Berberine relieves insulin resistance via the cholinergic anti-inflammatory pathway in HepG2 cells.
10.1007/s11596-016-1543-5
- Author:
Fen LI
1
;
Yun-bin ZHAO
2
;
Ding-kun WANG
3
;
Xin ZOU
3
;
Ke FANG
3
;
Kai-fu WANG
4
Author Information
1. Institute of Integrated Traditional Chinese and Western Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. kerenlifen@163.com.
2. College of Chemistry and Chemical Engineering, Huazhong University of Science and Technology, Wuhan, 430074, China.
3. Institute of Integrated Traditional Chinese and Western Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
4. Institute of Integrated Traditional Chinese and Western Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. wkf58@163.com.
- Publication Type:Journal Article
- Keywords:
alpha7 nicotinic acetylcholine receptor;
berberine;
cholinergic anti-inflammatory pathway;
glucose uptake;
inflammation
- MeSH:
Berberine;
pharmacology;
Glucose;
metabolism;
Hep G2 Cells;
Humans;
Hypoglycemic Agents;
pharmacology;
I-kappa B Kinase;
metabolism;
I-kappa B Proteins;
metabolism;
Insulin;
metabolism;
Insulin Resistance;
Interleukin-6;
metabolism;
Transcription Factor RelA;
metabolism;
alpha7 Nicotinic Acetylcholine Receptor;
genetics;
metabolism
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2016;36(1):64-69
- CountryChina
- Language:English
-
Abstract:
Berberine (BBR) is an isoquinoline alkaloid extracted from Rhizoma coptidis and has been used for treating type 2 diabetes mellitus (T2DM) in China. The development of T2DM is often associated with insulin resistance and impaired glucose uptake in peripheral tissues. In this study, we examined whether BBR attenuated glucose uptake dysfunction through the cholinergic anti-inflammatory pathway in HepG2 cells. Cellular glucose uptake, quantified by the 2-[N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl)-amino]-2-deoxy-D-glucose (2-NBDG), was inhibited by 21% after HepG2 cells were incubated with insulin (10(-6) mol/L) for 36 h. Meanwhile, the expression of alpha7 nicotinic acetylcholine receptor (α7nAChR) protein was reduced without the change of acetylcholinesterase (AChE) activity. The level of interleukin-6 (IL-6) in the culture supernatant, the ratio of phosphorylated I-kappa-B kinase-β (IKκβ) Ser181/IKKβ and the expression of nuclear factor-kappa B (NF-κB) p65 protein were also increased. However, the treatment with BBR enhanced the glucose uptake, increased the expression of α7nAChR protein and inhibited AChE activity. These changes were also accompanied with the decrease of the ratio of pIKKβ Ser181/IKKβ, NF-κB p65 expression and IL-6 level. Taken together, these results suggest that BBR could enhance glucose uptake, and relieve insulin resistance and inflammation in HepG2 cells. The mechanism may be related to the cholinergic anti-inflammatory pathway and the inhibition of AChE activity.
