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01.12.2014 | Research | Ausgabe 1/2014 Open Access

Chinese Medicine 1/2014

Effects of a novel curcumin derivative on insulin synthesis and secretion in streptozotocin-treated rat pancreatic islets in vitro

Zeitschrift:
Chinese Medicine > Ausgabe 1/2014
Autoren:
MohammedTalaat Abdel Aziz, Mohammed Farid El-Asmar, Ameen Mahmoud Rezq, MohammedAbdel Aziz Wassef, Hanan Fouad, Nagwa Kamal Roshdy, Hanan Hosni Ahmed, Laila Ahmed Rashed, Dina Sabry, Fatma Mohammed Taha, Amira Hassouna
Wichtige Hinweise

Electronic supplementary material

The online version of this article (doi:10.​1186/​1749-8546-9-3) contains supplementary material, which is available to authorized users.

Competing interests

The authors declare that they have no competing interests.

Authors’ contributions

AAMT, EAMF, RAM, WMA, and FH designed the study. RNK, AHH, RL, SD, TFM, and HA performed the experiments. AAMT, EAMF, RAM, WMA, FH, RNK, AHH, RL, SD, TFM, and HA analyzed and interpreted the data. RNK, AHH, RL, SD, TFM, and HA wrote the manuscript. All authors read and approved the final version of the manuscript.

Abstract

Background

Hyperglycemia induces activation of the c-Jun N-terminal kinase (JNK) pathway, which suppresses insulin gene expression and reduces DNA binding of pancreatic and duodenal homeobox factor (PDX)-1. This study aims to investigate the effects of a novel curcumin derivative (NCD) on JNK signaling pathway on insulin synthesis and secretion in streptozotocin (STZ)-treated rat pancreatic islets in vitro.

Methods

Isolated rat pancreatic islets were divided into five groups: untreated control group; group treated with NCD (10 μM); group exposed to STZ (5 mM); group treated with NCD (10 μM) and then exposed to STZ (5 mM); and group exposed to STZ (5 mM) and then treated with NCD (10 μM). The pancreatic islets from all groups were used for DNA fragmentation assays and quantitative assessments of the JNK, Pdx1, glucose transporter-2 (GLUT2), heme oxygenase (HO)-1, transcription factor 7-like 2 (TCF7L2), and glucagon-like peptide (GLP)-1 gene expression levels. The intracellular calcium, zinc, and the phosphorylated and total JNK protein levels were assessed. The insulin (secreted/total) and C-peptide levels were examined in islet culture medium.

Results

NCD protected pancreatic islets against STZ-induced DNA damage, improved total insulin (P = 0.001), secreted insulin (P = 0.001), and C-peptide levels (P = 0.001), normalized mRNA expressions of insulin, Pdx1, and GLUT2 (P = 0.0001), and significantly elevated calcium and zinc levels (P = 0.0001). All effects were significant when islets were treated with NCD before STZ (P = 0.05). JNK gene overexpression and JNK protein levels induced by STZ were significantly inhibited after NCD treatment of islets ( P = 0.0001). NCD-treated islets showed significantly elevated gene expressions of HO-1, TCF7L2, and GLP-1 (P = 0.0001), and these upregulated gene expressions were more significantly elevated with NCD treatment before STZ than after STZ (P = 0.05).

Conclusions

NCD improved insulin synthesis and secretion in vitro in isolated pancreatic islets treated with STZ through inhibition of the JNK pathway, up-regulation of the gene expressions of HO-1, TCF7L2, and GLP-1 and enhancing effects on calcium and zinc levels.
Zusatzmaterial
Additional file 1: GELATIN, A CURCUMIN DRUG CARRIER SYSTEM. (DOCX 53 KB)
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