Antioxidant effects of epigallocatechin-3-gallate on the aTC1-6 pancreatic alpha cell line

Journal Article · Mon Jan 15 04:00:00 EST 2018 · Biochemical and Biophysical Research Communications

DOI:https://doi.org/10.1016/J.BBRC.2017.11.006· OSTI ID:23100618

Cao, Ting ^[1]; Zhang, Xiong ^[2]; Yang, Dan; Wang, Yue-Qian; Qiao, Zheng-Dong; Huang, Jian-Ming ^[1]; Zhang, Peng ^[1]

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1. Center for Medical Research and Innovation, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai (China)
2. Department of Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Shanghai (China)

Highlights: • The ability of pancreatic α-cells respond to hypoglycemia becomes impaired in diabetes patients. • EGCG has antioxidant potential on pancreatic αTC1-6 cell lines. • EGCG protected the normal function of pancreatic α-cells from H{sub 2}O{sub 2}. • EGCG inhibited cell apoptosis via the activation of Akt and suppression of P38 and JNK pathway. • Combining the conventional anti-hyperglycemia therapy and antioxidant therapy would avert hypoglycemia in diabetes treatment. Hypoglycemia is a major barrier to achieving stable metabolic control in patients with diabetes which is a serious clinical concern. With progression of diabetes, the ability of pancreatic α-cells which respond to hypoglycemia becomes impaired; However, it is not clear whether the dysfunctional responses of α-cells during hypoglycemia are related with oxidative stress. In the present study, we investigated whether epigallocatechin-3-gallate (EGCG) has antioxidant potential on pancreatic alpha TC1-6 (αTC1-6) cell lines and protect the normal function of α-cells from H{sub 2}O{sub 2} induced oxidative stress. ROS production, cell viability, glucagon secretion, and cell apoptosis were assessed. EGCG reduced ROS production and cell apoptosis, while restored cell viability and glucagon secretion within a particular concentration range. Moreover, EGCG activated Akt signaling and inhibited P38 as well as JNK mitogen-activated protein kinase (MAPK) pathway. Taken together, EGCG prevented αTC1-6 cells from H{sub 2}O{sub 2} induced oxidative stress, restored dysfunction of glucagon secretion and inhibited cell apoptosis via the activation of Akt signaling and suppression of P38 and JNK pathway. These results provide rationale for combining the conventional anti-hyperglycemia therapy and antioxidant therapy in order to avert hypoglycemia in clinical treatment of diabetes.

• OSTI ID: 23100618
• Journal Information: Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 1 Vol. 495; ISSN 0006-291X; ISSN BBRCA9
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
APOPTOSIS
GLUCAGON
PANCREAS
PHOSPHOTRANSFERASES