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Article in Chinese | WPRIM | ID: wpr-707013


Objective To investigate the medicinal plant group and resource of Sect. Euthya in Paris L. in Shaanxi Province. Methods Through literature analysis and interview survey, combined with line transect method, the medicinal plant group, the natural distribution and the status of medicinal plant group and resources about Sect. Euthya in the specific county territory in Shaanxi Province were investigated.Results According to related records about the medicinal plants of Sect. Euthya in Paris L. included P. polyphylla, var. stenophylla, var. apetala, and Paris fargesii var. petiolatain in Shaanxi Province. Based on field investigation, it was found that, the medicinal plants of Sect.Euthya in Paris L.also included five variations of P.polyphylla var.latifolia,var.apperdiculata,var. thibetica, var. chinensis, and var. yunnanensis, which were new distribution records. No var. apetala was found under field investigation. Most of the rhizomes of the Sect. Euthya plants were used as Chinese materia medica Paridis Rhizoma, with wide distribution and good growth condition. The natural resources of these plants are endangered. Conclusion In this study, two species and six variations in the Sect. Euthya are identified as new distribution records. Consequently, the medicinal plant distribution record of Paris L. in Shaanxi Province is complete. The natural resources are investigated, which have laid the foundation for further research, development and protection.

Acta Pharmaceutica Sinica ; (12): 991-2016.
Article in Chinese | WPRIM | ID: wpr-779268


SWEET (sugars will be eventually exported transporters) constitute a large and conserved gene family of sugar transporters in eukaryotes, which are important in the cellular metabolisms, growth and development, and plant-microbe interaction in plants. In the present study, a full length cDNA of SWEET encoding gene, designed as DoSWEET1(GenBank accession No. KT957550), was identified in Dendrobium officinale using RT-PCR and RACE approaches. DoSWEET1 was 1150 bp in length and encoded a 262-aa protein with a molecular weight of 29.18 kD and an isoelectric point of 9.49. The deduced DoSWEET1 protein contained seven transmembrane regions and two conserved MtN3-slv domains (11-94, 130-212). Multiple sequence alignment revealed that DoSWEET1 had high identities (45%-54.6%) with SWEET proteins from various plants. A neighbor joining phylogenetic analysis suggests that DoSWEET1 belonged to the class II subgroup of the SWEET evolutionary tree, and was closely related to rice OsSWEET13, OsSWEET14, and OsSWEET15. qPCR analysis demonstrated that DoSWEET1 gene was differentially expressed in the three included organs of D. officinale, and the expression was most abundant in the roots at 9.88 fold over that of the stems, followed by that of the leaves with 2.85 fold higher. In the 3rd symbiotic germinating seeds infected by Tulasnella sp., the transcipts were dramatically induced by 1359.06 fold over that in the ungerniamted control seeds, suggesting a vital role of the gene in the D. officinale symbiotic germination process. Molecular cloning and characterization of the novel DoSWEET1 gene provides a foundation for the functional study of the gene in sugar translocation during the D. officinale symbiotic germination process.

Article in Chinese | WPRIM | ID: wpr-305335


The role of flavonoids of Echinps latifolius (FELT) in Wnt signaling was investigated in adjuvant arthritis (AA) rats. The therapeutic effects of FELT on AA rats were detected by rat arthritis score and MTT. The effect of FELT gavage treatment on the Wnt signaling key gene β-catenin, C-myc and cyclin D1 in synovium from AA rats was detected by Real-time qPCR, and the effects of FELT gavage treatment on the upstream negative regulation gene SFRP 1,2,4,5 in synovium from AA rats were detected by Real-time qPCR. The results showed that FELT gavage treatment significantly inhibited arthritis score and MTT values in AA rats, significantly inhibited the expression of the Wnt signaling gene β-catenin, C-myc and cyclin D1, significantly up-regulated the expression of the up- stream negative regulation gene SFRP 1,2,4. FELT has a better therapeutic effect for AA rats.

Animals , Arthritis, Experimental , Drug Therapy , Genetics , Metabolism , Asteraceae , Chemistry , Disease Models, Animal , Down-Regulation , Drugs, Chinese Herbal , Flavonoids , Humans , Intercellular Signaling Peptides and Proteins , Genetics , Metabolism , Male , Membrane Proteins , Genetics , Metabolism , Rats , Rats, Sprague-Dawley , Signal Transduction , Synovial Membrane , Metabolism , Wnt Signaling Pathway , beta Catenin , Metabolism
Chinese Journal of Traumatology ; (6): 314-319, 2015.
Article in English | WPRIM | ID: wpr-316792


<p><b>OBJECTIVE</b>The 8.12 Tianjin Port Explosion in 2015 caused heavy casualties. Pingjin Hospital, an affiliated college hospital in Tianjin, China participated in the rescue activities. This study aims to analyze the emergency medical response to this event and share experience with trauma physicians to optimize the use of medical resource and reduce mortality of critical patients.</p><p><b>METHODS</b>As a trauma centre at the accident city, our hospital treated 298 patients. We retrospectively analyzed the data of emergency medical response, including injury triage, injury type, ICU patient flow, and medical resource use.</p><p><b>RESULTS</b>There were totally 165 deaths, 8 missing, and 797 non-fatal injuries in this explosion. Our hospital treated 298 casualties in two surges of medical demand. The first one appeared at 1 h after explosion when 147 wounded were received and the second one at 4 h when 31 seriously injured patients were received, among whom 29 were transferred from Tianjin Emergency Center which was responsible for the scene injury triage. After reexamination and triage, only 11 cases were defined as critical ill patients. The over-triage rate reached as high as 62.07%. Seventeen patients underwent surgery and 17 patients were admitted to the intensive care unit.</p><p><b>CONCLUSIONS</b>The present pre-hospital system is incomplete and may induce two surges of medical demand. The first one has a much larger number of casualties than predicted but the injury level is mild; while the second one has less wounded but almost all of them are critical patients. The over-triage rate is high. The hospital emergency response can be improved by an effective re-triage and implementation of a hospital-wide damage control.</p>

Blast Injuries , Mortality , Therapeutics , China , Explosions , Female , Health Services Needs and Demand , Hospitals, University , Humans , Injury Severity Score , Male , Mass Casualty Incidents , Retrospective Studies , Surge Capacity , Trauma Centers , Triage
Article in English | WPRIM | ID: wpr-320342


<p><b>OBJECTIVE</b>Isoliquiritigenin (ISL), a licorice chalconoid, is considered to be a bioactive agent with chemopreventive potential. This study investigates the mechanisms involved in ISL-induced apoptosis in human cervical carcinoma HeLa cells.</p><p><b>METHODS</b>Cell viability was evaluated using a 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide (MTT) assay. Apoptosis was determined by flow cytometry using an Annexin V-FITC Apoptosis Detection Kit. The intracellular ROS levels were assessed using a 2, 7-dichlorofluorescein probe assay. The mitochondrial membrane potential was measured with the dual-emission potential-sensitive probe 5, 5', 6, 6'-tetra-chloro-1, 1', 3, 3'-tetraethyl-imidacarbocyanine iodide (JC-1). The degradation of poly-ADP-ribose polymerase (PARP) protein, the phosphorylation of PKR-like ER kinase (PERK), the phosphorylation of the α-subunit of eukaryotic initiation factor 2 (eIF2α), the expression of the 78 kD glucose-regulated protein (GRP 78), and the activation of caspase-12 were analyzed via western blot analysis.</p><p><b>RESULTS</b>ISL significantly inhibited the proliferation, the increase in ROS levels and apoptotic rates of HeLa cells in a concentration-dependent manner. Moreover, ISL induced mitochondrial dysfunction, caspase activation, and PARP cleavage, which displayed features of mitochondria dependent on apoptotic signals. Besides, exposure of HeLa cells to ISL triggered endoplasmic reticulum (ER) stress, as indicated by the increase in p-eIF2α and GRP78 expression, ER stress-dependent apoptosis is caused by the activation of ER-specific caspase-12.</p><p><b>CONCLUSION</b>The findings from our study suggest that ISL-induced oxidative stress causes HeLa cell apoptosis via the mitochondrion-dependent and the ER stress-triggered signaling pathways.</p>

Aldehyde Reductase , Apoptosis , Cell Survival , Chalcones , Pharmacology , Therapeutic Uses , Chemoprevention , Drug Screening Assays, Antitumor , Endoplasmic Reticulum Stress , HeLa Cells , Humans , Mitochondria , Neoplasms , Reactive Oxygen Species , Metabolism
Acta Pharmaceutica Sinica ; (12): 1477-1482, 2012.
Article in Chinese | WPRIM | ID: wpr-274635


This study is to investigate the mechanism of human promyelocytic leukemia HL-60 cells proliferation induced by alteronol in vitro. Human promyelocytic leukemia HL-60 cells cultured in vitro were treated with different concentrations of alteronol. Inhibition rate was detected by SRB assay. Cellular morphological changes were observed by Hoechst and AO/EB (acridine orange/ethidium bromide dye) staining. The apoptosis rate was determined by Annexin V-FITC/PI assay. Cell cycle distribution was determined by flow cytometry. Western blotting analysis was carried out to determine the cell cycle related proteins. The proliferation of HL-60 cells treated with alteronol was inhibited in a concentration-dependent manner. Based on cell viability assay, observation on cell morphology and apoptosis rate, it confirmed that alteronol played an obvious role in proliferation inhibition of human promyelocytic leukemia HL-60 cells, but it did not induce apoptosis in human promyelocytic leukemia HL-60 cells in different concentrations groups. Alteronol could effectively inhibit the proliferation of human promyelocytic leukemia HL-60 cells inducing cell cycle arrest at G1 phase, as well as, alteration expression of cell cycle proteins level of CyclinD1 and pRb.

Antineoplastic Agents , Pharmacology , Apoptosis , Cell Cycle , Cell Proliferation , Cyclin D1 , Metabolism , Dose-Response Relationship, Drug , HL-60 Cells , Humans , Naphthoquinones , Pharmacology , Phosphorylation , Retinoblastoma Protein , Metabolism