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Browsing by Subject "Diabetic retinopathy"

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    Effect of diabetes blood-stasis syndrome and Xuefu Zhuyu decoction on ERK1/2-VEGF signal pathway in rat retina Müller cells
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2022) Ye, Xiaofeng; Ren, Hui; Jiang, Tingting; Zhang, Ting; Li, Gang
    Aims. This research was aimed to investigate whether diabetic blood-stasis syndrome had a relationship with ERK1/2-VEGF signaling pathway in rat retina Müller cells and Traditional Chinese Drugs designed for promoting blood circulation to remove blood stasis had effectiveness for diabetic retinopathy (DR) treatment. Methods. Immunofluorescence was applied to determine purity of Müller cells. Müller cells were stimulated by blood serum obtained from rats with blood-stasis syndrome and then treated by Xuefu Zhuyu decoction. Western blot analysis, RT-PCR and ELISA were used to measure the expression of VEGF. Western blot analysis was used to determine the phosphorylation of ERK1/2. The status of AP-1 DNA binding activity was monitored by electrophoretic mobility shift assay (EMSA). Results. Stimulation of Müller cells by blood serum of rat with diabetic blood stasis increased the secretion of VEGF, activated ERK1/2 and AP-1 DNA-binding activity. And treatment of Xuefu Zhuyu decoction could weaken this phenomenon. What's more, ERK1/2 signaling pathway inhibitor U0126 also could inhibit the expression of VEGF. Conclusions. Diabetic blood-stasis syndrome in theory of traditional Chinese Medicine has positive role in regulating ERK1/2-VEGF signaling pathway. Traditional Chinese drugs for promoting blood circulation to remove blood stasis would be an effective therapy to treat DR.
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    Functional aspects of the somatostatinergic system in the retina and the potential therapeutic role of somatostatin in retinal disease
    (Murcia : F. Hernández, 2005) Casini, G.; Catalani, E.; Dal Monte, M.; Bagnoli, P.
    The somatostatinergic system of the retina has been investigated in a variety of studies. A considerable amount of experimental evidence is available concerning the patterns of expression of somatostatin (SRIF) and its receptors in vertebrate retinas. However the functional roles of this peptidergic system in retinal physiology are far from being elucidated. Nonetheless, data have been provided concerning the regulatory action of SRIF on the excitability of different retinal cell types and on the modulation of ion channels in different vertebrate retinas. The present review is focused on recent and unpublished investigations of the mouse retina relative to the involvement of specific SRIF receptors in the regulation of ion channels and transmitter release, the transduction pathways coupled to SRIF receptors, and the mechanisms regulating the expression of SRIF and its receptors as derived from studies in transgenic animal models. In these models, altered expression levels of SRIF or of specific SRIF receptors have also been found to affect the morphology of retinal cell types (namely the rod bipolar cells) and to result in functional alterations at the level of both ion channel regulation and transmitter release. These new pieces of evidence constitute an important step forward in the understanding of the functional actions of the retinal somatostatinergic system, although our current knowledge is far from being exhaustive. The ultimate goal of understanding SRIF functional actions in the retina is concerned with the possibility of using SRIF or its analogs as therapeutic agents to cure retinal diseases. Indeed, encouraging results are being obtained in clinical investigations focused on the use of SRIF analogs to treat diabetic retinopathy, a retinal disease with high social impact and originating as a complication of diabetes. The closing part of the present paper examines the evidence supporting SRIF as a promising therapeutic agent in this disease.
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    Novel features of neurodegeneration in the inner retina of early diabetic rats
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Énzsöly, Anna; Szabó, Arnold; Szabó, Klaudia; Szél, Ágoston; Németh, János; Lukáts, Ákos
    The literature indicates that in diabetes retinal dysfunctions related to neural retinal alterations exist prior to clinically detectable vasculopathy. In a previous report, a detailed description about the alteration of the outer retina was given, where diabetic degeneration preceded apoptotic loss of cells (Enzsöly et al., 2014). Here, we investigated the histopathology of the inner retina in early diabetes using the same specimens. We examined rat retinas with immunohistochemistry and Western blotting, 12 weeks after streptozotocin induction of diabetes. Glial reactivity was observed in all diabetic retinal specimens; however, it was not detectable all over the retina, but appeared in randomly arranged patches, with little or no glia activation in between. Similarly, immunoreactivity of parvalbumin (staining mostly AII amacrine cells) was also decreased only in some regions. We propose that these focal changes appear prior to affecting the whole retina and overt loss of cells. In contrast to these, most other markers used (calretinin, recoverin, tyrosin hydroxylase anti-Brn-3a and also calbindin in the optic part of the retina) did not show any major alterations in the intensity of immunoreactivity or in the number of stained elements. Interestingly, under diabetic conditions, the labeling pattern of PKC-α and calbindin in the ciliary retina showed a clear resemblance to the pattern described during development. This observation is in line with our previous study, reporting an increase in the number of dual cones, coexpressing two photopigments, which is another common feature with developing retinas. These data may indicate a previously uninvestigated regenerative capacity in diabetic retina
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    Quantification of Photoreceptors’ Changes in a Diabetic Retinopathy Model with Two-Photon Imaging Microscopy
    (MDPI, 2024-08-11) Bautista-Elivar, N.; Avilés-Trigueros, M.; Bueno, J.M; Avilés-Trigueros, M.; Bueno, J.M.; Oftalmología, Optometría, Otorrinolaringología y Anatomía Patológica
    settingsOrder Article Reprints Open AccessArticle Quantification of Photoreceptors’ Changes in a Diabetic Retinopathy Model with Two-Photon Imaging Microscopy by Nazario Bautista-Elivar 1ORCID,Marcelino Avilés-Trigueros 2ORCID andJuan M. Bueno 3,*ORCID 1 Departamento de Ingeniería Eléctrica y Electrónica, Tecnológico Nacional de México/Instituto Tecnológico de Pachuca, Pachuca 42082, Hidalgo, Mexico 2 Departamento de Oftalmología, Facultad de Medicina, Universidad de Murcia e Instituto Murciano de Investigación Biosanitaria Virgen de la Arrixaca, “Campus Mare Nostrum” de Excelencia International, 30100 Murcia, Spain 3 Laboratorio de Óptica, Instituto Universitario de Investigación en Óptica y Nanofísica, Universidad de Murcia, 30100 Murcia, Spain * Author to whom correspondence should be addressed. Int. J. Mol. Sci. 2024, 25(16), 8756; https://doi.org/10.3390/ijms25168756 Submission received: 28 June 2024 / Revised: 1 August 2024 / Accepted: 5 August 2024 / Published: 11 August 2024 (This article belongs to the Special Issue Retinal Degenerative Diseases: 2nd Edition) Downloadkeyboard_arrow_down Browse Figures Versions Notes Abstract Emerging evidence suggests that retinal neurodegeneration is an early event in the pathogenesis of diabetic retinopathy (DR), preceding the development of microvascular abnormalities. Here, we assessed the impact of neuroinflammation on the retina of diabetic-induced rats. For this aim we have used a two-photon microscope to image the photoreceptors (PRs) at different eccentricities in unstained retinas obtained from both control (N = 4) and pathological rats (N = 4). This technique provides high-resolution images where individual PRs can be identified. Within each image, every PR was located, and its transversal area was measured and used as an objective parameter of neuroinflammation. In control samples, the size of the PRs hardly changed with retinal eccentricity. On the opposite end, diabetic retinas presented larger PR transversal sections. The ratio of PRs suffering from neuroinflammation was not uniform across the retina. Moreover, the maximum anatomical resolving power (in cycles/deg) was also calculated. This presents a double-slope pattern (from the central retina towards the periphery) in both types of specimens, although the values for diabetic retinas were significantly lower across all retinal locations. The results show that chronic retinal inflammation due to diabetes leads to an increase in PR transversal size. These changes are not uniform and depend on the retinal location. Two-photon microscopy is a useful tool to accurately characterize and quantify PR inflammatory processes and retinal alterations.
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    The effectiveness of edible bird's nest in lowering VEGF, CD31, and PDGFR-β levels in diabetic retinopathy in rats with type 1 diabetes
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Komolkriengkrai, Manaras; Matsathit, Udomlak; Khimmaktong, Wipapan
    Aims. Diabetic eye disease, known as diabetic retinopathy (DR), is one of the problems that can arise from having high blood sugar for an extended period. This study aimed to investigate the effect of the edible bird’s nest (EBN) on retinal angiogenesis in diabetic rats. Methods. The 50 rats were separated into five different groups, each containing 10 rats: control, diabetes (DM), bird's nest-fed diabetes (75 mg/kg Body weight; BW), (EBN 75), (150 mg/kg BW) (EBN 150), and glyburide (GR) for an eight-week study. H&E and Masson’s trichrome staining were utilized to investigate the retinal tissue and vascular changes. The immunofluorescence study was used to detect angiogenic protein expression. The vascular corrosion cast/SEM method was also used to evaluate capillary plexus formation within the retinal layer. Results. From histological studies, DM rats have thinning of the retinal layer. Remarkably, the retinal vessels displayed dilations resembling ruptured blood vessels. The expression of vascular endothelial growth factor (VEGF) (30.51±2.62), cluster of differentiation 31 (CD31) (28.18±0.22), and platelet-derived growth factor receptor beta (PDGFR-β) (141.67±0.97) were increased. EBN 75 exhibited some small improvements in their blood vessels and eye tissue. At a dose of 150 mg/kg BW, EBN proved to be more effective. There was a significant decrease in VEGF and CD31 expression compared with the diabetic group (p<0.001 and p<0.01, respectively). Conclusions. These studies have demonstrated that EBN can lower the growth levels of VEGF, CD31, and PDGFR-β, which results in a decrease in angiogenesis and a recovery from a variety of diabetic retinopathy-related diseases

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