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Protective effect of spleen-yin-nourishing recipe on amyloid β-peptide-induced damage of primarily cultured rat hippocampal neurons and its mechanism

Keywords: Alzheimer disease , Zibu Piyin Recipe , amyloid beta-peptide , serum-inducible kinase , spine-associated Rap guanosine triphosphatase activating prote , receptors , N-methyl-D-aspartate , synapses

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Objective: To observe the relationship among amyloid β-peptide (Aβ)-induced neurotoxicity, serum-inducible kinase (SNK)-spine-associated Rap guanosine triphosphatase activating protein (SPAR) pathway and N-methyl-D-aspartate receptor (NMDAR), and to explore the mechanism of the protective effect of spleen-yin nourishing recipe (Zibu Piyin Recipe, ZBPYR) in hippocampal neurons against Aβ-induced neurotoxicity.Methods: The Aβ1-40 powder was dissolved in 1×PBS and incubated at 37 ℃, and then aggregated fibrillar Aβ1-40 was obtained 72 h later. We used rat primary hippocampal neurons as cell model. ZBPYR-containing serum was gained by the method of serum pharmacology. ZBPYR-containing serum was added to the culture 1 h before Aβ1-40 (5 μmol/L) exposure. Cells were harvested 2 h after Aβ1-40 exposure for total RNA extracting. Then the mRNA expression levels of SNK, SPAR and NMDAR subunits NR1, NR2A and NR2B were detected by reverse transcription-polymerase chain reaction (RT-PCR).Results: After 2-hour Aβ1-40 exposure, we found that the expression level of SNK mRNA was up-regulated and the expression levels of SPAR, NR1, NR2A and NR2B mRNAs were down-regulated in hippocampal neurons as compared with control group (P<0.01, P<0.05). While with ZBPYR-containing serum pretreatment, the expression level of SNK mRNA was down-regulated and the levels of SPAR, NR1, NR2A and NR2B were up-regulated as compared with Aβ1-40 exposure, and 2% ZBPYR-containing serum showed the best effect (P<0.05). Conclusion: Aβ-induced neurotoxicity was related to SNK-SPAR pathway and NMDAR; ZBPYR-containing serum can protect neurons from Aβ-induced neurotoxicity, and this protective effect may be performed by regulating the expression of NMDAR and blocking of the SNK-SPAR pathway. JCIM Open Access THIS ARTICLE Abstract Full text Download PDF file Send to a friend Related articles in JCIM Cited in JCIM Reader's comments Send a comment


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