Hydroxysafflor Yellow A Attenuates Lipopolysaccharide-Induced Neurotoxicity and Neuroinflammation in Primary Mesencephalic Cultures

Molecules. 2018 May 18;23(5):1210. doi: 10.3390/molecules23051210.

Abstract

Lipopolysaccharide (LPS)-induced neuroinflammation triggers and accelerates the pathogenesis of Parkinson's disease (PD). Carthamus tinctorius L., a traditional Chinese medicine, has been widely used for the treatment of cerebrovascular disease. Hydroxysafflor Yellow A (HSYA) is an active component of C. tinctorius. The purpose of this study was to investigate whether HSYA could attenuate LPS-induced neurotoxicity and neuroinflammation in primary mesencephalic cultures. Cell viability was measured by MTT and LDH assays. The number of tyrosine hydroxylase (TH) positive neuron was observed by immunohistochemistry. NF-κB p65 and iNOS expressions were evaluated with western blotting method. Pro-inflammatory cytokines including IL-1β and TNF-α were determined by ELISA kits. Nitric oxide (NO) content in the culture medium was assayed. The results showed that HSYA treatment significantly attenuated the LPS-induced dopaminergic neurons damage. HSYA partially inhibited the expressions of NF-κB p65 and iNOS. Furthermore, HSYA decreased the content of IL-1β, TNF-α and NO in the supernatants. Taken together, these results suggest that HSYA exerts protective effects on LPS-induced neurotoxicity in dopaminergic neurons and the mechanisms may be associated with the inhibition of inflammatory response.

Keywords: Hydroxysafflor Yellow A; lipopolysaccharide; neuroinflammation; neurotoxicity.

MeSH terms

  • Animals
  • Carthamus tinctorius / chemistry
  • Cell Survival / drug effects
  • Cells, Cultured
  • Chalcone / analogs & derivatives*
  • Chalcone / chemistry
  • Chalcone / pharmacology
  • Cytokines / metabolism
  • Humans
  • Inflammation / drug therapy*
  • Lipopolysaccharides / pharmacology*
  • Mesencephalon / cytology
  • Mice, Inbred C57BL
  • Neurons / drug effects*
  • Neurons / metabolism
  • Nitrogen Oxides
  • Primary Cell Culture
  • Quinones / chemistry
  • Quinones / pharmacology*
  • Signal Transduction
  • Tissue Distribution
  • Transcription Factor RelA / metabolism

Substances

  • Cytokines
  • Lipopolysaccharides
  • Nitrogen Oxides
  • Quinones
  • Transcription Factor RelA
  • lipopolysaccharide, E coli O55-B5
  • hydroxysafflor yellow A
  • Chalcone