Abstract | OBJECTIVE: METHOD: The 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. RESULT: Compared 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. CONCLUSION:
Berberine 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.
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Authors | Jing Xu, Hong Zhang, Fan Yang, Jin-Xin Yu |
Journal | Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
(Zhongguo Zhong Yao Za Zhi)
Vol. 38
Issue 9
Pg. 1327-30
(May 2013)
ISSN: 1001-5302 [Print] China |
PMID | 23944062
(Publication Type: English Abstract, Journal Article)
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Chemical References |
- Amyloid beta-Peptides
- Peptide Fragments
- Receptors, Interleukin-1 Type I
- Tumor Necrosis Factor-alpha
- amyloid beta-protein (25-35)
- Berberine
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Topics |
- 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)
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