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Secondary intervention with aminoguanidine retards the progression of diabetic retinopathy in the rat model (1995)

Hammes, H.-P. ; Strödter, D. ; Weiss, A. ; [et al.]

Springer

Diabetologia 38 (1995), S. 656-660

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ISSN: 1432-0428

Keywords: Key words Diabetic retinopathy ; rat model ; aminoguanidine ; glycation ; secondary intervention ; islet transplantation.

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Summary Primary prevention with aminoguanidine – an inhibitor of advanced glycation end product (AGE) formation – has been successfully employed to prevent diabetic retinopathy in the rat. However, it is unknown whether inhibition of AGE formation is still effective in a secondary intervention strategy. The present study addresses this question by comparing secondary intervention with aminoguanidine with syngeneic islet transplantation in the rat model. After 6 months of diabetes, one group was treated with aminoguanidine (50 mg/100 ml drinking water; D-AG) while another group received syngeneic transplantation of collagenase-ficoll isolated islets by intraportal injection (Tx). After an additional 4 months, both groups were compared to a normal (NC 10) and diabetic (DC 10) control group. Retinal autofluorescence was increased 2.5-fold after 6 months and increased 3.7-fold after 10 months of diabetes (p 〈 0.001). Aminoguanidine and islet Tx retarded the further accumulation of autofluorescence equally (p 〈 0.001 vs DC 10), although the values were higher than those observed in DC at 6 months (p 〈 0.001). Diabetes was associated with a 2.7-fold increase in acellular capillaries after 6 months and a 4.1-fold increase after 10 months. Treatment with aminoguanidine or islet Tx reduced but did not completely attenuate the progression of vascular occlusion (p 〈 0.001 vs DC 10; D-AG vs DC 6, p 〈 0.05; Tx vs DC 6, p 〈 0.01). Both treatments reduced endothelial proliferation (22.4 % after 10 months; p 〈 0.001) and completely arrested pericyte dropout (40 % after 10 months; p 〈 0.001). These data demonstrate that aminoguanidine is as effective as islet transplantation in retarding the progression of diabetic retinopathy in a secondary prevention setting. [Diabetologia (1995) 38: 656–660]

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00401835

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Aminoguanidine does not inhibit the initial phase of experimental diabetic retinopathy in rats (1995)

Hammes, H.-P. ; Ali, S. Syed ; Uhlmann, M. ; [et al.]

Springer

Diabetologia 38 (1995), S. 269-273

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ISSN: 1432-0428

Keywords: Key words Diabetic retinopathy ; rat model ; aminoguanidine ; glycation ; retinal basement membrane.

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Summary We have previously shown that long-term administration of aminoguanidine, an inhibitor of advanced glycosylation product formation, reduces the extent of experimental diabetic retinopathy in the rat by 85 %. In order to determine whether the residual retinopathy that developed despite aminoguanidine was attributable to advanced glycation endproduct formation, a time-course study was performed in three different groups of male Wistar rats: non-diabetic controls (NC), streptozotocin-diabetic controls (DC) and streptozotocin-diabetic rats treated with aminoguanidine HCL, 50 mg/100 ml drinking water (D-AG). Eyes were obtained at 24, 32, 44 and 56 weeks of diabetes/treatment duration and morphologic evaluation was done on retinal digest preparations. At 56 weeks, retinal basement membrane thickness was additionally measured. After 24 weeks of diabetes, the number of acellular capillaries was significantly elevated in DC (44.6 ± 5.7/mm2 of retinal area, NC 19.6 ± 4.9; p 〈 0.001) and increased continuously over time (DC 56 weeks 87.4 ± 15.1; p 〈 0.001 vs DC 24 weeks). In contrast, acellular capillaries in D-AG increased over the first 24 weeks and then remained constant for the rest of the study (D-AG 24 weeks 35.7 ± 5.18; p 〈 0.01 vs NC 24 weeks and NS vs DC 24 weeks; D-AG 56 weeks 42.0 ± 6.20; p NS vs D-AG 24 weeks). Diabetes-associated pericyte loss (DC 24 weeks 2310 ± 170/mm2 of capillary area; NC 24 weeks 3120 ± 190; p 〈 0.001; DC 56 weeks 1570 ± 230; NC 56 weeks 2960 ± 50; p 〈 0.001) was significantly prevented by aminoguanidine after diabetic-like changes over the initial 24 weeks (D-AG 24 weeks 2450 ± 75; p NS vs DC 24 weeks; D-AG 56 weeks 2350 ± 90; p 〈 0.001 vs DC 56 weeks). At 56 weeks, aminoguanidine treatment was associated with a 67.4 % reduction in retinal basement membrane thickening. This time-course study demonstrates that aminoguanidine prevents the progression of experimental diabetic retinopathy, and suggests that non AG-inhibitable mechanisms are involved in the initial phase of diabetic retinopathy. [Diabetologia (1995) 38: 269–273]

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF00400629

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Release of the angiogenesis inhibitor angiostatin in patients with proliferative diabetic retinopathy: association with retinal photocoagulation (2000)

Spranger, J. ; Hammes, H.-P. ; Preissner, K. T. ; [et al.]

Springer

Diabetologia 43 (2000), S. 1404-1407

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ISSN: 1432-0428

Keywords: Keywords Diabetes, angiostatin, VEGF, bFGF, angiogenesis, retinopathy, cytokine, growth factors, photocoagulation, retina.

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract Aims/hypothesis. Proliferative diabetic retinopathy is a major debilitating disease causing most cases of blindness in humans in the Western world. Photocoagulation is the established therapy of proliferative diabetic retinopathy, although the molecular mechanisms of its effects are still not known. Recently angiostatin has been characterized as a potent inhibitor of neovascularization. Apart from a possible down-regulation of angiogenic cytokines, release of angiostatin could initiate the anti-angiogenic effects of retinal photocoagulation.¶Methods. We investigated the regulation of angiostatin and the angiogenic cytokines vascular endothelial growth factor and basic fibroblast growth factor in vivo by comparing vitreal concentrations of 18 control patients and 34 patients with proliferative diabetic retinopathy with and without previous photocoagulation. Concentrations of basic fibroblast growth factor and angiostatin were additionally measured in serum, while vascular endothelial growth factor is known to be regulated locally in the eye. Cytokines were measured by immunological methods.¶Results. Angiostatin could be detected in 2 out of 18 control patients and in 25 out of 34 diabetic patients (p 〈 0.00 001). Most importantly, production of angiostatin in human vitreous correlated significantly with previous retinal photocoagulation (p 〈 0.0001) in patients with proliferative diabetic retinopathy. Only two patients (one control and one diabetic) had detectable serum concentrations of angiostatin. Additionally patients with proliferative diabetic retinopathy and with previous photocoagulation had significantly lower concentrations of vascular endothelial growth factor (0.9 ± 0.1 ng/ml; p 〈 0.0001) than diabetic patients without previous photocoagulation (4.0 ± 0.8 ng/ml). The investigation of vitreal and serum basic fibroblast growth factor concentrations yielded no significant differences between the groups.¶Conclusion/interpretation. Angiostatin is not a regularly expressed angiogenesis inhibitor in human vitreous. The alterations we observed suggest that local release of angiostatin and down-regulation of vascular endothelial growth factor mediate the therapeutic effects of retinal photocoagulation in proliferative diabetic retinopathy. [Diabetologia (2000) 43: 1404–1407]

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/s001250051546

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