High incidence of sebaceous gland inflammation in aldose reductase-deficient mice.

Aldose reductase is a member of the 1B1 subfamily of aldo-keto reductase gene superfamily. The action of aldose reductase (AR) has been implicated in the pathogenesis of a variety of disease states, most notably complications of diabetes mellitus including neuropathy, retinopathy, nephropathy, and cataracts. To explore for mechanistic roles for AR in disease pathogenesis, we established mutant strains produced using Crispr-Cas9 to inactivate the AKR1B3 gene in C57BL6 mice. Phenotyping AR-knock out (ARKO) strains confirmed previous reports of reduced accumulation of tissue sorbitol levels. Lens epithelial cells in ARKO mice showed markedly reduced epithelial-to-mesenchymal transition following lens extraction in a surgical model of cataract and posterior capsule opacification. A previously unreported phenotype of preputial sebaceous gland swelling was observed frequently in male ARKO mice homozygous for the mutant AKR1B3 allele. This condition, which was shown to be accompanied by infiltration of proinflammatory CD3+ lymphocytes, was not observed in WT mice or mice heterozygous for the mutant allele. Despite this condition, reproductive fitness of the ARKO strain was indistinguishable from WT mice housed under identical conditions. These studies establish the utility of a new strain of AKR1B3-null mice created to support mechanistic studies of cataract and diabetic eye disease.

Nonspecific Orbital Inflammation (NSOI): Unraveling the Molecular Pathogenesis, Diagnostic Modalities, and Therapeutic Interventions.

Nonspecific orbital inflammation (NSOI), colloquially known as orbital pseudotumor, sometimes presents a diagnostic and therapeutic challenge in ophthalmology. This review aims to dissect NSOI through a molecular lens, offering a comprehensive overview of its pathogenesis, clinical presentation, diagnostic methods, and management strategies. The article delves into the underpinnings of NSOI, examining immunological and environmental factors alongside intricate molecular mechanisms involving signaling pathways, cytokines, and mediators. Special emphasis is placed on emerging molecular discoveries and approaches, highlighting the significance of understanding molecular mechanisms in NSOI for the development of novel diagnostic and therapeutic tools. Various diagnostic modalities are scrutinized for their utility and limitations. Therapeutic interventions encompass medical treatments with corticosteroids and immunomodulatory agents, all discussed in light of current molecular understanding. More importantly, this review offers a novel molecular perspective on NSOI, dissecting its pathogenesis and management with an emphasis on the latest molecular discoveries. It introduces an integrated approach combining advanced molecular diagnostics with current clinical assessments and explores emerging targeted therapies. By synthesizing these facets, the review aims to inform clinicians and researchers alike, paving the way for molecularly informed, precision-based strategies for managing NSOI.

Radiation cataract in Heterogeneous Stock mice after γ-ray or HZE ion exposure.

Health effects of space radiation are a serious concern for astronauts on long-duration missions. The lens of the eye is one of the most radiosensitive tissues in the body and, therefore, ocular health risks for astronauts is a significant concern. Studies in humans and animals indicate that ionizing radiation exposure to the eye produces characteristic lens changes, termed "radiation cataract," that can affect visual function. Animal models of radiation cataractogenesis have previously utilized inbred mouse or rat strains. These studies were essential for determining morphological changes and dose-response relationships between radiation exposure and cataract. However, the relevance of these studies to human radiosensitivity is limited by the narrow phenotypic range of genetically homogeneous animal models. To model radiation cataract in genetically diverse populations, longitudinal cataract phenotyping was nested within a lifetime carcinogenesis study in male and female heterogeneous stock (HS/Npt) mice exposed to 0.4 Gy HZE ions (n = 609) or 3.0 Gy γ-rays (n = 602) and in unirradiated controls (n = 603). Cataractous change was quantified in each eye for up to 2 years using Merriam-Focht grading criteria by dilated slit lamp examination. Virtual Optomotry™ measurement of visual acuity and contrast sensitivity was utilized to assess visual function in a subgroup of mice. Prevalence and severity of posterior lens opacifications were 2.6-fold higher in HZE ion and 2.3-fold higher in γ-ray irradiated mice compared to unirradiated controls. Male mice were at greater risk for spontaneous and radiation associated cataracts. Risk for cataractogenesis was associated with family structure, demonstrating that HS/Npt mice are well-suited to evaluate genetic determinants of ocular radiosensitivity. Last, mice were extensively evaluated for cataract and tumor formation, which revealed an overlap between individual susceptibility to both cancer and cataract.

Oxidative stress and antioxidants in cataract development.

PURPOSE OF REVIEW: Oxidative stress plays a central role in cataract pathogenesis, a leading cause of global blindness. This review delves into the role of oxidative stress in cataract development and key biomarkers - glutathione (GSH), superoxide dismutase (SOD), malondialdehyde (MDA), and 4-hydroxynonenal (4-HNE) - to clarify their functions and potential applications in predictive diagnostics and therapies. RECENT FINDINGS: Antioxidants serve as pivotal markers in cataract pathogenesis. GSH affects the central lens due to factors such as enzyme depletion and altered connexin expression, impairing GSH diffusion. Age-related oxidative stress may hinder GSH transport via connexin channels or an internal microcirculation system. N-acetylcysteine, a GSH precursor, shows promise in mitigating lens opacity when applied topically. Additionally, SOD, particularly SOD1, correlates with increased cataract development and gel formulations have exhibited protective effects against posterior subscapular cataracts. Lastly, markers of lipid peroxidation, MDA and 4-HNE, have been shown to reflect disease severity. Studies suggest a potential link between 4-HNE and connexin channel modification, possibly contributing to reduced GSH levels. SUMMARY: Oxidative stress is a significant contributor to cataract development, underscoring the importance of antioxidants in diagnosis and treatment. Notably, GSH depletion, SOD decline, and lipid peroxidation markers are pivotal factors in cataract pathogenesis, offering promising avenues for both diagnosis and therapeutic intervention.

Oxidative stress in the eye and its role in the pathophysiology of ocular diseases.

Oxidative stress occurs through an imbalance between the generation of reactive oxygen species (ROS) and the antioxidant defense mechanisms of cells. The eye is particularly exposed to oxidative stress because of its permanent exposure to light and due to several structures having high metabolic activities. The anterior part of the eye is highly exposed to ultraviolet (UV) radiation and possesses a complex antioxidant defense system to protect the retina from UV radiation. The posterior part of the eye exhibits high metabolic rates and oxygen consumption leading subsequently to a high production rate of ROS. Furthermore, inflammation, aging, genetic factors, and environmental pollution, are all elements promoting ROS generation and impairing antioxidant defense mechanisms and thereby representing risk factors leading to oxidative stress. An abnormal redox status was shown to be involved in the pathophysiology of various ocular diseases in the anterior and posterior segment of the eye. In this review, we aim to summarize the mechanisms of oxidative stress in ocular diseases to provide an updated understanding on the pathogenesis of common diseases affecting the ocular surface, the lens, the retina, and the optic nerve. Moreover, we discuss potential therapeutic approaches aimed at reducing oxidative stress in this context.

[Mechanism of gigantol in transmembrane transport in human lens epithelial cells].

Gigantol is a phenolic component of precious Chinese medicine Dendrobii Caulis, which has many pharmacological activities such as prevent tumor and diabetic cataract. This paper aimed to investigate the molecular mechanism of gigantol in transmembrane transport in human lens epithelial cells(HLECs). Immortalized HLECs were cultured in vitro and inoculated in the laser scanning confocal microscopy(LSCM) medium at 5 000 cells/mL. The fluorescence distribution and intensity of gigantol marked by fluorescence in HLECs were observed by LSCM, and the absorption and distribution of gigantol were expressed as fluorescence intensity. The transmembrane transport process of gigantol in HLECs were monitored. The effects of time, temperature, concentration, transport inhibitors, and different cell lines on the transmembrane absorption and transport of gigantol were compared. HLECs were inoculated on climbing plates of 6-well culture plates, and the ultrastructure of HLECs was detected by atomic force microscopy(AFM) during the transmembrane absorption of non-fluorescent labeled gigantol. The results showed that the transmembrane absorption of gigantol was in time and concentration-dependent manners, which was also able to specifically target HLECs. Energy and carrier transport inhibitors reduced gigantol absorption by HLECs. During transmembrane process of gigantol, the membrane surface of HLECs became rougher and presented different degrees of pits, indicating that the transmembrane transport of gigantol was achieved by active absorption of energy and carrier-mediated endocytosis.

The role of mip in the development of lens in zebrafish.

Major intrinsic protein (MIP) functions as a water channel and a cell-junction molecule in the vertebrate eye lens. The pathogenic mechanism behind the loss of MIP function in the lens, which leads to degraded optical quality and cataract formation, is still unclear. In this study, a zebrafish model with the mipb mutant was produced. The expression of mipb mRNA and protein was dramatically reduced in the mutant. Immunological analysis reveals that loss function of mip leads to the diffuse distribution of ZL-1 in the mutant lens. Furthermore, in situ hybridization reveals that mip knockout results in a decrease in the transcripts of beaded filament structural protein 2 (Bfsp2) in the lens. Histology study shows that lens fibers in the mutants are less uniform in shape and the fiber arrangement is disrupted. The presented data provides evidence for the essential role of mipb in the development of lens fibers. The absence of mipb during lens formation is likely to result in aberrant lens fiber formation and impaired lens function.

A crystallin mutant cataract with mineral deposits.

Connexin mutant mice develop cataracts containing calcium precipitates. To test whether pathologic mineralization is a general mechanism contributing to the disease, we characterized the lenses from a nonconnexin mutant mouse cataract model. By cosegregation of the phenotype with a satellite marker and genomic sequencing, we identified the mutant as a 5-bp duplication in the γC-crystallin gene (Crygcdup). Homozygous mice developed severe cataracts early, and heterozygous animals developed small cataracts later in life. Immunoblotting studies showed that the mutant lenses contained decreased levels of crystallins, connexin46, and connexin50 but increased levels of resident proteins of the nucleus, endoplasmic reticulum, and mitochondria. The reductions in fiber cell connexins were associated with a scarcity of gap junction punctae as detected by immunofluorescence and significant reductions in gap junction-mediated coupling between fiber cells in Crygcdup lenses. Particles that stained with the calcium deposit dye, Alizarin red, were abundant in the insoluble fraction from homozygous lenses but nearly absent in wild-type and heterozygous lens preparations. Whole-mount homozygous lenses were stained with Alizarin red in the cataract region. Mineralized material with a regional distribution similar to the cataract was detected in homozygous lenses (but not wild-type lenses) by micro-computed tomography. Attenuated total internal reflection Fourier-transform infrared microspectroscopy identified the mineral as apatite. These results are consistent with previous findings that loss of lens fiber cell gap junctional coupling leads to the formation of calcium precipitates. They also support the hypothesis that pathologic mineralization contributes to the formation of cataracts of different etiologies.

Congenital glaucoma in a tiger (Panthera tigris).

OBJECTIVE: To describe a case of congenital glaucoma in atiger (Panthera tigris). ANIMAL STUDIED: An 8-month-old intact female tiger wasreferred for suspected glaucoma of the right eye. The right eye was buphthalmicwith moderate episcleral injection, circumferential superficial cornealneovascularization, moderate corneal edema, and a fixed dilated pupil. Tapetalreflection was absent due to a mature cataract. Rebound tonometry under generalanesthesia revealed 70 mmHg and 21 mmHg in the right and left eye, respectively. PROCEDURE: A trans-conjunctival enucleation was performedand the globe was submitted for histopathology. RESULTS: Histopathology revealed a thin sclera, amorphousmaterial contouring an imperforate and hypoplastic iridocorneal angle, ahypoplastic lens with severe anterior-posterior compression, subcapsularepithelial hyperplasia, and Morganian globules, and segmental moderate retinalatrophy. Periodic acid-Schiff stain highlighted segmental dilations of theDescemet's membrane. Masson trichrome stain highlighted a pre-irido collagenmembrane. CONCLUSION: The tiger's age and histopathologic findingsare consistent with congenital goniodysgenesis. This is the first known reportof congenital glaucoma in a tiger.

[Ocular alterations in patients with Alport syndrome-An update]. / Okuläre Veränderungen bei Patienten mit Alport-Syndrom ­ ein Update.

BACKGROUND AND OBJECTIVE: Alport syndrome (AS) is a rare hereditary systemic disease that results in alterations of the kidneys, inner ear, and various structures of the eye. It is caused by mutations in one of the genes encoding collagen type IV. In recent years, new and innovative imaging techniques have added characteristics of ocular alterations in AS and provided new insights, including into the pathogenesis of the disease. The aim of this paper is to provide an overview of the current knowledge of ocular changes in AS, as well as to present the Alport ocular pass. METHOD: Narrative review article. RESULTS: Ocular manifestations of AS include changes in the cornea, lens, and retina. Specifically, posterior polymorphic corneal dystrophy, anterior lenticonus (pathognomonic for AS), and various retinal changes have been described, which have been further characterized in recent years by newer imaging techniques. In particular, foveal changes in AS may present as both a thickened central retina in the context of foveal hypoplasia or a staircase-like thinning of the fovea. Both lesions could provide further insights into the role of type IV collagen in ocular structures. CONCLUSION: The AS can manifest in various structures of the eye. The staircase-like changes of the central retina in AS patients indicate the important role of collagen type IV in the homeostasis and regular function of the inner retinal layers. The often mild foveal hypoplasia may provide clues to the role of collagen type IV in retinal embryogenesis. While anterior lenticonus is pathognomonic for AS and can be treated easily by refractive lens exchange, the only option currently available for retinal alterations is close follow-up and, if necessary, treatment of systemic complications of AS.

In vitro assessment of the severity of deoxyribonucleic acid damage in different types of cataracts directly in lens epithelial cells.

Purpose: This study aimed to assess the severity of deoxyribonucleic acid (DNA) damage in lens epithelial cells (LECs) of senile cortical, nuclear, and posterior subcapsular cataracts. Methods: LECs were obtained from senile cortical, nuclear, and subcapsular types of cataracts after surgery. DNA damage in the cells was immediately assessed quantitatively using the CometScore™ software. Results: Comets were found in cataractous LECs. The formation of "comets" in the DNA of LECs can be visualized using single-cell gel electrophoresis and indicates DNA strand breaks because the damaged DNA migrates at a different rate than the nondamaged DNA. Maximal damage was observed in Grade 3 cortical, nuclear, and subcapsular forms of cataracts. Statistically significant DNA damage was seen between grades 1 and 3 of cortical type of cataract, grades 1 and 3 of nuclear type of cataract, and grades 2 and 3 and grades 1 and 3 of posterior subcapsular type of cataract. Conclusion: In patients with senile cataract, DNA of LECs was randomly damaged, and this type of damage was possibly caused by reactive oxygen species (ROS). Maximum DNA damage was found in patients with Grade 3 senile cortical, nuclear, and subcapsular type cataracts. The pathogenesis of senile cataracts is multifactorial and includes continuous molecular stress resulting from photooxidative stress, UV irradiation, and oxidative reactions.

New technology using crystalline lens autofluorescence for presbyopia and cataract grading.

PURPOSE: To investigate whether fundus autofluorescence (FAF) obtained using an ultra-wide field (UWF) fundus camera with an artificial opacity pattern can grade the degree of presbyopia and nuclear cataract. METHODS: Sixty eyes of 30 patients were enrolled in this prospective diagnostic study. The nuclear cataract (nuclear color/opalescence (NC/NO)) was graded according to the Lens Opacity Classification System III. The monocular near point of accommodation (NPA) was measured in eyes with NC3/NO3 or less. The mean gray value difference between the central 8 artificial opacity lesions and peripheral 8 artificial opacity lesions in the retinal AF was measured. The correlation between the mean gray value difference, NPA, and nuclear cataract grade was analyzed. RESULTS: The mean nuclear cataract grade of 60 eyes was 3.2 ± 1.6 and mean NPA of 37 eyes was 45.3 ± 16.1 cm. The mean gray value differences increased with increasing nuclear cataract grade (eyes with NC/NO grade 1, 53.3 ± 11.4; 2, 78.3 ± 13.6; 3, 95.2 ± 12.2; 4, 101.6 ± 11.9; 5, 109.0 ± 22.9; and 6, 121.1 ± 12.0; p < 0.001). The mean gray value difference was positively correlated with both the monocular NPA (R2 = 0.637; ß coefficient = 1.009; 95% CI, 0.748 to 1.271; p < 0.001) and nuclear cataract grade (R2 = 0.661; ß coefficient = 12.437; 95% CI, 10.097 to 14.778; p < 0.001). CONCLUSIONS: The FAF camera with an artificial opacity pattern attached can be used to effectively diagnose the degree of presbyopia and nuclear cataract.

Pre-hyperglycemia immune cell trafficking underlies subclinical diabetic cataractogenesis.

BACKGROUND: This work elucidates the first cellular and molecular causes of cataractogenesis. Current paradigm presupposes elevated blood glucose as a prerequisite in diabetic cataractogenesis. Novel evidence in our model of diabetic cataract challenges this notion and introduces immune cell migration to the lens and epithelial-mesenchymal transformation (EMT) of lens epithelial cells (LECs) as underlying causes. METHODS: Paucity of suitable animal models has hampered mechanistic studies of diabetic cataract, as most studies were traditionally carried out in acutely induced hyperglycemic animals. We introduced diabetic cataract in the Nile grass rat (NGR) that spontaneously develops type 2 diabetes (T2D) and showed its closeness to the human condition. Specialized stereo microscopy with dual bright-field illumination revealed novel hyperreflective dot-like microlesions in the inner cortical regions of the lens. To study immune cell migration to the lens, we developed a unique in situ microscopy technique of the inner eye globe in combination with immunohistochemistry. RESULTS: Contrary to the existing paradigm, in about half of the animals, the newly introduced hyper reflective dot-like microlesions preceded hyperglycemia. Even though the animals were normoglycemic, we found significant changes in their oral glucose tolerance test (OGTT), indicative of the prediabetic stage. The microlesions were accompanied with significant immune cell migration from the ciliary bodies to the lens, as revealed in our novel in situ microscopy technique. Immune cells adhered to the lens surface, some traversed the lens capsule, and colocalized with apoptotic nuclei of the lens epithelial cells (LECs). Extracellular degradations, amorphous material accumulations, and changes in E-cadherin expressions showed epithelial-mesenchymal transformation (EMT) in LECs. Subsequently, lens fiber disintegration and cataract progression extended into cortical, posterior, and anterior subcapsular cataracts. CONCLUSIONS: Our results establish a novel role for immune cells in LEC transformation and death. The fact that cataract formation precedes hyperglycemia challenges the prevailing paradigm that glucose initiates or is necessary for initiation of the pathogenesis. Novel evidence shows that molecular and cellular complications of diabetes start during the prediabetic state. These results have foreseeable ramifications for early diagnosis, prevention and development of new treatment strategies in patients with diabetes.

Evaluation of Vitreolenticular Interface in Eyes with Fuchs Uveitis.

PURPOSE: To investigate the vitreo-lenticular interface (Berger space) in Fuchs uveitis (FU). METHODS: This cross-sectional study included 20 FU patients (Group 1), the fellow eyes of patients (Group 2) and 20 healthy individuals (Group 3). RESULTS: Berger space was detected in all, and hyperreflective spots were identified in Berger spaces in 65% of FU eyes through optical coherence tomography (OCT). The measurements of Berger space the distance in central, nasal, and temporal 2 mm were 715 ± 101µ, 620 ± 66µ, and 676 ± 76µ in group 1; 370 ± 40µ, 321 ± 41µ, 297 ± 39µ in group 2 and 290 ± 37µ, 267 ± 32µ, 227 ± 28µ in group 3. There was a statistical difference between groups 1, 2nd, and 3rd in all the values. CONCLUSION: The detection of the Berger space is the crucial finding of this study. Visualizing the vitreolenticular area may reveal new insights for pathology and OCT-guided investigations.

Unusual case of double anterior segment with two lenses and double cataract in a 6-month child.

INTRODUCTION: Anterior segment duplicity with two lenses is a rare event which pathogenesis is still unknown. Different ocular and systemic abnormalities might be associated with such event. CASE OBSERVATIONS: Hereby we describe a case of a 6-months female child referred to our service due to signs of ocular malformation in the left eye. The ocular exam showed a double anterior segment with twin lenses in one single eye, associated with double lamellar opacity and persistence of the two hyaloid arteries. The patient underwent surgical treatment with lensectomy and vitrectomy aiming visual stimulation and prevention of definitive visual loss secondary to amblyopia. CONCLUSION: In any case of ocular malformation, efforts to provide adequate visual stimulus are necessary to avoid amblyopia. In our case, the opacified lenses were removed, the patient adapted contact lenses and will be followed-up for visual stimulation at the ophthalmic pediatric division aiming the best visual prognosis possible.

Exosomal microRNA-222-3p increases UVB sensitivity of lens epithelium cells by suppressing MGMT.

BACKGROUND: Age-related cataract (ARC) is a leading cause of blindness worldwide with multiple pathogenic factors. Oxidative damage of lens epithelium cells (LECs) is one of the well-accepted pathogenesis of ARC which can be regulated by DNA repair genes (DRGs). The present research aimed to clarify the regulatory mechanism of exosomal microRNAs (miRNAs) on DRGs in LECs. METHODS: The LECs oxidative damage model was established by UVB-irradiation on SRA01/04 (human lens epithelium cell line). Exosomes from UVB-irradiated cells (UVB-exo) and exosomes from normal control cells (NC-exo) were collected from the culture medium. To explore the functions of LECs exosomes, SRA01/04 were incubated with UVB-exo/NC-exo. Then, we detected SRA01/04 proliferation, viability and apoptosis respectively using 5'-ethynyl-2'-deoxyuridine (EdU), cell-counting kit-8 (CCK-8) and TdT-mediated dUTP Nick-End Labeling (TUNEL) assay. Next, the miRNA expression profiles of UVB-exo and NC-exo were identified by miRNA microarrays. RNA expression in exosomes, cells, and clinical samples was verified by qRT-PCR. The location and expression of MGMT and CD63 proteins were detected by immunofluorescence and western blot. The 3'UTR regulation of miR-222-3p to MGMT was verified by luciferase analyses. RESULTS: MGMT down-regulated while miR-222-3p up-regulated in LECs sub-central anterior capsule from ARC lenses. MGMT and miR-222-3p expressions in central and peripheral LECs from anterior lens capsules were differential. UVB-exo can transport the up-regulated miR-222-3p from oxidative-damaged LECs to normal LECs, which could suppress MGMT expression and increase UVB sensitivity of LECs. CONCLUSIONS: Findings on exosomal miRNA functions provided novel insights into pathogenesis of ARC. Exosomal miR-222-3p can be a potential target for prevention and cure of ARC.

Ocular lesions of captive cephalopods.

Ocular lesions are uncommonly reported and described in invertebrate species. In this study, cases from 2 diagnostic laboratories, in which lesions were noted in 33 diagnostic specimens from various species of cephalopods, including octopuses, squid, nautiluses, and cuttlefish, were reviewed. Clinical information and gross lesions were described in a minority of cases. The most common lesion was inflammation of varying severity and was most commonly within the anterior uvea (iris and ciliary papilla), followed by the posterior chamber and lens. More than half of the cases with inflammation had concurrent hyperplastic lesions of the iris and ciliary papilla, including posterior iris epithelial hyperplasia, cystic adenomatous hyperplasia, and/or posterior epithelial cysts. The most common clinical observation was cloudy eyes, which correlated histologically to anterior uveitis in all cases where it was documented. Dermatitis and cutaneous ulceration were the most frequent comorbidities in cases where clinical information was available.

Investigation of the antioxidant effect of Chrysin in an experimental cataract model created in chick embryos.

PURPOSE: Cataract, which occurs as a result of lens opacification, is one of the most common causes of vision loss. In the literature, deterioration of the antioxidant system due to the increase in reactive oxygen species and oxidant levels is shown among the causes of cataract formation. The aim of this study was to investigate the antioxidant effect of chrysin on steroid-induced cataract development in an experimental chick embryo model using morphological, histological and biochemical parameters. METHODS: Within the scope of the study, 150 specific pathogen free (SPF) fertilized eggs were used. Eggs were divided into 6 groups as control (group 1), corn oil (group 2), hydrocortisone hemisuccinate sodium (HC) (group 3), low dose chrysin (group 4), medium dose chrysin (group 5) and high dose chrysin (group 6). On the 15th day of incubation, Chrysin and HC were applicated to the air sac of the eggs with Hamilton and/or insulin injector. On day 17, the chick embryos were removed from the eggs and the bulbus oculi of the embryos were dissected. Lenses of 9 embryos were used for morpholigical cataract grading in each group, lens of 8 embryos for biochemical analysis and intact eyes of 7 embryos for histological evaluation (TUNEL method). RESULTS: No opacity was observed in any of the lenses in Group 1 and 2. Cataract was observed in all lenses in Group 3. The mean opacity grades in group 3 were statistically significantly higher when compared to group 1 and 2 (p<0.05). The difference between group 6 and group 3 was statistically significant (p<0.05). GSH and TAS levels in the lenses were statistically significantly decreased compared to the control group due to HC application (p<0.05). It was determined that the decreased GSH and TAS levels in the lenses increased in relation to the Chrysin application doses. The increased levels of MDA, TOS, caspase 3 and caspase 9 in the HC group decreased significantly depending to the chrysin doses (p<0.05). In addition, while the rate of apoptotic cells determined by the TUNEL method was statistically significantly higher in the HC administered group than in the control group (p<0.05), it was statistically significantly decreased in the chrysin-administered groups, in relation to the dose of chrysin (p<0.05). CONCLUSIONS: We think that anti-cataract effect of crhysin may be due to the antioxidant and antiapoptotic properties of chrysin. However, more research is needed to clarify the anti-cataract effects of chrysin.

Mechanism of gigantol in transmembrane transport in human lens epithelial cells / 中国中药杂志

Gigantol is a phenolic component of precious Chinese medicine Dendrobii Caulis, which has many pharmacological activities such as prevent tumor and diabetic cataract. This paper aimed to investigate the molecular mechanism of gigantol in transmembrane transport in human lens epithelial cells(HLECs). Immortalized HLECs were cultured in vitro and inoculated in the laser scanning confocal microscopy(LSCM) medium at 5 000 cells/mL. The fluorescence distribution and intensity of gigantol marked by fluorescence in HLECs were observed by LSCM, and the absorption and distribution of gigantol were expressed as fluorescence intensity. The transmembrane transport process of gigantol in HLECs were monitored. The effects of time, temperature, concentration, transport inhibitors, and different cell lines on the transmembrane absorption and transport of gigantol were compared. HLECs were inoculated on climbing plates of 6-well culture plates, and the ultrastructure of HLECs was detected by atomic force microscopy(AFM) during the transmembrane absorption of non-fluorescent labeled gigantol. The results showed that the transmembrane absorption of gigantol was in time and concentration-dependent manners, which was also able to specifically target HLECs. Energy and carrier transport inhibitors reduced gigantol absorption by HLECs. During transmembrane process of gigantol, the membrane surface of HLECs became rougher and presented different degrees of pits, indicating that the transmembrane transport of gigantol was achieved by active absorption of energy and carrier-mediated endocytosis.