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Diabetic keratopathy is one of the common ocular complications of diabetes, and diabetic patients are often accompanied by changes in the morphological structure of the corneal endothelium.Oxidative stress, inflammation, apoptosis, glucose metabolism disorders, mitochondrial injury, and endoplasmic reticulum stress are the main mechanisms of the occurrence and progression of diabetic keratopathy.Studies have shown that advanced glycation end products can activate and induce the formation of a large number of reactive oxygen species (ROS), which in turn causes cell damage and even apoptosis.Mitochondria are the source of ROS, which will be damaged when a large amount of ROS accumulate, and mitochondrial autophagy will be formed when the body removes damaged mitochondria.Mitophagy refers to the process of eliminating aging, dysfunctional, damaged mitochondria through selective autophagy, which is a key mechanism for mitochondria to maintain function.The decrease in the level of mitophagy will lead to the destruction of the hexagonal structure of the diabetic corneal endothelium and its dysfunction, and upregulating the level of mitophagy can play a protective role on corneal endothelium in oxidative stress.The role of mitophagy in diabetic corneal endothelial lesions were reviewed in this article.
ABSTRACT
Diabetic keratopathy is a chronic complication of diabetes caused by abnormal metabolites accumulation, oxidative stress, abnormal inflammation and corneal neuropathy.It can result in delayed corneal epithelial healing and decreased corneal sensitivity under the stimulation of ocular trauma or surgery which bring great challenges to clinicians.Activation of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammatory is one of the factors that cause chronic complications of diabetes, and is also an important factor for delaying the healing of diabetic wounds.The NLRP3 inflammatory signaling pathway is closely related to corneal oxidative stress, delayed epithelium healing and development of corneal neuropathy.In this paper, the research status and prospects of NLRP3 inflammatory signaling pathway and diabetic keratopathy were reviewed to provide new ideas for studying the mechanism and treatment of diabetic keratopathy.
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@#It is estimated that currently, about 46%-64% of patients with diabetes mellitus(DM)suffer from diabetic keratopathy(DK). With the increasing prevalence of DM, DK has gradually been concerned by ophthalmologists. Nevertheless, its pathogenesis is not yet clear. Oxidative stress is a pathological process that causes excessive production of reactive oxygen species(ROS)and reactive nitrogen species(RNS)in the body, which damages tissues and cells. It participates in the occurrence and development of many diseases, including the ocular complications of DM. This study aims to review the research progress of oxidative stress in the pathogenesis and the treatment of diabetic corneal lesions, thus providing references for clinical diagnosis and treatment of DK.
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Objeetive To explore the influence of extracellular high glucose on the proliferation,migration and biomarkers of corneal limbal stem cells.Methods Establishment of a model of high glucose in cultured human limbal stem cells to observe and investigate the effects of extracellular high glucose on the proliferation and migration of corneal limbal stem cells by immunoflurescence,CCK-8 and Transwell assay,respectively.Totally 16 SPF rats were collected and induced diabetic model by streptozotocin as the high-glucose group,and the normal rats of the same age served as the control group.Corneal epidermises of rats in both groups were scraped to observe the repair of corneal epithelium.And the corneas were treated with HE staining and immunohistochemical staining to detect the expression of biomarkers of corneal limbal stem cells and the modality changes of cells.Results The proliferation rate of human limbal epithelial cells was significantly decreased when exposed to high glucose,and the rate at 24 h,48 h and 72 h was 0.728,0.345 and 0.395,respectively,which was markedly lower than that in the control group,with a significant difference (P ＜ 0.05);meanwhile the cell migration rate of the high-glucose group was 17.6％ at 48 h,which was significantly slower than that of the control group (100％).And the inhibition was accompanied by the decreased expression of β-catenin and vimentin.Furthermore,the expression levels of β-catenin and vimentin mRNA and protein were down-regulated,with abnormal location,in the high-glucose group.And diabetic rats had poor corneal epithelial healing.The epithelial layer became thinner and the structures were disorganized in diabetic rats through HE staining.The immunohistochemical assay revealed the expression of β-catenin and vimentin of cornea limbal stem cells was down-regulated in high-glocose group when compared with the control group.Conclusion High glucose can significantly inhibit the proliferation and migration of cornea limbal stem cells,and its main damage mechanism is correlated with the abnormalities of β-catenin and vimentin.
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·AIM: To observe the effect of two kinds of bandage contact lenses on epithelial erosions and corneal thickness after vitreoretinal surgery for proliferative diabetic retinopathy ( PDR) .· METHODS: In this prospective, nonrandomized, comparative clinical study, 69 eyes of 69 patients with PDR were divided into two groups. They underwent vitreoretinal surgery. Group A, 36 eyes of 36 cases, the bandage contact lens with diameter of 13. 8mm were covered on corneal surface during surgery under noncontact wide-angle viewing systems. Group B, 33 eyes of 33 cases, the bandage contact lens with diameter of 14. 0mm were covered on corneal surface during the same surgery. Visual acuity, intraocular pressure, slit-lamp examination, corneal fluorescein sodium staining, count of corneal endothelium cells, measure of corneal thickness before and after operation were assessed.·RESULTS: Pre-operation, corneal fluorescein sodium staining positive rate was 42% in Group A and 42% in Group B (x2=0. 004, P=0. 949). At 1d after surgery, the positive rate of was 47% in Group A and 45% in Group B (x2=0. 022, P=0. 883). At 2d after surgery, the positive rate of was 44% in Group A and 45% in Group B ( x2 =0. 007, P=0. 933). At 3d after surgery, the positive rate of was 44% in Group A and 42% in Group B (x2=0. 029, P=0. 886). At 7d after surgery, the positive rate of was 42%in Group A and 39% in Group B (x2=0. 037, P=0. 848). Count of corneal endothelium cells showed no significant difference between Group A and Group B(P>0. 05). Count of corneal endothelium cells of Group A before surgery and at 7d after surgery were 2779. 25 ± 329. 55 /mm2 , 2777. 14±331. 17 /mm2, without significant difference (t=0. 551, P=0. 585);those of Group B were 2678. 61±335. 64/mm2 , 2672. 45 ± 336. 25 /mm2 , without significant difference(t = 1. 774, P = 0. 086). Measure of corneal thickness was 519. 25±23. 42μm before surgery and 542. 03± 25.94μm after surgery in Group A (t=-6.854, P<0.001). Measure of corneal thickness was 525. 64 ± 20. 97μm before surgery and 551. 33±27. 87μm after surgery in Group B (t=-7. 204, P<0. 001).·CONCLUSION:Two kinds of bandage contact lenses are used in vitreoretinal surgery in diabetic patients. The corneal epithelial integrity shows no difference before and after surgery. Both the bandage contact lens could protect the corneal epithelium and maintain good corneal transparency during vitreoretinal surgery.
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AIM: To discuss the establishment of immediate diabetic keratopathy animal model of C57BL/6 mouse induced by ahigh-fat and high-glucose diet. METHODS: Diabetes mellitus was induced by a high-fat and high-glucose diet in C57BL/6 mouse. 1% rose bengal was stained on the cornea to examine the integrality of the corneal epithelium at 2 ~ 12mo after completion of the model. Corneal epithelial wound healing was observed using a vivo epithelial debridement model which was dyed by sodium fluorescein. Corneal morphology histology was examined by pathological methods. RESULTS: The high-fat and high-glucose diet C57BL/6 mouse in 2mo had showed general symptoms of diabetes: polydipsia, polyphagia, polyuria, weight loss etc. The model had a steady-state high glucose (≥18mmol/L), also the weight was lower compared with normal control mouse. 1% rose bengal corneal staining had dot coloring at 2mo after completion of the model, the stained area and extent were gradually increased with the extension of the duration of diabetes, almost all the cornea was stained at 12mo after completion of the model. With the passage of time into a mold, the cornea epithelial healing time become longer: 2mo was about 40h;3mo was about 120h; 4, 6, 12mo was about 144h;the coloboma were gradually increased at 12mo after completion of the model, then the area was reduced gradually until complete healing, the time was 96~120h, showed repeating phenomenon. CONCLUSION: The mouse were induced by high-fat and high-glucose diet can be used as animal models of diabetic keratopathy: the damage of epithelium for corneal and delay healing on epithelium and other symptoms.