One important purpose to investigate medicinal plants is to understand genes and enzymes that govern the biological metabolic process to produce bioactive compounds.Genome wide high throughput technologies such as genomics,transcriptomics,proteomics and metabolomics can help reach that goal.Such technologies can produce a vast amount of data which desperately need bioinformatics and systems biology to process,manage,distribute and understand these data.By dealing with theomicsdata,bioinformatics and systems biology can also help improve the quality of traditional medicinal materials,develop new approaches for the classification and authentication of medicinal plants,identify new active compounds,and cultivate medicinal plant species that tolerate harsh environmental conditions.In this review,the application of bioinformatics and systems biology in medicinal plants is briefly introduced.

Germination of the seeds of Bupleurum chinense and B. falcatum activated by exogenous hormones of dif ferent concentrations was studied. The hormones used were GA3, 6-BA and IAA. The optimum concentration of the 3 hormones that activated the seed germination of B. chinense was 50?g/ml,while that for B. falcatum was 200?g/ml, 100?g/ml and 25?g/ml respectively. Among the 3 hormones, 6-BA showed the greatest effect on the 2 species of Bupleurum L. 50?g/ml 6-BA raised the germination rate of the seeds of B. chinese from 57.5 % to 84. 5 % and 100?g/ml 6-BA raised the germination rate of the seeds of B.falcatum from 28. 5 % to 76.0%

A new dibenzocyclooctadiene lignan, renchangianin E (1) was isolated from the stems of Kadsura renchangiana. Its structure and stereochemistry were elucidated by spectroscopic methods, including 2D-NMR techniques.

Objective To evaluate the effect of dexmedetomidine pretreatment on Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling pathway during intestinal ischemia-reperfusion (I/R) in rats.Methods Twenty-four male Spragne-Dawley rats,weighing 180-220 g,were divided into 3 groups (n =8 each) using a random number table method:sham operation group (S group),intestinal I/R group (I group) and dexmedetomidine pretreatment group (DP group).Intestinal I/R model was established by occlusion of the superior mesenteric artery for 1 h followed by 2-h reperfusion in anesthetized rats.Dexmedetomidine 100 μg/kg was intraperitoneally injected at 30 min before ischemia in DP group.Blood samples were collected from hearts at the end of reperfusion for determination of the serum intestinal fatty acid binding protein (I-FABP) level by enzyme-linked immunosorbent assay.The intestinal tissues were obtained at the end of reperfusion for examination of pathologic changes and for determination of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) contents (by enzyme-linked immunosorbent assay) and expression of TLR4,MyD88,phosphorylated NF-κB p65 (p-NF-κB p65) in total protein and NF-κB p65 in nucleoprotein (by Western blot).The degree of intestinal tissue damage was graded using Chiu's scoring system.Results Compared with S group,the Chiu's score and concentrations of IFABP in serum and contents of TNF-α and IL-1β in intestinal tissues were significantly increased,and the expression of TLR4,MyD88 and p-NF-κB p65 in total protein and NF-κB p65 in nucleoprotein was up-regulated in I/R group,and the Chiu's score was significantly increased,the expression of MyD88 and p-NF-κB p65 was up-regulated (P＜0.05),and no significant change was found in serum I-FABP concentration,contents of TNF-α and IL-1β,or expression of TLR4 in total protein and NF-κB p65 in nucleoprotein in DP group (P＞0.05).Compared with I/R group,the Chiu's score,serum I-FABP concentration,and contents of TNF-α and IL-1β were significantly decreased,and the expression of TLR4,MyD88 and p-NF-κB p65 in total protein and NF-κB p65 in nucleoprotein was down-regulated in DP group (P＜0.05).Conclusion The mechanism by which dexmedetomidine pretreatement mitigates intestinal I/R injury may be related to inhibiting activation of TLR4/NF-κB signaling pathway in rats.