Development of microsatellite markers for the dove tree, Davidia involucrata (Nyssaceae), a rare endemic from China.

PREMISE OF THE STUDY: Microsatellite primers were developed for the endangered Davidia involucrata to assess the population genetics and infer its evolutionary history. METHODS AND RESULTS: Using both the modified magnetic bead hybridization method and the dual-suppression PCR method, we isolated and characterized 12 polymorphic microsatellite loci using 134 individuals from five populations in southwestern China. The number of alleles per locus ranged from six to 21 (mean = 10.8). The expected heterozygosity per locus ranged from 0.404 to 0.918 and observed heterozygosity ranged from 0.015 to 0.821. CONCLUSIONS: All of the 12 microsatellite markers developed for D. involucrata are polymorphic, and lay a solid foundation for further studies of the population genetics of this famous tree.

[Inhibitory action of hydroxysafflor yellow A on inflammatory signal transduction pathway related factors in rats with cerebral cortex ischemia].

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.