EXPERIMENTAL RESEARCH
Thymoquinone activates imidazoline receptor to enhance glucagon-like peptide-1 secretion in diabetic rats
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1
Department of Food Science, College of Agriculture, National Pingtung University of Science and Technology, Neipu Township, Pingtung County, Taiwan
2
Cardiovascular Center, Kaohsiung Veterans General Hospital, Kaohsiung City, Zuoying District, Taiwan
3
Department of Medical Research, Chi-Mei Medical Center, Tainan City, Yongkang District, Taiwan
Submission date: 2019-04-25
Final revision date: 2019-06-05
Acceptance date: 2019-06-26
Online publication date: 2019-07-26
 
Arch Med Sci 2022;18(6)
 
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ABSTRACT
Introduction:
Thymoquinone (TQ) is one of the principal bioactive ingredients proven to exhibit anti-diabetic effects. Recently, glucagon-like peptide-1 (GLP-1) has been found to be involved in antidiabetic effects in rats. The aim of this study was to evaluate the mediation of GLP-1 in the antidiabetic effect of TQ and to understand the possible mechanisms.

Material and methods:
NCI-H716 cells and CHO-K1 cells were used to investigate the effects of TQ on GLP-1 secretion in vitro. In type 1 diabetic rats, the changes in plasma glucose and GLP-1 levels were evaluated with TQ treatment.

Results:
The direct effect of TQ on imidazoline receptors (I-Rs) was identified in CHO-K1 cells overexpressing I-Rs. Additionally, in the intestinal NCI-H716 cells that may secrete GLP-1, TQ treatment enhanced GLP-1 secretion in a dose-dependent manner. However, these effects of TQ were reduced by ablation of I-Rs with siRNA in NCI-H716 cells. Moreover, these effects were inhibited by BU224, the imidazoline I2 receptor (I-2R) antagonist. In diabetic rats, TQ increased plasma GLP-1 levels, which were inhibited by BU-224 treatment. Functionally, TQ-attenuated hyperglycemia is also evidenced through GLP-1 using pharmacological manipulations.

Conclusions:
This report demonstrates that TQ may promote GLP-1 secretion through I-R activation to reduce hyperglycemia in type-1 diabetic rats.

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ISSN:1734-1922