alexa Anti-Diabetic Action of Cydonia oblonga Seed Extract: I
e-ISSN: 2321-6182 p-ISSN: 2347-2332

Research & Reviews: Journal of Pharmacognosy and Phytochemistry
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Research Article

Anti-Diabetic Action of Cydonia oblonga Seed Extract: Improvement of Glucose Metabolism via Activation of PI3K/AKT Signaling Pathway

Dan Tang1, Lian-Zhen Xie1,2, Xue-Lei Xin1, and H. A. Aisa1*

1The Key Laboratory of Plant Resources and Chemistry of Arid Zone and State Key Laboratory Basis of Xinjiang Indigenous Medicinal Plants Resource Utilization, Xinjiang Technical Institute of Physics and Chemistry, Chinese Academy of Sciences, Urumqi 830011, People’s Republic of China

2University of Chinese Academy of Sciences, Beijing 100039, People’s Republic of China

*Corresponding Author:
H. A. Aisa
Xinjiang Technical Institute of Physics and Chemistry
Chinese Academy of Sciences
40-1 Beijing Road, Urumqi
Xinjiang 830011
P. R.,China
E-mail: [email protected]

Received date: 12/04/2016; Accepted date: 10/06/2016; Published date: 17/06/2016



Context: Diabetes mellitus is one of the most common metabolic syndromes characterized by hyperglycemia. Cydonia oblonga Miller (Rosaceae) is used in traditional uyghur medicine and is proved to have antioxidant and antihypertensive properties, but the anti-diabetic activity of C. oblonga Mill. seeds extracts (CSE) is not yet explored.

Objective: The anti-diabetic ability of CSE and the underlying mechanism of action of CSE were investigated in L6 skeletal muscle cells.

Methods: CSE were evaluated for their inhibitory activity against protein tyrosine phosphatase 1B (PTP1B) in vitro. L6 myoblasts were differentiated to myotubes and treated with CSE (0 μg/ml to 100 μg/ ml) for 1 h. Cell viability was assessed by MTT assay and cell cytotoxicity was detected by lactate dehydrogenase (LDH) release from L6 cells. The phosphorylation levels of four key proteins (IRS-1, AKT, GSK-3β and AMPK) involve in PI3K/AKT signaling pathway were examined by western blotting.

Results: CSE possess good anti-PTP1B activity with an IC50 value of 3.5 μg/mL. Treatment of L6 skeletal muscle cells with CSE (0 μg/ml to 100 μg/ml) did not affect cell viability. CSE at 12.5 μg/ml increased glucose consumption and glycogen synthesis in L6 myotubes. Western blotting results showed that CSE increased the phosphorylation of IRS- 1, AKT and GSK-3β protein in the present of insulin.

Discussion and Conclusion: These results suggested that CSE promoted glucose metabolism by activating PI3K/AKT signaling pathway in L6 cells. The study reported the anti-diabetic effect of CSE on in vitro cell model for the first time, which providing potential drug candidates for prevention and treatment of diabetes.


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