RESUMO
Paris is famous in China for its medicinal value and has been included in the Chinese Pharmacopoeia. Inaccurate identification of these species could confound their effective exploration, conservation, and domestication. Due to the plasticity of the morphological characteristics, correct identification among Paris species remains problematic. In this regard, we report the complete chloroplast genome of P. thibetica and P. rugosa to develop highly variable molecular markers. Comparing three chloroplast genomes, we sought out the most variable regions to develop the best cpDNA barcodes for Paris. The size of Paris chloroplast genome ranged from 162,708 to 163,200 bp. A total of 134 genes comprising 81 protein coding genes, 45 tRNA genes and 8 rRNA genes were observed in all three chloroplast genomes. Eight rapidly evolving regions were detected, as well as the difference of simple sequence repeats (SSR) and repeat sequence. Two regions of the coding gene ycf1, ycf1a and ycf1b, evolved the quickest and were proposed as core barcodes for Paris. The complete chloroplast genome sequences provide more integrated and adequate information for better understanding the phylogenetic pattern and improving efficient discrimination during species identification.
Assuntos
Código de Barras de DNA Taxonômico/métodos , Genoma de Cloroplastos , Melanthiaceae/genética , Genes de Plantas , Melanthiaceae/classificação , Repetições de Microssatélites , Filogenia , Plantas Medicinais/classificação , Plantas Medicinais/genéticaRESUMO
OBJECTIVE: To investigate the effects of the proprietary Chinese Medicine "anti-hepatic-fibrosis 268" on hepatic fibrosis and the related mechanisms. METHODS: The model of CCl4-induced hepatic damage was established in SD rats. 54 male rats were divided into four groups, namely high dose and low dose "anti-hepatic-fibrosis 268" groups, colchicine control group, and model control group. Using Masson stain and light microscope, the authors examined the rats' hepatic tissues and counted the hepatic fiber components, then examined and counted TGF-beta1, alpha-SMA, FN, Type I, III collagen by means of immunohistochemical technique. The groups were compared and the internal relationships of the data were analyzed. RESULTS: The levels of FN, LN, Type I and III collagen, TGF-beta1, and alpha-SMA of the CCl4 damaged rats increased (P<0.01). After 3 weeks of high dose "anti-hepatic-fibrosis 268" treatment, the levels of TGF-beta1, alpha-SMA, FN, LN, Type I and III collagen decreased (P<0.01) and the degree hepatic fibrosis took a favorable turn significantly (P<0.05) as compared with the model control. In the rats of the low dose group, the levels of TGF-beta1, alpha-SMA, FN, Type III collagen significantly decreased (P<0.05), the levels of LN, Type I collagen were not different from the model control; The hepatic fibrosis improved to a certain extent (P<0.05). CONCLUSION: The mechanism of reversing hepatic fibrosis by "anti-hepatic-fibrosis 268" in this experiment is that the medicine regulates TGF-beta1 and further affects alpha-SMA, thus resulting in the decline of FN, Type I, III collagen levels in liver extracellular matrix.