bioplatform will inspire the development of future smart tattoo sensors in various diagnostic and monitoring scenarios.

Alleviation effect of lutein Pickering emulsion formed by casein-dextran conjugates through Maillard reaction against blue light retinal degeneration

With the increasing prevalence of electronic devices, awareness of the risks linked to blue light exposure has significantly heightened. Lutein, a powerful antioxidant, safeguards eye tissue by filtering blue light, while supplementation with docosahexaenoic acid (DHA) enhances retinal function. Adequate intake of these nutrients can help reduce the potential damage from prolonged blue light exposure. The protective effects of lutein and algal oil stabilized with Pickering emulsion were investigated using casein-dextran (CD) conjugates via Maillard reaction. Microstructural analysis revealed a three-dimensional network structure surrounding oil droplets formed by CD conjugates. With the increase of the oil phase ratio from 55 % to 80 %, the average size of Pickering emulsion droplets decreased. Pickering emulsion demonstrated higher viscoelasticity, excellent recovery, thixotropy, and good thermal stability as the oil phase ratio increased. The retention of lutein in CD-75 % Pickering emulsions showed significant improvement under various conditions. Simulated gastrointestinal digestion demonstrated that CD-75 % Pickering emulsions effectively enhanced the lutein bioaccessibility from 19.97 % to 48.99 %. In vivo experiments showed that lutein-loaded Pickering emulsion could effectively relieve blue light-induced retinal degeneration in mice. These findings suggested that Pickering emulsion can serve as a delivery system to protect lutein, offering a nutritional intervention to mitigate blue light-induced retinal degeneration.

Comparison of Nocifensive Behavior in NaV1.7-, NaV1.8-, and NaV1.9-Channelrhodopsin-2 Mice by Selective Optogenetic Activation of Targeted Sodium Channel Subtype-Expressing Afferents.

Voltage-gated sodium channels, including NaV1.7, NaV1.8, and NaV1.9, play important roles in pain transmission and chronic pain development. However, the specific mechanisms of their action remain unclear, highlighting the need for invivo stimulation studies of these channels. Optogenetics, a novel technique for targeting the activation or inhibition of specific neural circuits using light, offers a promising solution. In our previous study, we used optogenetics to selectively excite NaV1.7-expressing neurons in the dorsal root ganglion of mice to induce nocifensive behavior. Here, we further characterize the impact of nocifensive behavior by activation of NaV1.7, NaV1.8, or NaV1.9-expressing neurons. Using CRISPR/Cas9-mediated homologous recombination, NaV1.7-iCre, NaV1.8-iCre, or NaV1.9-iCre mice expressing iCre recombinase under the control of the endogenous NaV1.7, NaV1.8, or NaV1.9 gene promoter were produced. These mice were then bred with channelrhodopsin-2 (ChR2) Cre-reporter Ai32 mice to obtain NaV1.7-ChR2, NaV1.8-ChR2, or NaV1.9-ChR2 mice. Blue light exposure triggered paw withdrawal in all mice, with the strongest response in NaV1.8-ChR2 mice. These light sensitivity differences observed across NaV1.x-ChR2 mice may be dependent on ChR2 expression or reflect the inherent disparities in their pain transmission roles. In conclusion, we have generated noninvasive pain models, with optically activated peripheral nociceptors. We believe that studies using optogenetics will further elucidate the role of sodium channel subtypes in pain transmission.

Protective Effects of Purple Corn (Zea mays L.) Byproduct Extract on Blue Light-Induced Retinal Damage in A2E-Accumulated ARPE-19 Cells.

This study investigated the antioxidative characteristics of Zea mays L. purple corn cob and husk extract (PCHE) and its potential protective effects against blue light (BL)-induced damage in N-retinylidene-N-retinylethanolamine (A2E)-accumulated ARPE-19 retinal pigment epithelial cells. PCHE had a 2,2-diphenyl-1-picrylhydrazyl radical-scavenging capacity and Trolox equivalent antioxidant capacity of 1.28±0.43 mM Trolox equivalents (TE)/g and 2,545.41±34.13 mM TE/g, respectively. Total content of anthocyanins, polyphenols, and flavonoids in the PCHE was 11.13±0.10 mg cyanidin-3-glucoside equivalents/100 g, 227.90±7.38 mg gallic acid equivalents/g, and 117.75±2.46 mg catechin equivalents/g, respectively. PCHE suppressed the accumulation of A2E and the photooxidation caused by BL in a dose-dependent manner. After initial treatment with 25 µM/mL A2E and BL, ARPE-19 cells showed increased cell viability following additional treatment with 15 µg/mL PCHE while the expression of the p62 sequestosome 1 decreased, whereas that of heme oxygenase-1 protein increased compared with that in cells without PCHE treatment. This suggests that PCHE may slow the autophagy induced by BL exposure in A2E-accumulated retinal cells and protect them against oxidative stress.

Maintaining KEAP1 levels in retinal pigment epithelial cells preserves their viability during prolonged exposure to artificial blue light

Exposure to artificial blue light, one of the most energetic forms of visible light, can increase oxidative stress in retinal cells, potentially enhancing the risk of macular degeneration. Retinal pigment epithelial (RPE) cells play a crucial role in this process; the loss of RPE cells is the primary pathway through which retinal degeneration occurs. In RPE cells, Kelch-like ECH-associated protein 1 (KEAP1) is located in both the nucleus and cytosol, where it binds to nuclear factor erythroid 2-related factor 2 (NRF2) and p62 (sequestosome-1), respectively. Blue light exposure activates the NRF2-heme oxygenase 1 (HMOX1) axis through both canonical and noncanonical p62 pathways thereby reducing oxidative damage, and initiates autophagy, which helps remove damaged proteins. These protective responses may support the survival of RPE cells. However, extended exposure to blue light drastically decreases the viability of RPE cells. This exposure diminishes the ability of KEAP1 to bind to p62 and reduces the level of KEAP1. Inhibition of autophagy does not prevent KEAP1 degradation, the NRF2-HMOX1 axis, or blue-light-induced cytotoxicity. However, proteasome inhibitor along with a transient increase in the amount of KEAP1 in RPE cells, partially restores the p62-KEAP1 complex and reduces blue-light-induced cytotoxicity. In vivo studies confirmed the downregulation of KEAP1 in damaged RPE cells. Mice subjected to periodic blue light exposure exhibited significant atrophy in the outer retina, particularly in the peripheral areas. Additionally, there was a significant decrease in c-wave electroretinography and pupillary light reflex, indicating functional impairments in both visual and nonvisual physiological processes. These data underscore the essential role of KEAP1 in managing oxidative defense and autophagy pathways triggered by blue light exposure in RPE cells.

Nvestigating How Blue Light Exposure Affects the Health of the Cornea

nvestigating How Blue Light Exposure Affects the Health of the Cornea

Is blue light solely detrimental for human eyes?

It has long been assumed that blue light is solely detrimental to the eyes and that it is a serious risk factor for a number of ocular diseases. In order to gain a more nuanced comprehension of the impact of blue light on the eye and to ascertain whether there are any beneficial aspects to this influence, this article presents a synthesis of the relevant research and offers updates on the current understanding of the subject matter. The review encompasses the environmental and societal changes that result in increased light exposure, the working principle and reasons for the prevalence of light-emitting diodes, and the safety classification of artificial light sources. Subsequently, we present the impact of blue light on ocular growth and the known mechanisms by which blue light affects different areas of the eye, including the cornea, conjunctiva, lens and retina. Finally, we discuss the validity of blue-blocking lenses and review other recommended strategies aimed at minimising the negative effects of blue light exposure.

Alkaline electrolyzed water-assisted ultrasonic extraction of lutein from daylily (Hemerocallis spp.): Structural preservation and activity evaluation

During lutein extraction, isomerization from all-trans to cis form reduced stability and antioxidant capacity. Alkaline electrolyzed water (AEW), with its reduced-state and small molecular clusters, effectively extracted bioactive substances and inhibited oxidation. Thus, an AEW-assisted ultrasonic extraction method was used to extract lutein from daylily. Compared to ultrasonic extraction alone, AEW treatment increased the lutein yield by 60 %. Structural analysis confirmed the preservation of all-trans lutein by AEW. Assess AEW extraction's impact on lutein's bioactivity by examining its protection against blue light cell damage. The results showed that that lutein extracted using AEW exhibited enhanced antioxidant capacity, significantly boosting the viability of ARPE-19 cells and the activity of intracellular antioxidant enzymes, thereby mitigating oxidative stress damage to the retina caused by blue light exposure. This study provided an effective method for efficiently extracting bioactive substances and preventing the impact of the extraction process on their structure and function.

Optogenetic induction of mechanical muscle stress identifies myosin regulatory ubiquitin ligase NHL-1 in C. elegans

Mechanical stress during muscle contraction is a constant threat to proteome integrity. However, there is a lack of experimental systems to identify critical proteostasis regulators under mechanical stress conditions. Here, we present the transgenic Caenorhabditis elegans model OptIMMuS (Optogenetic Induction of Mechanical Muscle Stress) to study changes in the proteostasis network associated with mechanical forces. Repeated blue light exposure of a muscle-expressed Chlamydomonas rheinhardii channelrhodopsin-2 variant results in sustained muscle contraction and mechanical stress. Using OptIMMuS, combined with proximity labeling and mass spectrometry, we identify regulators that cooperate with the myosin-directed chaperone UNC-45 in muscle proteostasis. One of these is the TRIM E3 ligase NHL-1, which interacts with UNC-45 and muscle myosin in genetic epistasis and co-immunoprecipitation experiments. We provide evidence that the ubiquitylation activity of NHL-1 regulates myosin levels and functionality under mechanical stress. In the future, OptIMMuS will help to identify muscle-specific proteostasis regulators of therapeutic relevance.

Betahistine mesylate reduces the damage of blue light exposure in Drosophila model

Previous studies have demonstrated the efficacy of betahistine mesylate in treating vertigo and angioneurotic headache, enhancing microcirculation, and facilitating histamine release. However, limited research has been conducted on the drug's potential in mitigating blue light-induced damage. Thus, this study utilized Drosophila as the model organism and employed the Siler model to investigate the impact of various concentrations of betahistine mesylate on the lifespan, under 3000 lx blue light irradiation. At the same time we measure food intake, spontaneous activity, and sleep duration of Drosophila. The findings of this study indicate that a high concentration of betahistine mesylate can decrease the initial mortality (b0) in male flies, mitigating the damage of blue light to Drosophila. Consequently, this delays the aging process in male Drosophila and extends their average lifespan. After betahistine mesylate ingestion, locomotor activity upon blue light exposure decreased significantly in male Drosophila. In conclusion, this study offers initial evidence supporting the investigation of the regulatory mechanisms of betahistine mesylate on lifespan and its potential anti-blue light effects.

Light-responsive adipose-hypothalamus axis controls metabolic regulation

Light is fundamental for biological life, with most mammals possessing light-sensing photoreceptors in various organs. Opsin3 is highly expressed in adipose tissue which has extensive communication with other organs, particularly with the brain through the sympathetic nervous system (SNS). Our study reveals a new light-triggered crosstalk between adipose tissue and the hypothalamus. Direct blue-light exposure to subcutaneous white fat improves high-fat diet-induced metabolic abnormalities in an Opsin3-dependent manner. Metabolomic analysis shows that blue light increases circulating levels of histidine, which activates histaminergic neurons in the hypothalamus and stimulates brown adipose tissue (BAT) via SNS. Blocking central actions of histidine and denervating peripheral BAT blunts the effects of blue light. Human white adipocytes respond to direct blue light stimulation in a cell-autonomous manner, highlighting the translational relevance of this pathway. Together, these data demonstrate a light-responsive metabolic circuit involving adipose-hypothalamus communication, offering a potential strategy to alleviate obesity-induced metabolic abnormalities.

Blue light photobiomodulation induced osteosarcoma cell death by facilitating ferroptosis and eliciting an incomplete tumor cell stress response

To investigate the potential of blue light photobiomodulation (PBM) in inducing ferroptosis, a novel form of regulated cell death, in OS cells, considering its known effectiveness in various cancer models. In this investigation, we exposed human OS cell lines, HOS and MG63, to different wavelengths (420, 460 and 480 nm) of blue light at varying irradiances, and examined cellular responses such as viability, apoptosis, levels of reactive oxygen species (ROS), and mitochondrial membrane potential (MMP). Transcriptome sequencing was employed to unravel the molecular mechanisms underlying blue light-induced effects, with validation via quantitative real-time PCR (qRT-PCR). Our findings revealed a wavelength- and time-dependent decrease in cell viability, accompanied by increased apoptosis and oxidative stress. Transcriptomic analysis identified differential expression of genes associated with ferroptosis, oxidative stress, and iron metabolism, further validated by qRT-PCR. These results implicated ferroptosis as a significant mechanism in the blue light-induced death of OS cells, potentially mediated by ROS generation and disruption of iron homeostasis. Also, An incomplete stress response was observed in MG63 cells induced by blue light exposure. Hence, blue light PBM holds promise as a therapeutic approach in OS clinical investigations; however, additional exploration of its underlying mechanisms remains imperative.

Protective effect and mechanism of Lycium ruthenicum Murray anthocyanins against retinal damage induced by blue light exposure.

Lycium ruthenicum Murray (LR) is a medicine and edible plant in Northwest China, and L. ruthenicum Murray anthocyanins (LRA) are green antioxidants with various pharmacological activities, such as antioxidant and anti-inflammatory activities. However, the protective effect and mechanism of LRA against retinal damage induced by blue light exposure are poorly understood. This study explored the protective effects and potential mechanisms of LRA on retinal damage induced by blue light exposure invitro and invivo. The results showed that LRA could ameliorate oxidative stress injury by activating the antioxidant stress nuclear factor-related factor 2 pathway, promoting the expression of phase II detoxification enzymes (HO-1, NQO1) and endogenous antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase), and reducing reactive oxygen species and malondialdehyde levels. Additionally, LRA could inhibit inflammatory response by decreasing the expression of blue light exposure-induced nuclear factor-κB (NF-κB) pathway-related proteins (NF-κB and p-IκBα), as well as interleukin (IL)-6, tumor necrosis factor-α, IL-1β pro-inflammatory factors and pro-inflammatory chemokine VEGF, and increasing the expression of anti-inflammatory factor IL-10. Furthermore, LRA could ameliorate oxidative stress-induced apoptosis by upregulating Bcl-2 and downregulating Bax and Caspase-3 protein expression. All these results indicate that LRA can be used as an antioxidant dietary supplement for the treatment or prevention of retinal diseases.

Decrease of alpha-crystallin A by miR-325-3p in retinal cells under blue light exposure

Exposure to blue light can lead to retinal degeneration, causing adverse effects on eye health. Although the loss of retinal cells due to blue light exposure has been observed, the precise molecular mechanisms underlying this process remain poorly understood. In this study, we investigate the role of alpha crystallin A (CRYAA) in neuro-retinal degeneration and their regulation by blue light. We observed significant apoptotic cell death in both the retina of rats and the cultured neuro-retinal cells. The expressions of Cryaa mRNA and protein were significantly down-regulated in the retina exposed to blue light. We identified that miR-325-3p reduces Cryaa mRNA and protein by binding to its 3'-untranslated region (UTR). Up-regulation of miR-325-3p destabilized Cryaa mRNA and suppresses CRYAA, whereas down-regulation of miR-325-3p increased both expressions. Blue light-induced neuro-retinal cell death was alleviated by CRYAA overexpression. These results highlight the critical role of Cryaa mRNA and miR-325-3p molecular axis in blue light-induced retinal degeneration. Consequently, targeting CRYAA and miR-325-3p presents a potential strategy for protecting against blue light-induced retinal degeneration.