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Proanthocyanidins Prevent High Glucose-Induced Eye Malformation by Restoring Pax6 Expression in Chick Embryo.

Tan RR, Zhang SJ, Li YF, Tsoi B, Huang WS, Yao N, Hong M, Zhai YJ, Mao ZF, Tang LP, Kurihara H, Wang Q, He RR - Nutrients (2015)

Bottom Line: In this study, we used chick embryo to establish a GDM model to study the protective effects of proanthocyanidins on eye development.However, proanthocyanidins could not decrease the glucose concentration of embryo eye.Moreover, the key genes regulating eye development, Pax6, was down-regulated by high glucose.

View Article: PubMed Central - PubMed

Affiliation: Anti-stress and Health Center, Pharmacy College, Jinan University, Guangzhou 510632, China. tanruirong@foxmail.com.

ABSTRACT
Gestational diabetes mellitus (GDM) is one of the leading causes of offspring malformations, in which eye malformation is an important disease. It has raised demand for therapy to improve fetal outcomes. In this study, we used chick embryo to establish a GDM model to study the protective effects of proanthocyanidins on eye development. Chick embryos were exposed to high glucose (0.2 mmol/egg) on embryo development day (EDD) 1. Proanthocyanidins (1 and 10 nmol/egg) were injected into the air sac on EDD 0. Results showed that both dosages of proanthocyanidins could prevent the eye malformation and rescue the high glucose-induced oxidative stress significantly, which the similar effects were showed in edaravone. However, proanthocyanidins could not decrease the glucose concentration of embryo eye. Moreover, the key genes regulating eye development, Pax6, was down-regulated by high glucose. Proanthocyanidins could restore the suppressed expression of Pax6. These results indicated proanthocyanidins might be a promising natural agent to prevent high glucose-induced eye malformation by restoring Pax6 expression.

No MeSH data available.


Related in: MedlinePlus

Proanthocyanidins had no effect on glucose concentration in high-glucose-treated eye of chick embryo. Glucose concentration (A) and GLUT1 gene expression (B) were detected in the eye of EDD 3.5 chick embryo. Values were expressed as mean ± SD in each group (n = 10). ** p < 0.01 vs. control. CON: control, GLU: high glucose, ProL: 1 nmol/egg proanthocyanidins, ProH: 10 nmol/egg proanthocyanidins, EDA: edaravone.
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nutrients-07-05299-f004: Proanthocyanidins had no effect on glucose concentration in high-glucose-treated eye of chick embryo. Glucose concentration (A) and GLUT1 gene expression (B) were detected in the eye of EDD 3.5 chick embryo. Values were expressed as mean ± SD in each group (n = 10). ** p < 0.01 vs. control. CON: control, GLU: high glucose, ProL: 1 nmol/egg proanthocyanidins, ProH: 10 nmol/egg proanthocyanidins, EDA: edaravone.

Mentions: Glucose concentration of eye was determined in EDD 3.5 embryo to further determine the effect of high glucose. Results showed that the injection of 0.2 mmol/egg glucose raised glucose concentration in the eyes of EDD 3.5 embryos, which confirmed that the leading effect was hyperglycemia on embryonic eye malformation. However, the increased glucose content could not be reduced by both proanthocyanidins and edaravone (Figure 4A). Glucose transporters facilitate the transport of glucose across the plasma membrane of a cell, and Glucose transporter 1 (Glut1) is one of the major Gluts existing in the eye. Glut1 was measured after high glucose treatment and agents’ administration. Consistently, the gene expression of Glut1 was decreased in the eye of hyperglycemia-treated embryos. Neither proanthocyanidins nor edaravone recovered their expression (Figure 4B).


Proanthocyanidins Prevent High Glucose-Induced Eye Malformation by Restoring Pax6 Expression in Chick Embryo.

Tan RR, Zhang SJ, Li YF, Tsoi B, Huang WS, Yao N, Hong M, Zhai YJ, Mao ZF, Tang LP, Kurihara H, Wang Q, He RR - Nutrients (2015)

Proanthocyanidins had no effect on glucose concentration in high-glucose-treated eye of chick embryo. Glucose concentration (A) and GLUT1 gene expression (B) were detected in the eye of EDD 3.5 chick embryo. Values were expressed as mean ± SD in each group (n = 10). ** p < 0.01 vs. control. CON: control, GLU: high glucose, ProL: 1 nmol/egg proanthocyanidins, ProH: 10 nmol/egg proanthocyanidins, EDA: edaravone.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4555138&req=5

nutrients-07-05299-f004: Proanthocyanidins had no effect on glucose concentration in high-glucose-treated eye of chick embryo. Glucose concentration (A) and GLUT1 gene expression (B) were detected in the eye of EDD 3.5 chick embryo. Values were expressed as mean ± SD in each group (n = 10). ** p < 0.01 vs. control. CON: control, GLU: high glucose, ProL: 1 nmol/egg proanthocyanidins, ProH: 10 nmol/egg proanthocyanidins, EDA: edaravone.
Mentions: Glucose concentration of eye was determined in EDD 3.5 embryo to further determine the effect of high glucose. Results showed that the injection of 0.2 mmol/egg glucose raised glucose concentration in the eyes of EDD 3.5 embryos, which confirmed that the leading effect was hyperglycemia on embryonic eye malformation. However, the increased glucose content could not be reduced by both proanthocyanidins and edaravone (Figure 4A). Glucose transporters facilitate the transport of glucose across the plasma membrane of a cell, and Glucose transporter 1 (Glut1) is one of the major Gluts existing in the eye. Glut1 was measured after high glucose treatment and agents’ administration. Consistently, the gene expression of Glut1 was decreased in the eye of hyperglycemia-treated embryos. Neither proanthocyanidins nor edaravone recovered their expression (Figure 4B).

Bottom Line: In this study, we used chick embryo to establish a GDM model to study the protective effects of proanthocyanidins on eye development.However, proanthocyanidins could not decrease the glucose concentration of embryo eye.Moreover, the key genes regulating eye development, Pax6, was down-regulated by high glucose.

View Article: PubMed Central - PubMed

Affiliation: Anti-stress and Health Center, Pharmacy College, Jinan University, Guangzhou 510632, China. tanruirong@foxmail.com.

ABSTRACT
Gestational diabetes mellitus (GDM) is one of the leading causes of offspring malformations, in which eye malformation is an important disease. It has raised demand for therapy to improve fetal outcomes. In this study, we used chick embryo to establish a GDM model to study the protective effects of proanthocyanidins on eye development. Chick embryos were exposed to high glucose (0.2 mmol/egg) on embryo development day (EDD) 1. Proanthocyanidins (1 and 10 nmol/egg) were injected into the air sac on EDD 0. Results showed that both dosages of proanthocyanidins could prevent the eye malformation and rescue the high glucose-induced oxidative stress significantly, which the similar effects were showed in edaravone. However, proanthocyanidins could not decrease the glucose concentration of embryo eye. Moreover, the key genes regulating eye development, Pax6, was down-regulated by high glucose. Proanthocyanidins could restore the suppressed expression of Pax6. These results indicated proanthocyanidins might be a promising natural agent to prevent high glucose-induced eye malformation by restoring Pax6 expression.

No MeSH data available.


Related in: MedlinePlus