4.4 Article

Effects of andrographolide on postoperative cognitive dysfunction and the association with NF-κB/MAPK pathway

Journal

ONCOLOGY LETTERS
Volume 14, Issue 6, Pages 7367-7373

Publisher

SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2017.7088

Keywords

Morris water maze test; aged rats; neuron-specific enolase; human soluble protein-100 beta; NF-kappa B/MAPK

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Funding

  1. Traditional Chinese Medicine Science and Technology Development of Project of Shandong Province, China [2015-416]
  2. National Science Foundation of Shandong Province, China [ZR2016HL17]

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The present study investigated the effects of andrographolide on postoperative cognitive dysfunction (POCD) in aged rats to gain insight of the underlying mechanism, which may provide theoretical basis for the clinical application of andrographolide to prevent POCD in older patients. Thirty aged male rats were randomly assigned to 3 groups: Control, model and andrographolide groups. The Morris water maze test was used to examine the spatial memory and learning ability of the rats postoperatively. The histological alterations of neuronal cells in the hippocampus were visualized by H&E staining. The serum levels of neuron-specific enolase (NSE), human soluble protein-100 beta (S-100 beta) and the inflammation factors of interluekin (IL)-1 beta, IL-6 and TNF-alpha involved in the nuclear factor kappa B (NF-kappa B)/mitogen-activated protein kinase (MAPK) signaling pathway were detected by ELISA. The NF-kappa B/MAPK signaling pathway-associated proteins in rat serum were detected by western blotting. Following andrographolide treatment, the rats significantly gained learning ability after surgery. Is it ameliorated hippocampal neuronal injury in rats following surgery. Andrographolide decreased NSE, S-100 beta, and the inflammation factors, IL-6, IL-1 beta and TNF-alpha in serum. Andrographolide reduced NF-kappa B/MAPK pathway-associated protein expression. Andrographolide ameliorated POCD in aged rats following surgery. The underlying mechanism may be associated with the downregulation the inflammatory factors and NF-kappa B/MAPK-associated protein expression.

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