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The Extract of Aster Koraiensis Prevents Retinal Pericyte Apoptosis in Diabetic Rats and Its Active Compound, Chlorogenic Acid Inhibits AGE Formation and AGE/RAGE Interaction

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ABSTRACT

Retinal capillary cell loss is a hallmark of early diabetic retinal changes. Advanced glycation end products (AGEs) are believed to contribute to retinal microvascular cell loss in diabetic retinopathy. In this study, the protective effects of Aster koraiensis extract (AKE) against damage to retinal vascular cells were investigated in streptozotocin (STZ)-induced diabetic rats. To examine this issue further, AGE accumulation, nuclear factor-kappaB (NF-κB) and inducible nitric oxide synthase (iNOS) were investigated using retinal trypsin digests from streptozotocin-induced diabetic rats. In the diabetic rats, TUNEL (Terminal deoxynucleotidyl transferase mediated dUTP Nick End Labeling)-positive retinal microvascular cells were markedly increased. Immunohistochemical studies revealed that AGEs were accumulated within the retinal microvascular cells, and this accumulation paralleled the activation of NF-κB and the expression of iNOS in the diabetic rats. However, AKE prevented retinal microvascular cell apoptosis through the inhibition of AGE accumulation and NF-κB activation. Moreover, to determine the active compounds of AKE, two major compounds, chlorogenic acid and 3,5-di-O-caffeoylquinic acid, were tested in an in vitro assay. Among these compounds, chlorogenic acid significantly reduced AGE formation as well as AGE/RAGE (receptor for AGEs) binding activity. These results suggest that AKE, particularly chlorogenic acid, is useful in inhibiting AGE accumulation in retinal vessels and exerts a preventive effect against the injuries of diabetic retinal vascular cells.

No MeSH data available.


Advanced glycation end products/receptor for AGE (AGE/RAGE) binding activity of AKE (A); Chlorogenic acid and 3,5-di-O-caffeoylquinic acid (B). The percentages of AGE/RAGE binding activities were calculated relative to the vehicle control (0 concentration). The IC50 values were calculated from the dose inhibition curves. All data are presented as the mean ± the SD (n = 4).
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nutrients-08-00585-f002: Advanced glycation end products/receptor for AGE (AGE/RAGE) binding activity of AKE (A); Chlorogenic acid and 3,5-di-O-caffeoylquinic acid (B). The percentages of AGE/RAGE binding activities were calculated relative to the vehicle control (0 concentration). The IC50 values were calculated from the dose inhibition curves. All data are presented as the mean ± the SD (n = 4).

Mentions: The inhibitions of AGE-BSA binding to RAGE at various concentrations of 3,5-di-O-caffeoylquinic acid and chlorogenic acid were tested (Figure 2). In this assay, AKE and chlorogenic acid and dose-dependently markedly reduced AGE-BSA/RAGE binding activity, and the IC50 values of AKE and chlorogenic acid were 84.91 ± 9.32 and 378.78 ± 14.16 μg/mL, respectively. However, 3,5-di-O-caffeoylquinic acid did not affect AGE/RAGE binding activity or the binding of AGE–BSA and RAGE.


The Extract of Aster Koraiensis Prevents Retinal Pericyte Apoptosis in Diabetic Rats and Its Active Compound, Chlorogenic Acid Inhibits AGE Formation and AGE/RAGE Interaction
Advanced glycation end products/receptor for AGE (AGE/RAGE) binding activity of AKE (A); Chlorogenic acid and 3,5-di-O-caffeoylquinic acid (B). The percentages of AGE/RAGE binding activities were calculated relative to the vehicle control (0 concentration). The IC50 values were calculated from the dose inhibition curves. All data are presented as the mean ± the SD (n = 4).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037569&req=5

nutrients-08-00585-f002: Advanced glycation end products/receptor for AGE (AGE/RAGE) binding activity of AKE (A); Chlorogenic acid and 3,5-di-O-caffeoylquinic acid (B). The percentages of AGE/RAGE binding activities were calculated relative to the vehicle control (0 concentration). The IC50 values were calculated from the dose inhibition curves. All data are presented as the mean ± the SD (n = 4).
Mentions: The inhibitions of AGE-BSA binding to RAGE at various concentrations of 3,5-di-O-caffeoylquinic acid and chlorogenic acid were tested (Figure 2). In this assay, AKE and chlorogenic acid and dose-dependently markedly reduced AGE-BSA/RAGE binding activity, and the IC50 values of AKE and chlorogenic acid were 84.91 ± 9.32 and 378.78 ± 14.16 μg/mL, respectively. However, 3,5-di-O-caffeoylquinic acid did not affect AGE/RAGE binding activity or the binding of AGE–BSA and RAGE.

View Article: PubMed Central - PubMed

ABSTRACT

Retinal capillary cell loss is a hallmark of early diabetic retinal changes. Advanced glycation end products (AGEs) are believed to contribute to retinal microvascular cell loss in diabetic retinopathy. In this study, the protective effects of Aster koraiensis extract (AKE) against damage to retinal vascular cells were investigated in streptozotocin (STZ)-induced diabetic rats. To examine this issue further, AGE accumulation, nuclear factor-kappaB (NF-κB) and inducible nitric oxide synthase (iNOS) were investigated using retinal trypsin digests from streptozotocin-induced diabetic rats. In the diabetic rats, TUNEL (Terminal deoxynucleotidyl transferase mediated dUTP Nick End Labeling)-positive retinal microvascular cells were markedly increased. Immunohistochemical studies revealed that AGEs were accumulated within the retinal microvascular cells, and this accumulation paralleled the activation of NF-κB and the expression of iNOS in the diabetic rats. However, AKE prevented retinal microvascular cell apoptosis through the inhibition of AGE accumulation and NF-κB activation. Moreover, to determine the active compounds of AKE, two major compounds, chlorogenic acid and 3,5-di-O-caffeoylquinic acid, were tested in an in vitro assay. Among these compounds, chlorogenic acid significantly reduced AGE formation as well as AGE/RAGE (receptor for AGEs) binding activity. These results suggest that AKE, particularly chlorogenic acid, is useful in inhibiting AGE accumulation in retinal vessels and exerts a preventive effect against the injuries of diabetic retinal vascular cells.

No MeSH data available.