title: [Inhibitory action of hydroxysafflor yellow A on inflammatory signal transduction pathway related factors in rats with cerebral cortex ischemia].
abstract: Hydroxysafflor yellow A (HSYA) is a main active monomer purified from Carthamus tinctorius L. The research is to study the inhibitory effect of HSYA on the inflammatory signal transduction pathway related factors which were induced by permanent cerebral ischemia in rats. By using the successive administration at a 30 min interval of HSYA and the rats permanent focal cerebral ischemia model established by a intraluminal suture occlusion method. After cerebral artery occlusion 3, 6, 12 and 24 h, cortex was removed for the next experiments. Western blotting was used to detect the expression of p65 protein and the phospho-IkappaB-alpha (pIkappaB-alpha) in the cytoplasm and nucleus. Nuclear factor-kappaB (NF-kappaB) DNA binding activity was measured by Trans-AM transcription factor assay kits. mRNA expression of cytokines TNF-alpha, IL-1beta, IL-6 and IL-10 was measured by the RT-PCR method. The result showed that intravenous injection of HSYA (10 mg x kg(-1)) to rats after cerebral occlusion, the p65 translocation activity and the phosphorylation of IkappaB-alpha were significantly inhibited. At the same time, HSYA suppressed p65 binding activity and the transcriptional level of pro-inflammatory cytokines including TNF-alpha, IL-1beta and IL-6, and promoted the mRNA expression of anti-inflammatory cytokine IL-10. In conclusion, the anti-cerebral ischemic mechanism of HSYA may be due to its inhibition of NF-kappaB activity and the mRNA expression of cytokines in the inflammatory transduction pathway.
authors.affiliation: Key Laboratory of Bioactive Substances and Resources Utilization of Chinese Herbal Medicine Affiliated Ministry of Education, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
authors.forename: Ting-Ting
authors.initials: TT
authors.lastname: Chen
authors.forename: Yu-Juan
authors.initials: YJ
authors.lastname: Du
authors.forename: Xiao-Lei
authors.initials: XL
authors.lastname: Liu
authors.forename: Hai-Bo
authors.initials: HB
authors.lastname: Zhu
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism*; D031178:Carthamus / Q000737:chemistry; D002599:Chalcone / Q000031:analogs & derivatives* / Q000302:isolation & purification / Q000494:pharmacology; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics; D035264:Flowers / Q000737:chemistry; D020672:I-kappa B Proteins / Q000378:metabolism; D016753:Interleukin-10 / Q000096:biosynthesis / Q000235:genetics; D053583:Interleukin-1beta / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000096:biosynthesis / Q000235:genetics; D008297:Male; D000072000:NF-KappaB Inhibitor alpha; D018696:Neuroprotective Agents / Q000302:isolation & purification / Q000494:pharmacology; D010766:Phosphorylation / Q000187:drug effects; D010946:Plants, Medicinal / Q000737:chemistry; D021381:Protein Transport; D011809:Quinones / Q000302:isolation & purification / Q000494:pharmacology*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects*; D051996:Transcription Factor RelA / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D020672:I-kappa B Proteins; D053583:Interleukin-1beta; D015850:Interleukin-6; D018696:Neuroprotective Agents; C000606206:Nfkbia protein, rat; D011809:Quinones; D012333:RNA, Messenger; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D000072000:NF-KappaB Inhibitor alpha; C085278:hydroxysafflor yellow A; D002599:Chalcone