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

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.

• Authors: Tian Wang, Yu-Xin Ding, Jie He, Cheng-Jun Ma, Yue Zhao, Zhen-Hua Wang, Bing Han
• Journal: Molecules (Basel, Switzerland) (Molecules) Vol. 23 Issue 5 (May 18 2018) ISSN: 1420-3049 [Electronic] Switzerland
• PMID: 29783643 (Publication Type: Journal Article)

Chemical References

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

Topics

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