Complete chloroplast genome of adonis amurensis (ranunculaceae), an important cardiac folk medicinal plant in east asia.

Adonis amurensis Regel et Radde is an important cardiac folk medicinal plant which endemic to Northeast Asia. We determined the first complete chloroplast genome of A. amurensis using genome skimming approach. The cp genome was 157,032 bp long, with a large single-copy region (LSC) of 86,218 bp and a small single-copy region (SSC) of 18,212 bp separated by a pair of inverted repeats (IRs) of 26,301 bp. It encodes 129 genes, including 84 protein-coding genes, 37 tRNA genes, and 8 ribosomal RNA genes. We also reconstructed the phylogeny of Adonideae and Isopyreae using maximum likelihood (ML) method, including our data and previously reported cp genomes of related taxa. The phylogenetic analysis indicated that A. amurensis is close related with Adonis sutchuenensis.

[Effects of icariin on proliferation of vascular smooth muscle cell induced by ox-LDL via impacting MAPK signaling pathway].

This paper was aimed to study the effects of icariin (ICA) on the proliferation of vascular smooth muscle cell (VSMC) induced by oxidized low density lipoprotein (ox-LDL), and the molecular mechanism of the expression of proliferating cell nuclear antigen (PCNA) and MAPK signaling pathway. In this study, VSMC was induced by ox-LDL (50 mg•L⁻¹),the effect of ICA on the proliferation of VSMC was detected by MTT assay, Western blot and Real-time PCR. The results showed that after stimulation of ox-LDL, the proliferation activity of VSMC was increased, S phase, G2/M phase cells were increased, G0/G1 phase cells were decreased, PCNA protein expression was enhanced; ICA (40, 20, 10 µmol•L⁻¹) could effectively inhibit ox-LDL-induced VSMC proliferation, S phase and G2/M phase cells were decreased, the percentage of cells in G0/G1 phase were increased, PCNA expression was decreased, p38MAPK and ERK1/2 activation were inhibited. These results indicate that ICA can inhibit the proliferation of VSMC by reducing the expression of PCNA and blocking the p38MAPK and ERK1/2 signaling pathway.

[Effect and mechanism of icariin on myocardial ischemia-reperfusion injury model in diabetes rats].

To study the therapeutic effect and possible mechanism of icariin on myocardial ischemia-reperfusion injury ( MIRI) model in diabetes rats. The model of diabetic rats were induced by Streptozotocin (STZ), then the model of MIRI was established by ligating the reversible left anterior descending coronary artery for 30 min, and then reperfusing for 120 min. totally 40 male SD were randomly divided into five groups: the control group (NS), the ischemia reperfusion group (NIR), the diabetes control group (MS), the diabetic ischemia reperfusion group (MIR) and the diabetic ischemia reperfusion with icariin group (MIRI). The changes in blood glucose, body weight and living status were observed; the enzyme activity of serum CK-MB, LDH, GSH-Px and myocardium SOD and the content MDA and NO in myocardium were detected; the myocardial pathological changes were observed by HE staining; the myocardial Caspase-3, the Bcl-2, Bax protein expressions were detected by Western blot. The result showed that the diabetes model was successfully replicated; myocardial ischemia-reperfusion injury was more serious in diabetes rats; icariin can increase NO, SOD, GSH-Px, Bcl-2 protein expression, decrease MDA formation, CK-MB and LDH activities and Caspase-3 and Bcl-2 protein expressions and myocardial damage. The result suggested that icariin may play a protective role against ischemia reperfusion myocardial injury in diabetes rats by resisting oxidative stress and inhibiting cell apoptosis.