Publications by authors named "Dujuan Xu"

13 Publications

  • Page 1 of 1

Carvacrol alleviates liver fibrosis by inhibiting TRPM7 and modulating the MAPK signaling pathway.

Eur J Pharmacol 2021 May 26;898:173982. Epub 2021 Feb 26.

Inflammation and Immune Mediated Diseases Laboratory of Anhui, Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, China; The Key Laboratory of Anti-inflammatory and Immune Medicines, Ministry of Education, Hefei, China; Institute for Liver Diseases of Anhui Medical University, Hefei, China; Department of Pharmacy, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China. Electronic address:

Liver fibrosis is a compensatory response to the tissue repair process. The activation and proliferation of hepatic stellate cells (HSCs) are thought to be related to the occurrence of hepatic fibrosis. Therefore, inhibiting the activation and proliferation of HSCs is a key step in alleviating liver fibrosis. As a non-specific inhibitor of transient receptor potential melastatin 7 (TRPM7), carvacrol has anti-tumor, anti-inflammatory and anti-hepatic fibrosis activities. This study aimed to explore the protective effect of carvacrol on liver fibrosis and related molecular mechanisms. A CCl-induced liver fibrosis mouse model and platelet-derived growth factor (PDGF-BB)-activated HSC-T6 cells (a rat hepatic stellate cell line) were employed for in vivo and in vitro experiments. C57BL/6J mice were orally administered different concentrations of carvacrol every day for 6 weeks during the development of CCl-induced liver fibrosis. The results show that carvacrol could effectively reduce liver damage and the progression of liver fibrosis in mice, which are expressed as fibrotic markers levels were reduced and histopathological characteristics were improved. Moreover, carvacrol inhibited the proliferation and activation of HSC-T6 cells induced by PDGF-BB. In addition, it was found that carvacrol inhibits the expression of TRPM7 and mediated through mitogen-activated protein kinases (MAPK). Collectively, our study shows that carvacrol can reduce liver fibrosis by inhibiting the activation and proliferation of hepatic stellate cells, and the MAPK signaling pathway might be involved in this process.
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http://dx.doi.org/10.1016/j.ejphar.2021.173982DOI Listing
May 2021

PD-1/PD-L1 enhanced cisplatin resistance in gastric cancer through PI3K/AKT mediated P-gp expression.

Int Immunopharmacol 2021 May 10;94:107443. Epub 2021 Feb 10.

School of Pharmacy, Anhui Medical University, Hefei, China; The First Affiliated Hospital of Anhui Medical University, Hefei, China. Electronic address:

Background: Programmed cell death receptor 1 (PD-1) is an immunosuppressive molecule expressed on T cells, and its ligand (PD-L1) which expressed on tumor cells play pivotal roles in regulating host immune responses. However, little is known whether PD-1/PD-L1 axis could directly activates intracellular oncogenic signaling pathways in tumor cells, leading to tumor resistance.

Methods: In the present study, the expression of PD-1 and PD-L1 in the tissues of gastric cancer was detected by western blot and immunofluorescence. The effect of PD-L1-Fc and cisplatin on resistant gastric cancer cells was examined by MTT assay and Flow Cytometry. In addition. The effect of PD-L1-Fc on the expression of P-gp in gastric cancer cells and resistant gastric cancer cells was detected by quantitative real-time reverse-transcription PCR (qRT-PCR) and western blot. The molecular mechanisms of the regulation of cisplatin and PD-L1-Fc treatment were evaluated by western blot.

Results: We found that the level of PD-1 was significantly increased in human gastric cancer tissues and drug-resistant gastric cancer cells and P-gp was the same result. The PD-L1 could reduce the level of cell damage caused by cisplatin. In addition, we found PD-L1 can also up-regulate the expression of P-gp. Mechanistically, PD-L1 activated the PI3K/AKT signaling pathway in which PI3K/AKT pathway inhibition attenuated the upregulation of P-gp.

Conclusion: PD-1/PD-L1 enhanced cisplatin resistance in gastric cancer through PI3K/AKT mediated P-gp expression.
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http://dx.doi.org/10.1016/j.intimp.2021.107443DOI Listing
May 2021

Cigarette smoke extract amplifies NADPH oxidase-dependent ROS production to inactivate PTEN by oxidation in BEAS-2B cells.

Food Chem Toxicol 2021 Apr 10;150:112050. Epub 2021 Feb 10.

Collaborative Innovation Center for Chinese Medicine and Respiratory Diseases Co-constructed by Henan Province & Education Ministry of P.R. China, Henan University of Chinese Medicine, Zhengzhou, China; Henan Key Laboratory of Chinese Medicine for Respiratory Disease, Henan University of Chinese Medicine, Zhengzhou, China; Department of Respiratory Diseases, The First Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, 450000, China. Electronic address:

Chronic obstructive pulmonary disease (COPD) is widely recognized as a global public health problem and the third leading cause of mortality worldwide by 2020. Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a dual-specificity protein and lipid phosphatase that plays an important role in COPD. However, the redox regulation of PTEN in the development of COPD was poorly studied. Our results showed that cigarette smoke extract (CSE) could oxidize PTEN in a time-dependent manner in BEAS-2B cells, whereas PTEN oxidation exposed to CSE was delayed compared to that of HO Additionally, we found that ROS derived from DUOX1 and 2 of NADPH oxidases were mainly responsible for oxidative inactivation PTEN, also simultaneously led to Trx-1 inactivation by dimerization. Oxidative mechanism of PTEN exposed to CSE was mediated by forming a disulfide bond between Cysand Cys, similar to HO. Inactivation of PTEN resulted in the increased phosphorylation of Akt. In conclusion, CSE exposure could elevate the intracellular ROS mainly from DUOX1 and 2 to oxidize PTEN and Trx-1 resulting in Akt activation, eventually cause the occurrence of COPD, suggesting that PTEN is a potential target for new therapies in COPD.
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http://dx.doi.org/10.1016/j.fct.2021.112050DOI Listing
April 2021

The triglyceride glucose index (TyG) and CDKAL1 gene rs10946398 SNP are associated with NAFLD in Chinese adults.

Minerva Endocrinol 2020 Dec 3. Epub 2020 Dec 3.

Department of Ultrasonography, Xuzhou Central Hospital, Xuzhou Clinical School of Xuzhou Medical University, Xuzhou, Jiangsu, China -

Aim: Non-alcoholic fatty liver disease (NAFLD) has a higher prevalence worldwide, and its pathogenesis is not clear. Genetic factors, dyslipidaemia and dysglycaemia have been proven to be associated with NAFLD. It has not been reported whether the triglyceride glucose index (TyG), which is estimated by triglyceride and fasting glucose, has a relationship with NAFLD in people from North China. Whether the CDKAL1 gene rs10946398 SNP, which has been found to be associated with BMI, has a relationship with TyG and NAFLD is not clear.

Methods: We recruited a total of 1,760 subjects in this study, and we measured the clinical characteristics, abdominal ultrasound, and genotype of those participants.

Results: The results showed that 527 (29.9%) subjects suffered from NAFLD, the TyG index was associated with NAFLD (OR=5.456, 95% CI (3.526~8.442)), and the CDKAL1 gene rs10946398 SNP has a relationship with NAFLD (OR=1.509, 95% CI (1.046~2.178)). The distribution of the C allele of rs10946398 was statistically significant at different levels of the TyG index.

Conclusions: We identified an association between the rs10946398 genotypes of CDKAL1 and NAFLD and the TyG index, and the TyG index was related to the risk of NAFLD.
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http://dx.doi.org/10.23736/S0391-1977.20.03273-3DOI Listing
December 2020

Therapeutic Potential of Diosgenin and Its Major Derivatives against Neurological Diseases: Recent Advances.

Oxid Med Cell Longev 2020 6;2020:3153082. Epub 2020 Mar 6.

Collaborative Innovation Center for Respiratory Disease Diagnosis and Treatment and Chinese Medicine Development of Henan Province, Henan Key Laboratory of Chinese Medicine for Respiratory Disease, Henan University of Chinese Medicine, China.

Diosgenin (DG), a well-known steroidal sapogenin, is present abundantly in medicinal herbs such as , , , , and . DG is utilized as a major starting material for the production of steroidal drugs in the pharmaceutical industry. Due to its wide range of pharmacological activities and medicinal properties, it has been used in the treatment of cancers, hyperlipidemia, inflammation, and infections. Numerous studies have reported that DG is useful in the prevention and treatment of neurological diseases. Its therapeutic mechanisms are based on the mediation of different signaling pathways, and targeting these pathways might lead to the development of effective therapeutic agents for neurological diseases. The present review mainly summarizes recent progress using DG and its derivatives as therapeutic agents for multiple neurological disorders along with their various mechanisms in the central nervous system. In particular, those related to therapeutic efficacy for Parkinson's disease, Alzheimer's disease, brain injury, neuroinflammation, and ischemia are discussed. This review article also critically evaluates existing limitations associated with the solubility and bioavailability of DG and discusses imperatives for translational clinical research. It briefly recapitulates recent advances in structural modification and novel formulations to increase the therapeutic efficacy and brain levels of DG. In the present review, databases of PubMed, Web of Science, and Scopus were used for studies of DG and its derivatives in the treatment of central nervous system diseases published in English until December 10, 2019. Three independent researchers examined articles for eligibility. A total of 150 articles were screened from the above scientific literature databases. Finally, a total of 46 articles were extracted and included in this review. Keywords related to glioma, ischemia, memory, aging, cognitive impairment, Alzheimer, Parkinson, and neurodegenerative disorders were searched in the databases based on DG and its derivatives.
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http://dx.doi.org/10.1155/2020/3153082DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7079249PMC
October 2020

Aidi Injection, a Traditional Chinese Medicine Injection, Could Be Used as an Adjuvant Drug to Improve Quality of Life of Cancer Patients Receiving Chemotherapy: A Propensity Score Matching Analysis.

Integr Cancer Ther 2019 Jan-Dec;18:1534735418810799. Epub 2018 Nov 27.

1 School of Pharmacy, Anhui Medical University, Hefei, China.

Background: Clinical research has paid increasing attention to quality of life (QoL) in recent years, but the assessment of QoL is difficult, hampered by the subjectivity, complexity, and adherence of patients and physicians. According to previous studies, QoL in cancer patients is related to performance status (PS) and influenced by chemotherapy-related toxicity. Aidi injection, a traditional Chinese medicine injection, is used as an adjuvant drug to enhance effectiveness of chemotherapy. The study aims to investigate whether Aidi injection could improve QoL by improving PS and reducing toxicity caused by chemotherapy.

Methods: A retrospective cohort study was performed at the First Affiliated Hospital of Anhui Medicine University. Data of consecutive patients diagnosed with cancers between January 2014 and June 2017 were retrieved from the electronic medical record system. After a 1:1 propensity score match, patients were then divided into 2 groups based on the therapies used, that is, Aidi injection combined with chemotherapy and chemotherapy alone, and the PS, chemotherapy-related toxicity, and combined medication information were compared. The effect of different dosages of Aidi injection on patients was further explored.

Results: A total of 3200 patients were included in this study. Aidi injection combined with chemotherapy exhibited significantly benefit in PS ( P < .001, odds ratio [OR] 3.4, 95% confidence interval [CI] 2.4-4.8) compared with chemotherapy alone after adjusting for the factors that affect PS. The improvement rate of PS in the Aidi group was significantly higher than in the control group across the stratification of gender, age, tumor type, TNM stage, body mass index, nodal metastasis, prior chemotherapy, chemotherapy regimens, other Chinese tradition medicines, and chemotherapy cycle. Meanwhile, Aidi injection used synchronously with chemotherapeutic drugs could decrease the incident rate of damage to liver and kidney function, myelosuppression, and gastrointestinal reactions caused by chemotherapy.

Conclusion: It was indicated that the integrative approach combining chemotherapy with Aidi injection, especially with the conventional dosage of Aidi injection, had significant benefit on QoL in cancer patients.
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http://dx.doi.org/10.1177/1534735418810799DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6432675PMC
December 2019

Proteomic analysis of cell cycle arrest and differentiation induction caused by ATPR, a derivative of all-trans retinoic acid, in human gastric cancer SGC-7901 cells.

Proteomics Clin Appl 2017 07 6;11(7-8). Epub 2017 Mar 6.

School of Pharmacy, Anhui Medical University, Hefei, China.

Purpose: 4-amino-2-trifluoromethyl-phenyl retinate (ATPR) was reported to potentially inhibit proliferation and induce differentiation activity in some tumor cells. In this study, a proteomics approach was used to investigate the possible mechanism by screening the differentially expressed protein profiles of SGC-7901 cells before and after ATPR-treatment in vitro.

Experimental Design: Peptides digested from the total cellular proteins were analyzed by reverse phase LC-MS/MS followed by a label-free quantification analysis. The SEQUEST search engine was used to identify proteins and bioinformatics resources were used to investigate the involved pathways for the differentially expressed proteins.

Results: Thirteen down-regulated proteins were identified in the ATPR-treated group. Bioinformatics analysis showed that the effects of ATPR on 14-3-3ε might potentially involve the PI3K-AKT-FOXO pathway and P27Kip1 expression. Western blot and RT-PCR analysis showed that ATPR could inhibit AKT phosphorylation, up-regulate the expression of FOXO1A and P27Kip1 at both the protein and mRNA levels, and down-regulate the cytoplasmic expression of cyclin E and CDK2. ATPR-induced G0/G1 phase arrest and differentiation can be ablated if the P27kip1 gene is silenced with sequence-specific siRNA or in 14-3-3ε overexpression of SGC-7901 cells.

Conclusion And Clinical Relevance: ATPR might cause cell cycle arrest and differentiation in SGC-7901 cells by simultaneously inhibiting the phosphorylation of AKT and down-regulating 14-3-3ε. This change would then enhance the inhibition of cyclin E/CDK2 by up-regulating FOXO1A and P27Kip1. Our findings could be of value for finding new drug targets and for developing more effective differentiation inducer.
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http://dx.doi.org/10.1002/prca.201600099DOI Listing
July 2017

ASIC1a mediates the drug resistance of human hepatocellular carcinoma via the Ca/PI3-kinase/AKT signaling pathway.

Lab Invest 2017 01 5;97(1):53-69. Epub 2016 Dec 5.

School of Pharmacy, Anhui Medical University, Hefei, China.

Chemotherapy is the main treatment method of patients with advanced liver cancer. However, drug resistance is a serious problem in the treatment of hepatocellular carcinoma (HCC). Acid sensing ion channel 1a (ASIC1a) is a H-gated cation channel; it mediates tumor cell migration and invasion, which suggests that it is involved in the development of malignant tumors. Therefore, we studied the relationship between ASIC1a and drug resistance in human hepatocellular carcinoma. In our study, we found that ASIC1a is highly expressed in human HCC tissue, and that its levels were significantly increased in resistant HCC cells Bel7402/FU and HepG2/ADM. Inhibiting the activity of ASIC1a enhances the chemosensitivity of Bel7402/FU and HepG2/ADM cells. The overexpression of ASIC1a contributed to drug resistance in Bel7402 and HepG2 cells, whereas knockdown of ASIC1a overcame drug resistance in Bel7402/FU and HepG2/ADM cells. We further demonstrated that ASIC1a mediated calcium influx, which resulted in the activation of PI3K/AKT signaling and increased drug resistance. These data suggest that ASIC1a/Ca/PI3K/AKT signaling represents a novel pathway that regulates drug resistance, thus offering a potential target for chemotherapy of HCC.
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http://dx.doi.org/10.1038/labinvest.2016.127DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5220138PMC
January 2017

Curdione attenuates thrombin-induced human platelet activation: β1-tubulin as a potential therapeutic target.

Fitoterapia 2017 Jan 30;116:106-115. Epub 2016 Nov 30.

College of Pharmacy, Anhui Medical University, Hefei, PR China; Department of Pharmacy, The First Affiliated Hospital of Anhui Medical University, Hefei, PR China. Electronic address:

Rhizoma Curcumae, the dry rhizomes derived from Curcuma aromatica Salisb., are a classical Chinese medicinal herb used to activate blood circulation, remove blood stasis and alleviate pain. Our previous study proved that curdione, a sesquiterpene compound isolated from the essential oil of Curcuma aromatica Salisb. can inhibit platelet activation suggesting its significant anticoagulant and antithrombotic effects. However, the underlying mechanism of curdione mediated anti-platelet effect has not been fully elucidated. Platelet proteins extracted from washed human platelets, including normal group (treated with normal saline), thrombin group and curdione group were digested and analysed by nano ESI-LC-MS/MS. UniProt database and SIEVE software were employed to identify and reveal the differentially expressed proteins. Furthermore, possible mechanisms involved were explored by Ingenuity Pathway Analysis (IPA) Software and validated by western blot experiments. Twenty-two differentially expressed proteins between the normal and thrombin group were identified. Compared with the thrombin group, the curdione treatment was significantly down-regulated only 2 proteins (Talin1 and β1-tubulin). Bioinformatics analysis showed that Talin1 and β1-tubulin could be involved in the integrin signal pathway. The results of western blot analysis were consistent with that of the proteomics data. Vinculin, identified in IPA database was involved in the formation of cell cytoskeletal. The down-regulation of β1-tubulin facilitated the decrease in vinculin/Talin1. Curdione regulated the expression of vinculin and Talin1 by β1-tubulin affecting the integrin signalling pathway and eventually inhibiting platelet activation. The β1-tubulin may be a potential target of curdione, which attenuates thrombin-induced human platelet activation.
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http://dx.doi.org/10.1016/j.fitote.2016.11.016DOI Listing
January 2017

AstragalosideII inhibits autophagic flux and enhance chemosensitivity of cisplatin in human cancer cells.

Biomed Pharmacother 2016 Jul 16;81:166-175. Epub 2016 Apr 16.

Department of Pharmacy, The First Affiliated Hospital of Anhui Medical University, Hefei 230032, Anhui, China; Third-Grade Pharmaceutical Chemistry Laboratory of State Administration of Traditional Chinese Medicine, Hefei, 230032 Anhui, China.

Inhibition of autophagy has been daily served as a promising anti-cancer treatment strategies. AstragalosideII (ASII), a main compound isolated from traditional Chinese medicine Radix Astragali, has been demonstrated to inhibit autophagy and reverse multidrug resistance in human hepatic cancer cells Bel-7402/5-FU. In this study, we inspected the function and mechanisms of ASII and cisplatin on autophagy in human cancer cells, and assessed the effect of ASII on cisplatin-induced apoptosis. We found ASII increased LC3II protein level, p62 protein level and GFP-LC3 puncta accumulation in human cancer cells. Furthermore, we found that ASII downregulated the expression of lysosomal cathepsinB/L (CTSB/L) in EBSS medium and affected the lysosomal acidification. Finally, we demonstrated that cisplatin induced protective autophagy which was involved of PI3K/Akt/mTOR pathway. Moreover, ASII in conjunction with cisplatin significant reduced cell viability, arrested in S phase and increased apoptosis. In conclusion, these findings suggested that ASII served as autophagy inhibitor which restored chemosensitivity of anticancer agent cisplatin and enhanced tumor cell death.
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http://dx.doi.org/10.1016/j.biopha.2016.03.025DOI Listing
July 2016

Reversal of P-glycoprotein-mediated multidrug resistance of human hepatic cancer cells by Astragaloside II.

J Pharm Pharmacol 2012 Dec 8;64(12):1741-50. Epub 2012 Jun 8.

School of Pharmacy, Anhui Medical University, The First Affiliated Hospital of Anhui Medical University, China.

Objectives: Chemoresistance is the main obstacle encountered in cancer treatment and is frequently associated with multidrug resistance (MDR). Astragaloside is a saponin which is widely used in traditional Chinese medicine. It has been reported that Astragaloside has antitumour effects on hepatocellular carcinoma Bel-7402 cells in vitro and in vivo. The purpose of this study was to examine the effects of Astragaloside II on the reversal of MDR and its molecular mechanism in vitro.

Methods: In this study, Bel-7402 and Bel-7402/FU cell lines were used as the experimental model. Drug sensitivity was determined using the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay, accumulation and efflux of Rh123 were analyzed by flow cytometer, the mRNA level of mdr1 was determined by RT-PCR and the protein levels of P-glycoprotein (P-gp) and mitogen-activated protein kinase were determined by Western blot.

Key Findings: Astragaloside II (0.08 mg/ml) showed strong potency to increase 5-fluorouracil cytotoxicity toward 5-fluorouracil-resistant human hepatic cancer cells Bel-7402/FU. The mechanism of Astragaloside II on P-gp-mediated MDR demonstrated that Astragaloside II significantly increased the intracellular accumulation of rhodamine 123 via inhibition of P-gp transport function. Based on the analysis of P-gp and mdr1 gene expression using Western blot and RT-PCR, the results revealed that Astragaloside II could downregulate the expression of the P-gp and mdr1 gene. In addition, Astragaloside II suppressed phosphorylation of extracellular signal regulated kinase 1/2, p38 and c-Jun N-terminal kinase.

Conclusions: The results suggested that Astragaloside II is a potent MDR reversal agent and may be a potential adjunctive agent for hepatic cancer chemotherapy.
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http://dx.doi.org/10.1111/j.2042-7158.2012.01549.xDOI Listing
December 2012

Antifibrosis effects of total glucosides of Danggui-Buxue-Tang in a rat model of bleomycin-induced pulmonary fibrosis.

J Ethnopharmacol 2011 Jun 21;136(1):21-6. Epub 2011 Mar 21.

Pharmaceutical preparation section, Third-Grade Pharmaceutical Chemistry Laboratory of State Administration of Traditional Chinese Medicine (TCM-2009-202), the First Affiliated Hospital of Anhui Medical University, Hefei 230022, Anhui, China.

Aim Of The Study: The present study examined the antifibrosis effects of DBTG (total glucosides of Danggui-Buxue-Tang) on bleomycin-induced pulmonary injury and fibrosis in rats.

Materials And Methods: Animals were randomly divided into six groups: (1) saline control group; (2) Bleomycin group in which rats were endotracheally instillated with bleomycin (5mg/kg); (3-5) Bleomycin and DBTG group, in which DBTG were given to rats daily (16.32 or 64mg/kg/day, i.g.) one day after bleomycin injection for 4 weeks until the end of the treatment; (6) Bleomycin and positive control group. Animals were sacrificed at 7, 14, and 28 days post bleomycin administration and lungs were removed. Lung specimens were stained with hematoxylin and eosin (HE) and Masson trichrome for histological evaluation of lung injury and fibrosis by light microscopy. Body weight and lung index from various groups were measured, as well as TNF-α, TGF-β1 and type I collagen concentrations in lung homogenates.

Results: DBTG reduced bleomycin-induced weight loss, decreased the lung index and histological evidence supported the ability of DBTG to attenuate bleomycin-induced lung fibrosis and consolidation. DBTG could partly dose-dependently decrease TNF-α and TGF-β1 activity, as well as it decrease type I collagen expression in lung tissues.

Conclusions: The findings of the present study provide evidence that DBTG may serve as a novel target for potential therapeutic treatment of lung fibrosis.
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http://dx.doi.org/10.1016/j.jep.2011.03.013DOI Listing
June 2011

Preparation of icariside II from icariin by enzymatic hydrolysis method.

Fitoterapia 2010 Jul 22;81(5):437-42. Epub 2009 Dec 22.

Department of Pharmacy, Third-Grade Pharmaceutical Chemistry Laboratory of State Administration of Traditional Chinese Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, PR China.

It has been reported that icariin and icariside II, two flavonoid glycosides coming from herba epimedii, which have a closely structural relationship, show some pharmacological effects such as preventing osteoporosis, cancer and depression. The content of natural icariside II is very low in herba epimedii, but it is the main component in vivo after the administration of herba epimedii. More icariside II can be obtained from icariin by enzymatic hydrolysis method than by traditional isolation method. This study focuses on finding a simple and feasible method to prepare icariside II from icariin by enzymatic hydrolysis, so as to meet the request for further pharmacologic actions study. Icariin was obtained successively with 90% ethanol extraction, isolation on macroporous resin and purification on silica gel chromatography. Enzymatic hydrolysis conditions were tested for the bioconversion of icariin into icariside II by orthogonal array design. The structures of isolated icariin and produced icariside II were identified by UV, IR, ESIMS, (1)H NMR, (13)C NMR, and DEPT spectroscope. Enzymatic hydrolysis experiment showed that icariin could be transformed into icariside II with the action of beta-glucosidase and the optimum reaction conditions were determined as follows: 50 degrees C, 0.2 M disodium hydrogen phosphate and citric acid buffer system (pH6.0), the ratio of icariin/enzyme is 1:1 and reaction time 5 h. By using this enzymatic condition, 95.5 mg icariside II (with the purity of 99.1%) was obtained eventually by transforming 200 mg icariin.
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http://dx.doi.org/10.1016/j.fitote.2009.12.006DOI Listing
July 2010