Intervention effect of berberine on expressions of TNF-alpha and receptor type I in Abeta25-35-induced inflammatory reaction in SH-SY5Y cell lines.
- Author:
Jing XU
1
;
Hong ZHANG
;
Fan YANG
;
Jin-Xin YU
Author Information
- Publication Type:Journal Article
- MeSH: Amyloid beta-Peptides; toxicity; Berberine; pharmacology; Cell Line; Humans; Inflammation; chemically induced; metabolism; Peptide Fragments; toxicity; Receptors, Interleukin-1 Type I; metabolism; Tumor Necrosis Factor-alpha; metabolism
- From: China Journal of Chinese Materia Medica 2013;38(9):1327-1330
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of berberine on expressions of tumor necrosis factor alpha (TNF-alpha) and receptor type I (TNFR1) in Abeta25-35-induced inflammatory reaction in SH-SYSY cell lines.
METHODThe 5 micromol . L-1 Abeta25-35 was used to treat SH-SY5Y cells for 24 hours, in order to establish the Alzheimer's disease (AD) model. Before modeling, berberine was given for pretreatment for 2 hours. The experiment included the normal control group, the AD model group, and indometacin low dose and high dose groups. Spectrophotometry was adopted to detect the activity of LDH. Meanwhile, the level of TNF-alpha was determined by ELISA, and the expression of TNFR1 genes was detected by RT-PCR.
RESULTCompared with the normal control group, the AD cell model group showed significant increase in LDH, TNF-alpha, and TNFR1 gene and protein expressions in the culture media. After intervention with berberine, the activity of LDH and TNF-alpha reduced in cell supernatant. The intervention with berberine could down-regulate TNFR1 gene and protein expressions, particularly 1, 10 x 10(-6) mol . L-l berberine showed a more notable effect in regulating TNFR1.
CONCLUSIONBerberine has the protective effect in Abeta-induced inflammatory injury in SH-SY5Y cells. Its mechanism may be related to the expression of its anti inflammatory factor TNF-alpha and its type I receptor TNFR1. Specifically, its regulation to TNFR1 shows dose dependence.