[Complete chloroplast genome sequencing and phylogeny of wild Atractylodes lancea from Yuexi, Anhui province].

This study investigated the choroplast genome sequence of wild Atractylodes lancea from Yuexi in Anhui province by high-throughput sequencing, followed by characterization of the genome structure, which laid a foundation for the species identification, analysis of genetic diversity, and resource conservation of A. lancea. To be specific, the total genomic DNA was extracted from the leaves of A. lancea with the improved CTAB method. The chloroplast genome of A. lancea was sequenced by the high-throughput sequencing technology, followed by assembling by metaSPAdes and annotation by CPGAVAS2. Bioiformatics methods were employed for the analysis of simple sequence repeats(SSRs), inverted repeat(IR) border, codon bias, and phylogeny. The results showed that the whole chloroplast genome of A. lancea was 153 178 bp, with an 84 226 bp large single copy(LSC) and a 18 658 bp small single copy(SSC) separated by a pair of IRs(25 147 bp). The genome had the GC content of 37.7% and 124 genes: 87 protein-coding genes, 8 rRNA genes, and 29 tRNA genes. It had 26 287 codons and encoded 20 amino acids. Phylogenetic analysis showed that Atractylodes species clustered into one clade and that A. lancea had close genetic relationship with A. koreana. This study established a method for sequencing the chloroplast genome of A. lancea and enriched the genetic resources of Compositae. The findings are expected to lay a foundation for species identification, analysis of genetic diversity, and resource conservation of A. lancea.

Naoluo Xintong Decoction Ameliorates Cerebral Ischemia-Reperfusion Injury by Promoting Angiogenesis through Activating the HIF-1α/VEGF Signaling Pathway in Rats.

Background: Naoluo Xintong decoction (NLXTD) is a traditional Chinese medicine (TCM) formula which has been used to improve neuronal functional recovery after cerebral ischemic stroke. However, the molecular mechanism underlying NLXTD's amelioration of ischemic stroke remains unclear. The present study was designed to explore the effect and mechanism of NLXTD on brain angiogenesis in a rat model with cerebral ischemia-reperfusion (I/R) injury targeting the hypoxia-inducible factor-1α (HIF-1α)/vascular endothelial growth factor (VEGF) pathway. Materials and Methods: Cerebral I/R model was established by the classical middle cerebral artery occlusion (MCAO) method. Sprague-Dawley (SD) male rats (n = 80) were randomly divided into the sham-operation group, the model group, the HIF-1α inhibitor 2-methoxyestradiol (2ME2) group, the 2ME2 with NLXTD group, and the NLXTD group. Neurological deficit test, TTC staining, H&E staining, TUNEL staining, immunohistochemistry (IH), immunofluorescence (IF), western blot, and quantitative RT-PCR were performed to evaluate the effect of NLXTD after MCAO. Results: Administration of NLXTD significantly decreased neuron deficiency scores, reduced brain infarct volume, and lowered damaged and apoptotic cells after brain I/R injury in rats. Meanwhile, NLXTD had a protective effect on angiogenesis by increasing the MVD and the expressions of BrdU and CD34, which enhanced the number of endothelial cells in the ischemic penumbra brain. NLXTD treatment significantly raised the protein and mRNA levels of HIF-1α, VEGF, VEGFR2, and Notch1 compared with the model treatment. In contrast, a specific HIF-1α inhibitor, 2ME2, inhibited the improvement of neurological function and angiogenesis in NLXTD-induced rats with cerebral I/R injury, suggesting that NLXTD played a positive role in ischemic brain injury by activating the HIF-1α/VEGF signaling pathway. Conclusions: NLXTD exerts neuroprotection targeting angiogenesis by upregulating the HIF-1α/VEGF signaling pathway on cerebral I/R injury rats.

[Establishment and evaluation of a rat model of ulcerative colitis with syndrome of dampness stagnancy due to spleen deficiency].

OBJECTIVE: To establish a rat model of ulcerative colitis with syndrome of spleen deficiency and dampness stagnancy. METHODS: Sixty rats were divided into normal control group, ulcerative colitis group, ulcerative colitis with syndrome of spleen deficiency and dampness stagnancy group (model group) and strengthening spleen for resolving dampness group. Ulcerative colitis in rats was induced by enema containing trinitrobenzene sulfonic acid (TNBS) and ethanol. The rats in the model group were suffered from standing in water, limiting sleeping time and abnormal diet based on administration of TNBS and ethanol. The rats in the spleen strengthening and dampness resolving group were gastrically administered with Shenlin Baizhu Powder, a compound traditional Chinese herbal medicine. Symptoms, signs and pathological changes in colon tissue of rats were observed after modeling. The levels of interleukin (IL)-6, IL-8 and tumor necrosis factor-α (TNF-α) in serum of rats were measured by enzyme-linked immunosorbent assay. RESULTS: The rats in the model group showed lethargy, poor appetite, loss of energy, diarrhea and bloody stool. Their body weight decreased significantly compared with the normal control group, and similar changes were found in the comparison of food intake, drinking amount, urine amount, stool wet weight and assay of spontaneous activity (P<0.05). When observed under a light microscope, the colon tissues of rats in the model group showed mucosal edema, congestion, inflammatory cell infiltration and ulceration. The degree of colon injury and IL-6, IL-8 and TNF-α levels were significantly increased (P<0.05) as compared to those in the normal control group. The changes mentioned above were improved by Shenlin Baizhu Powder (P<0.05). CONCLUSION: The rat model of ulcerative colitis with syndrome of spleen deficiency and dampness stagnancy is successfully induced and has the characteristics of ulcerative colitis of humans both in pathological changes and in syndrome.

[Comparative study on effects of three traditional Chinese medicinal compounds on energy metabolism related enzymes in cerebral tissue of rats after focal cerebral ischemia and reperfusion].

OBJECTIVE: To compare the effects of three traditional Chinese medicinal compounds on energy metabolism related enzymes in cerebral tissue of rats after focal cerebral ischemia and reperfusion (I/R). METHODS: The local cerebral I/R model was established by ligation of the middle cerebral arteries (MCA). The animals were divided into the sham-operative group, the model group, the Yiqi Huoxue Recipe (YHR) group, the Zhengan Xifeng Decoction (ZXD) group and the Xinglou Chengqi Decoction (XCD) group. The mitochondria in brain tissue was obtained by density-centrifugation and differential centrifugation, then the activities of succinate dehydrogenase (SDH), Na+ -K+ -ATPase, creatine kinase-BB (CK-BB) in homogenate of brain tissue were measured by chemical chromometry. RESULTS: Activities of SDH and Na+-K+ -ATPase were lower and that of CK-BB was higher in the model group than those in the sham -operative group at all time points after I/R (P< 0.01). Compared with those in the model group, activity of Na+ -K+ -ATPase was higher only in the ZXD group at 24 h after I/R, while at 48 h and 72 h after I/R, activities of both SDH and Na+ -K+ -ATPase were higher in all the treatment groups. As for the activity of CK-BB, it was lower in all the treatment groups (P < 0.05). The optimal effect was shown in the ZXD group at 24 h, in the XCD group at 48 h, and in the YHR group at 72 h after I/R. CONCLUSION: The three traditional Chinese medicinal compounds could reduce pathologic injury after focal cerebral I/R in rats by promoting activity of SDH and Na+ -K+ -ATPase and inhibiting that of CK-BB, the optimal effect of ZXD was shown at 24 h after I/R, that of XCD at 48 h after I/R and of YHR at 72 h after I/R.