Clinical, Imaging Characteristics and Outcome of Intracerebral Hemorrhage Caused by Structural Vascular Lesions.

BACKGROUND: The objective of this study was to investigate the clinical, imaging, and outcome characteristics of intracerebral hemorrhage (ICH) caused by structural vascular lesions. METHODS: We retrospectively analyzed data from a prospective observational cohort study of patients with spontaneous ICH admitted to the First Affiliated Hospital of Chongqing Medical University between May 2016 and April 2021. Good outcome was defined as modified Rankin Scale score of 0-3 at 3 months. The clinical and imaging characteristics were compared between primary ICH and ICH caused by structural vascular lesions. Multivariable logistic regression analysis was performed to test the associations of etiology with clinical outcome. RESULTS: All patients enrolled in this study were Asian. Compared with patients with primary ICH, those with structural vascular lesions were younger (48 vs. 62 years, P < 0.001), had a lower incidence of hypertension (26.4% vs. 81.7%, P < 0.001) and diabetes (7.4% vs. 16.2%, P = 0.003), and had mostly lobar hemorrhages (49.1% vs. 22.8%). ICH from structural vascular lesions had smaller baseline hematoma volume (8.4 ml vs. 13.8 ml, P = 0.010), had lower mortality rate at 30 days and 3 months (5.8% vs. 12.0%, P = 0.020; 6.7% vs. 14.8%, P = 0.007), and are associated with better functional outcome at 3 months (88% vs.70.3%, P < 0.001). CONCLUSIONS: Compared with primary ICH, ICH due to vascular lesions has smaller hematoma volume and less severe neurological deficit at presentation and better functional outcomes.

A randomized controlled comparative study of different fluid exchange modes in urgent-start peritoneal dialysis in patients with end-stage renal disease: automated peritoneal dialysis combined with manual fluid exchange vs. manual fluid exchange alone.

During urgent-start peritoneal dialysis (USPD) in end-stage renal disease (ESRD) patients, both adequate dialysis and skill training for fluid exchange are essential. However, automated peritoneal dialysis (APD) alone or manual fluid exchange peritoneal dialysis (MPD) alone could meet the above demands. Therefore, our study combined APD with MPD (A-MPD), and compared A-MPD with MPD, aiming to find the most appropriate treatment mode. This was a single-center, prospective, randomized controlled study. All eligible patients were randomized into the MPD and A-MPD groups. All patients underwent a five-day USPD treatment 48 h after catheter implantation, and they were followed up for six months after discharge. Overall, 74 patients were enrolled in this study. Among these, 14 and 60 patients quit due to complications during USPD and completed the study (A-MPD = 31, MPD = 29), respectively. Compared with MPD, the A-MPD treatment mode had a better effect on removing serum creatinine, blood urea nitrogen, and potassium and improving serum carbon dioxide combining power levels; it had less time expenditure on the fluid exchange by nurses (p < 0.05). In addition, patients in the A-MPD group had higher scores on the skill tests than those in the MPD group (p = 0.002). However, no significant differences in short-term peritoneal dialysis (PD) complications, PD technical survival rate, or mortality were found between the two groups. Therefore, the A-MPD mode could be recommended as an adoptable and suitable PD modality for USPD in the future.

Enhancing Permeation of Drug Molecules Across the Skin via Delivery in Nanocarriers: Novel Strategies for Effective Transdermal Applications.

The transdermal route of administration provides numerous advantages over conventional routes i.e., oral or injectable for the treatment of different diseases and cosmetics applications. The skin also works as a reservoir, thus deliver the penetrated drug for more extended periods in a sustained manner. It reduces toxicity and local irritation due to multiple sites for absorption and owes the option of avoiding systemic side effects. However, the transdermal route of delivery for many drugs is limited since very few drugs can be delivered at a viable rate using this route. The stratum corneum of skin works as an effective barrier, limiting most drugs' penetration posing difficulty to cross through the skin. Fortunately, some non-invasive methods can significantly enhance the penetration of drugs through this barrier. The use of nanocarriers for increasing the range of available drugs for the transdermal delivery has emerged as a valuable and exciting alternative. Both the lipophilic and hydrophilic drugs can be delivered via a range of nanocarriers through the stratum corneum with the possibility of having local or systemic effects to treat various diseases. In this review, the skin structure and major obstacle for transdermal drug delivery, different nanocarriers used for transdermal delivery, i.e., nanoparticles, ethosomes, dendrimers, liposomes, etc., have been discussed. Some recent examples of the combination of nanocarrier and physical methods, including iontophoresis, ultrasound, laser, and microneedles, have also been discussed for improving the therapeutic efficacy of transdermal drugs. Limitations and future perspectives of nanocarriers for transdermal drug delivery have been summarized at the end of this manuscript.

The complete mitochondrial genome of soft coral Sinularia penghuensis Ofwegen and Benayahu, 2012 (Octocorallia: Alcyonacea): the analysis of mitogenome organization and phylogeny.

The complete mitochondrial genome of Sinularia penghuensis was sequenced and analyzed using next-generation sequencing. The present mitochondrial genome was 18730 bp in length, containing 14 protein-coding genes (PCGs) (cox1-cox3.nad1-nad6, nad4L, atp6, atp8, cytb, and MutS), two ribosomal RNA genes (rRNAs) (12S and 16S), and one transfer RNA gene (Met-tRNA). The phylogenetic analysis of family Alcyoniidae revealed that S. penghuensis and Sinularia maxima cluster together. Five species in Sinularia reveals high identity in mitogenome sequences that the lowest variable sites (SNPs) were found between S. penghuensis and S. maxima.

RNA-Seq Provides New Insights into the Molecular Events Involved in "Ball-Skin versus Bladder Effect" on Fruit Cracking in Litchi.

Fruit cracking is a disorder of fruit development in response to internal or external cues, which causes a loss in the economic value of fruit. Therefore, exploring the mechanism underlying fruit cracking is of great significance to increase the economic yield of fruit trees. However, the molecular mechanism underlying fruit cracking is still poorly understood. Litchi, as an important tropical and subtropical fruit crop, contributes significantly to the gross agricultural product in Southeast Asia. One important agricultural concern in the litchi industry is that some famous varieties with high economic value such as 'Nuomici' are susceptible to fruit cracking. Here, the cracking-susceptible cultivar 'Nuomici' and cracking-resistant cultivar 'Huaizhi' were selected, and the samples including pericarp and aril during fruit development and cracking were collected for RNA-Seq analysis. Based on weighted gene co-expression network analysis (WGCNA) and the "ball-skin versus bladder effect" theory (fruit cracking occurs upon the aril expanding pressure exceeds the pericarp strength), it was found that seven co-expression modules genes (1733 candidate genes) were closely associated with fruit cracking in 'Nuomici'. Importantly, we propose that the low expression level of genes related to plant hormones (Auxin, Gibberellins, Ethylene), transcription factors, calcium transport and signaling, and lipid synthesis might decrease the mechanical strength of pericarp in 'Nuomici', while high expression level of genes associated with plant hormones (Auxin and abscisic acid), transcription factors, starch/sucrose metabolism, and sugar/water transport might increase the aril expanding pressure, thereby resulting in fruit cracking in 'Nuomici'. In conclusion, our results provide comprehensive molecular events involved in the "ball-skin versus bladder effect" on fruit cracking in litchi.

miR-106b-5p induces immune imbalance of Treg/Th17 in immune thrombocytopenic purpura through NR4A3/Foxp3 pathway.

BACKGROUND: Immune imbalance of regulatory T cells (Treg)/T helper 17 cells (Th17) contributes to the development of immune thrombocytopenic purpura (ITP). The dysregulation of miRNAs is important in the development of ITP. However, the role of miR-106b-5p in Treg/Th17 imbalance remains unknown in ITP. MATERIALS AND METHODS: Peripheral blood was collected from patients with ITP and healthy controls, and CD4 + T cells were further isolated. miR-106b-5p, nuclear receptor subfamily 4 group A member 3 (NR4A3), forkhead box protein 3 (Foxp3), IL-17A, and TGF-ß expressions were detected by qRT-PCR, western blot, or ELISA. The effect of miR-106b-5p on NR4A3 was detected by dual-luciferase reporter gene assay. RESULTS: Compared with healthy controls, miR-106b-5p was elevated in peripheral blood of patients with ITP, and NR4A3 expression was decreased. sh-NR4A3 significantly decreased Foxp3 and TGF-ß expressions, indicating that NR4A3 may regulate Treg differentiation via Foxp3. Additionally, NR4A3 was identified to be a target of miR-106b-5p, and miR-106b-5p was able to negatively modulate NR4A3 expression. Moreover, we found miR-106b-5p induced immune imbalance of Treg/Th17 through NR4A3. In vivo experiments revealed that silencing miR-106b-5p promoted Treg differentiation and increased the number of platelets, suggesting the relief of ITP. CONCLUSION: miR-106b-5p regulated immune imbalance of Treg/Th17 in ITP through the NR4A3/Foxp3 pathway.

[Pathogenesis of Immune Thrombocytopenic Purpura (ITP) by MiRNA-30a-Mediated Th17 Cell Differentiation].

OBJECTIVE: To investigate whether miRNA-30a is involved in the pathogenesis of ITP by affecting the differentiation of Th17 cells, and to explore its possible mechanism of miRNA-30a involved in the pathogenesis of ITP through the verification of the target gene SOCS3 for the prediction of miRNA-30a. METHODS: Firstly, a chronic ITP mouse model was established. The expression of miRNA-30a and RORγt in the spleen mononuclear cells were detected and their correlation were analyzed. Secondly, the luciferase vector containing 3'UTR of the target gene and green fluorescent vector containing miRNA were constructed. Luciferase fluorescence detection, real-time fluorescent quantitative PCR (qPCR) and Western blot were used to verify whether SOCS3 is the target gene of miRNA-30a. RESULTS: The platelet count of mice in experimental group decreased to below 20% of normal ones after 48 hours of injection of anti-mouse platelet serum (APS), which was maintained for 14 days at least; the expression of miRNA-30a and RORγt in the spleen mononuclear cells in experimental group were higher than those in the control group(P＜0.05), moreover, there was a positive correlation between them (r=0.54); the activity of luciferase in PMDH-GFP-miRNA-30a and pMIR-report-UTR was significantly lower than that in PMDH-GFP empty plasmid and pMIR-report-UTR(P＜0.05); The expression of SOCS3 at mRNA and protein level was not different from that in the control group. CONCLUSION: Chronic ITP mouse model has been established successfully; miRNA-30a expression in spleen mononuclear cells of ITP mouse increase, and positively correlated with the expression of RORγt, which contribute to the pathogenesis of ITP by affecting the differentiation of Th17 cells; SOCS3 is able to bind to the target site of miRNA-30a, but might not be its functional target gene.

[Protective effect of paeoniflorin against PM2.5-induced damage in BEAS-2B cells].

OBJECTIVE: To investigate the protective effects of paeoniflorin against PM2.5-induced damage in BEAS-2B cells and explore the possible mechanism. METHODS: With a factorial design, this study was performed to observe the protective effects of different doses of paeoniflorin against PM2.5-induced BEAS-2B cell growth inhibition and the effects of paeoniflorin on the contents of malondialdehyde (MDA) and intracellular reactive oxygen species (ROS) in the cell cultures. RESULTS: Exposure to increased PM2.5 concentrations caused significant decrease in the cell survival rate (P<0.05) with a clear dose-response relationship (r=-0.759, P<0.05). Treatment of the cells with paeoniflorin significantly attenuated PM2.5-induced inhibition of BEAS-2B cell survival (P<0.05), but the effect of paeoniflorin was not dose-dependent (P>0.05). PM2.5 exposure also significantly increased the contents of MDA and intracellular ROS (P<0.05), and paeoniflorin obviously antagonized these effects of PM2.5. CONCLUSION: Paeoniflorin can protect BEAS-2B cells from PM2.5-induced growth inhibition, and the mechanism might be related to the anti-oxidant effects of paeoniflorin.

[Snitrosylating protein disulphide isomerase mediates increased expression of α synuclein caused by methamphetamine in mouse brain].

OBJECTIVE: To investigate the role of Snitrosylation of protein disulphide isomerasec in methamphetamine (METH)-induced expression of alpha synuclein (αSN) in mouse hippocampus and striatum neurons. METHODS: Forty C57BL/6 mice were randomized equally into saline control group, METH group, L-NNA (a NOS inhibitor) group and L-NNA plus METH group. All the agents were injected intraperitoneally at an interval of 12 h, and a total of 8 injections were administered; in L-NNA plus METH group, METH was injected 30 min after LNNA in each treatment. Western Blotting was used to detect the expression of nitric oxide synthase (NOS), αSN, PDI and Snitrosylation of protein disulphide isomerase (PDI-SNO) in the hippocampus and striatum of the mice, and nitric oxide (NO) levels were determined using a NO assay kit. RESULTS: In METH group, the levels of NOS, PDISNO, αSN and NO all increased significantly compared with those in the control group (P<0.05). Combined treatment with L-NNA and METH, compared with METH alone, resulted in significantly lowered expression of NOS, NO, PDI-SNO and αSN in the hippocampus and striatum of the mice (all P<0.05). No significant differences were found in NOS, NO, PDI-SNO or αSN expressions among METH+L-NNA, L-NNA and control groups (P>0.05). CONCLUSION: METH induces the activation of NOS and increases NO level to cause the occurrence of PDI-SNO, leading subsequently to increased expression of αSN in mouse striatum and hippocampus. L-NNA, the inhibitor of NOS, can partly relieve nervous system toxicity induced by METH.

[Effect of methamphetamine exposure on S-nitrosylation of protein disulphide isomerase in PC12 cells].

OBJECTIVE: To study the effect of methamphetamine (METH) exposure on S-nitrosylation of protein disulphide isomerase and the neurotoxicity of METH in PC12 cells. METHODS: PC12 cells were exposed to different concentrations of METH, and the cell viability was assessed using the cell-counting kit-8. PC12 cells exposed to METH in the presence of the NOS inhibitor N-nitro-L-arginine (L-NNA) were examined for cell viability and S-nitrosylation of protein disulphide isomerase using the biotin-switch method, and the changes in cell morphology were examined with HE staining. RESULTS: METH exposure obviously decreased the cell viability and increased S-nitrosylation of protein disulphide isomerase, and the effect of METH was obviously inhibited by L-NNA treatment. CONCLUSION: METH can cause obvious neurotoxicity and promote S-nitrosylation of protein disulphide isomerase in PC12 cells.

[Effect of low-selenium diet on expressions of CCR7, CD206 and CD163 in the liver and kidney of rats].

OBJECTIVE: To investigate the effect of low-selenium diet on the liver and kidneys of rats and explore the role of macrophage polarization into M1 and M2 phenotypes in liver and kidney injuries. METHODS: Twenty-four rats (12 female and 12 male) were randomly divided into control group and low-selenium group and fed with normal chow (dietary selenium of 0.18 mg/kg) and low-selenium diet (dietary selenium of 0.02 mg/kg) for 109 days. After the feeding, the rats were sacrificed for HE staining to observe liver and kidney pathologies, and immunohistochemistry was performed for analyzing CCR7, CD206, CD163-positive cell numbers in the liver and kidneys. RESULTS: The rats in low-selenium group showed severer fibrosis in the liver and kidney than the control group. In either male or female rats in low-selenium group, CCR7 and CD206 expressions in the liver were comparable with those in control group, but CD163 expression was lower than that in the control group (P<0.05 for both female and male rats). In the kidney, the proximal tubule showed a slightly higher while the distal tubule showed a slightly lower CCR7 expression in low selenium group than in the control group (P>0.05). In low-selenium group, a significantly lower CD163 expression in the distal tubule and a significantly higher CD206 expression in the proximal tubule were noted as compared with the control group (P<0.05 in both female and male rats). Compared with the control rats, the male rats in low-selenium group, but not the female rats, showed a significantly lower CD163 expression in the proximal tubule of the kidney (P<0.05); the female but not the male rats in low-selenium group show a higher CD206 expression in the distal tubule (P<0.05). CONCLUSION: Low-selenium diet can cause liver and kidney fibrosis in rats and may inhibit macrophage activation into the M2 phenotype.

Long non-coding RNA MEG3 inhibits microRNA-125a-5p expression and induces immune imbalance of Treg/Th17 in immune thrombocytopenic purpura.

BACKGROUND: The imbalance of Treg/Th17 cells is an important pathogenic factor for immune thrombocytopenic purpura (ITP). We previously reported miR-125a-5p targeted CXCL13 and participated in the process of ITP. In the present study, the role of miR-125a-5p in regulating Treg/Th17 ratio and its potential molecular mechanism were investigated. METHOD: A total of 30 adults with ITP and 30 healthy subjects were included. MEG3 expression in peripheral blood derived CD4+ T cells from ITP patients and healthy subjects were detected by real-time PCR. In vitro experiments, the effects of inhibiting or overexpressing MEG3 on the expression of miR-125a-5p, Foxp3 and ROTγt in CD4+ T cells were investigated. RESULTS: MEG3 expression was increased in CD4+ T cells of patients with ITP. Dexamethasone decreased MEG3 expression level of CD4+ T cells in vitro. MEG3 directly interacted with miR-125a-5p and MEG3 overexpression inhibited miR-125a-5p expression in CD4+ T cells exposed to dexamethasone. MEG3 down-regulation or miR-125a-5p overexpression promoted Foxp3 expression and inhibited RORγt expression. CONCLUSION: MEG3 interacted with miR-125a-5p and inhibited its expression, and MEG3/miR-125a-5p contributed to induce immune imbalance of Treg/Th17 in ITP.

MicroRNA-125-5p targeted CXCL13: a potential biomarker associated with immune thrombocytopenia.

BACKGROUND: Immune thrombocytopenia (ITP) is an acquired and autoimmune disease of adults and children characterized by decreased platelet production. CXC chemokine ligand-13 (CXCL13) participates in multiple immunological responses. However, it is still unknown the relationship between CXCL13 and ITP. METHODS: Plasma CXCL13 was detected in ITP (n = 30) children. CD4+ T cells was isolated from peripheral blood mononuclear cells (PBMCs) from healthy volunteers. Treated CD4+ T cells with dexamethasone and/or miR-125-5p mimic/inhibitor, to observe the regulation of CXCL13. RESULTS: Compared with controls, ITP children had elevated plasma CXCL13, the concentration of which was reduced after treatment. In vitro, dexamethasone decreased CXCL13 level in in dose- dependent and in time-dependent manner. MiR-125-5p mimic decreased CXCL13 level and miR-125-5p inhibitor increased CXCL13 level in CD4+ T cells. CXCL13 was implied to be target gene of miR-125-5p. MiR-125-5p inhibitor also canceled dexamethasone induced decrease of CXCL13. CONCLUSION: CXCL13 is the target gene of miR-125-5p, which is possibly involved in the pathological process of ITP.

Multi-responses extraction optimization combined with high-performance liquid chromatography-diode array detection-electrospray ionization-tandem mass spectrometry and chemometrics techniques for the fingerprint analysis of Aloe barbadensis Miller.

A quality control strategy using high-performance liquid chromatography-diode array detector-electrospray ionization-tandem mass spectrometry (HPLC-DAD-ESI-MS/MS) coupled with chemometrics analysis was proposed for Aloe barbadensis Miller. Firstly, the extraction conditions including methanol concentration, extraction time and solvent-to-material ratio were optimized by multi-responses optimization based on response surface methodology (RSM). The optimum conditions were achieved by Derringer's desirability function and experimental validation implied that the established model exhibited favorable prediction ability. Then, HPLC fingerprint consisting of 27 common peaks was developed among 15 batches of A. barbadensis samples. 25 common peaks were identified using HPLC-DAD-ESI-MS/MS method by their spectral characteristics or comparison with the authentic standards. Chemometrics techniques including similarity analysis (SA), principal components analysis (PCA) and hierarchical clustering analysis (HCA) were implemented to classify A. barbadensis samples. The results demonstrated that all A. barbadensis samples shared similar chromatographic patterns as well as differences. These achievements provided an effective, reliable and comprehensive quality control method for A. barbadensis.

Natural phosphodiesterase-4 inhibitors from the leaf skin of Aloe barbadensis Miller.

The ethanolic extract of Aloe barbadensis Miller leaf skin showed inhibitory activity against phosphodiesterase-4D (PDE4D), which is a therapeutic target of inflammatory disease. Subsequent bioassay-guided fractionation led to the isolation of two new anthrones, 6'-O-acetyl-aloin B (9) and 6'-O-acetyl-aloin A (11), one new chromone, aloeresin K (8), together with thirteen known compounds. Their chemical structures were elucidated by spectroscopic methods including UV, IR, 1D and 2D NMR, and HRMS. All of the isolates were screened for their inhibitory activity against PDE4D using tritium-labeled adenosine 3',5'-cyclic monophosphate ((3)H-cAMP) as substrate. Compounds 13 and 14 were identified as PDE4D inhibitors, with their IC50 values of 9.25 and 4.42 µM, respectively. These achievements can provide evidences for the use of A. barbadensis leaf skin as functional feed additives for anti-inflammatory purpose.

S-Nitrosylating protein disulphide isomerase mediates α-synuclein aggregation caused by methamphetamine exposure in PC12 cells.

Methamphetamine (METH) belongs to Amphetamine-type stimulants, METH abusers are at high risk of neurodegenerative disorders, including Parkinson's disease (PD). However, there are still no effective treatments to METH-induced neurodegeneration because its mechanism remains unknown. In order to investigate METH's neurotoxic mechanism, we established an in vitro PD pathology model by exposing PC12 cells to METH. We found the expression of nitric oxide synthase (NOS), nitric oxide (NO) and α-synuclein (α-syn) was significantly increased after METH treatment for 24h, in addition, the aggregattion of α-syn and the S-nitrosylation of protein disulphideisomerase(PDI) were also obviously enhanced. When we exposed PC12 cells to the NOS inhibitor N-nitro-L-arginine(L-NNA) with METH together, the L-NNA obviously inhibited these changes induced by METH. While when we exposed PC12 cells to the precursor of NO L-Arginine together with METH, the L-Arginine resulted in the opposite effect compared to L-NNA. And when we knocked down the PDI gene, the L-NNA did not have this effect. Therefore, PDI plays a significant role in neurological disorders related to α-syn aggregation, and it suggests that PDI could be as a potential target to prevent METH-induced neurodegeneration.

Evaluation of analgesic, sedative effects and antimigraine mechanism of Qilong Toutong Granule () in rodents.

OBJECTIVE: To evaluate the analgesic and sedative effects of Qilong Toutong Granule (, QTG) and explore its possible mechanisms. METHODS: Kunming mice were randomly divided into 6 groups: normal control group, Zhengtian Pill (, ZTP) group, Western medicine group, and high-dose (5.2 g/kg), medium-dose (2.6 g/kg) and low-dose (1.3 g/kg) of QTG groups. After completing the prophylactic treatment for 3 days, hot-plate test and acetic acid-induced writhing test were used to assess the analgesic effect, and spontaneous locomotor test and sodium pentobarbital-induced hypnosis activity were adopted to estimate the sedative effect. Sprague-Dawley rats were grouped into normal control group, model group, ZTP group, rizatriptan group, and high-dose (3.6 g/kg), medium-dose (1.8 g/kg), and low-dose (0.9 g/kg) of QTG groups. After gavage for continuous 7 days, rats were intraperitoneally injected nitroglycerin, and 4 h later, blood samples were collected from postcava for measuring the levels of plasma calcitonin gene-related peptide (CGRP) and beta-endorphin (ß-EP) by radioimmunoassay. Subsequently, rats were perfused transcardially and the brain tissues containing the trigeminal nucleus caudalis (TNC) were achieved for detecting the number of Fos-immunoreactive cells by immunohistochemical method. RESULTS: In the mice experiments, compared with the normal control group, high- and medium-dose of QTG groups significantly raised the pain threshold (P<0.01), reduced the number of writhing response (P<0.01) and spontaneous activity (P<0.01), but had no influence on the sleeping rate of mice (P>0.05), and low-dose of QTG group also raised the pain threshold at 120 min (P=0.007), as well as lowered locomotor activity of mice at 2 h (P=0.003). On the study of migraine model rats, high- and medium-dose of QTG groups remarkably down-regulated the levels of plasma CGRP (P<0.01), up-regulated the levels of plasma ß-EP (P<0.01) and inhibited the expression of Fos protein in TNC (P<0.01), compared with the model group. CONCLUSIONS: QTG has obvious analgesic and sedative action and its mechanism on relieving migraine may be through regulating the levels of neurotransmitters and/or neuropeptides, and inhibiting the activation of Fos pathway.

One-step separation and purification of two chromones and one pyrone from Aloe barbadensis Miller: a comparison between reversed-phase flash chromatography and high-speed counter current chromatography.

INTRODUCTION: Chromones and pyrones are the major secondary metabolites of Aloe barbadensis Miller. As they are minor components of the plant, an efficient purification procedure for them is of great importance for promoting their pharmacological studies. OBJECTIVE: To develop efficient methods for one-step separation and purification of two chromones (5-((S)-2'-oxo-4'-hydroxypentyl)-2-hydroxymethylchromone (1) and 5-((4E)-2'-oxo-pentenyl)-2-hydroxymethylchromone (3)) and one pyrone (aloenin aglycone (2)) from A. barbadensis via reversed-phase flash chromatography (RP-FC) and high-speed counter current chromatography (HSCCC). METHODS: The RP-FC separation was performed using methanol:water (26:74, v/v) as the mobile phase at a flow rate of 20 mL/min. A solvent system composed of dichloromethane:methanol:water (3:1.5:1, v/v/v) was used for the HSCCC separation, at a flow rate of 2.0 mL/min. RESULTS: A one-step RP-FC operation within 110 min was successfully used for the purification of compounds 1 (27.9 mg, 96.5%), 2 (32.4 mg, 98.2%) and 3 (4.1 mg, 99.0%) from 129 mg of crude sample, and a one-step HSCCC separation within 95 min was successfully implemented for the purification of compounds 1 (31.1 mg, 97.6%), 2 (35.8 mg, 96.7%) and 3 (2.7 mg, 98.1%) from 134 mg of crude sample. CONCLUSION: The developed procedures were efficient, with low cost and high yield, which would afford sufficient amounts of high-purity compounds for chromatographic purposes and pharmacological activity screening.

[A novel naphthalene derivative from Aloe barbadensis].

To investigate the chemical constituents of A. barbadensis, aqueous extract of the plant was subjected to preparative medium pressure liquid chromatography (MPLC). The chemical structures were mainly determined by spectroscopic evidences (UV, IR, HR-MS, 1H NMR, 13C NMR, HSQC, 1H-1H COSY and HMBC) and chemical methods. A new O, O, O-triglucosylated naphthalene derivative, together with two known 6-phenyl-2-pyrone derivatives and four 5-methylchromones, were isolated and identified as 1-((3-((4- O-beta-D-glucopyranosyl)-beta-D-xylopyranosyloxymethyl)-1-hydroxy-8-alpha-L-rhamnopyranosyloxy)naphthalene-2-y])-ethanone (1), 10-O-beta-D-glucopyranosyl aloenin (2), aloenin B (3), aloesin (4), 8-C-glucosyl-(R)-aloesol (5), 8-C-glucosyl-7-O-methyl-(S)-aloesol (6), and isoaloeresin D (7). Compound 1 is a novel naphthalene derivative and named as aloveroside B, compounds 2-3 are isolated from this Aloe species for the first time.