Modified Si-Miao-San ameliorates pancreatic B cell dysfunction by inhibition of reactive oxygen species-associated inflammation through AMP-kinase activation.
10.1016/S1875-5364(14)60043-1
- Author:
Shu-Wan SHANG
1
;
Jiang-Lin YANG
1
;
Fang HUANG
1
;
Kang LIU
2
,
3
;
Bao-Lin LIU
2
,
4
Author Information
1. State key laboratory of Natural Medicines, Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing 211198, China.
2. State key laboratory of Natural Medicines, Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing 211198, China
3. Jiangsu Collaborative Innovation Center of Chinese Medicinal Resources Industrialization, Nanjing University of Chinese Medicines, Nanjing 210046, China.
4. Jiangsu Collaborative Innovation Center of Chinese Medicinal Resources Industrialization, Nanjing University of Chinese Medicines, Nanjing 210046, China. Electronic address: zhongyao440@163.com.
- Publication Type:Journal Article
- Keywords:
AMP-kinase;
Advanced glycation end products;
Inflammation;
Modified Si-Miao-San;
Pancreatic B cells
- MeSH:
AMP-Activated Protein Kinases;
genetics;
metabolism;
Animals;
Apoptosis;
drug effects;
Cell Line, Tumor;
Drugs, Chinese Herbal;
pharmacology;
Glucose;
metabolism;
Glycation End Products, Advanced;
metabolism;
Humans;
Inflammation;
drug therapy;
enzymology;
genetics;
metabolism;
Insulin-Secreting Cells;
cytology;
drug effects;
enzymology;
metabolism;
Phosphorylation;
Rats;
Reactive Oxygen Species;
metabolism
- From:
Chinese Journal of Natural Medicines (English Ed.)
2014;12(5):351-360
- CountryChina
- Language:English
-
Abstract:
AIM:To observe the effect of modified Si-Miao-San (mSMS) on advanced glycation end products (AGEs)-induced pancreatic B cell dysfunction, as well as examining the underlying mechanisms.
METHOD:Pancreatic B cells (INS-1) were stimulated with advanced glycation end products (AGEs, 200 μg·mL(-1)) for 24 h to produce dysfunction in pancreatic B cells and the effects of mSMS observed on insulin secretion, NF-κB (p65) phosphorylation, reactive oxygen species (ROS) production, mitochondria membrane potential (Δψm), cell apoptosis, phosphorylation of AMP-kinase (AMPK), and caspase 3 activity.
RESULTS:The AGEs challenge resulted in increased basal insulin secretion, but decreased insulin secretion in response to high glucose, whereas this situation was reversed by mSMS treatment. AGEs stimulation induced NF-κB (p65) phosphorylation and reactive oxygen species (ROS) production, as well as Δψm collapse and cell apoptosis. mSMS inhibited ROS production and inhibited NF-κB activation by attenuating p65 phosphorylation. Meanwhile, AGEs-induced Δψm collapse and cell apoptosis were also reversed by mSMS treatment. Compound C, an inhibitor of AMP-Kinase (AMPK), abolished the beneficial effects of mSMS on the regulation of B cell function, indicating the involvement of AMPK.
CONCLUSION:mSMS ameliorated AGEs-induced B cell dysfunction by suppressing ROS-associated inflammation, and this action was related to its beneficial regulation of AMPK activity.
