Dian-Dong Li

Peking Union Medical College Hospital, Peping, Beijing, China

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Publications (25)38.63 Total impact

  • Bin Li · Xiu-jun Liu · Liang Li · Sheng-hua Zhang · Yi Li · Dian-dong Li · Yong-su Zhen
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    ABSTRACT: A novel polymer–protein conjugate, Dex–rLDP, was prepared through conjugation of recombinant apoprotein (rLDP) of antitumor antibiotic lidamycin (LDM) to a macromolecular carrier, dextran T40, by the periodate oxidation–hydroboron reduction method. Its structure was verified by means of SDS-PAGE, HPLC, FT-IR, CD and MALDI-TOF MS. The weight-average molecular weight (Mw) of the glycoconjugate was 66.6 kDa, determined by MALDI-TOF MS, suggesting that approximately 3 mol of rLDP was attached per mole of oxidized dextran. The particle size, zeta potential and thermal stability of the dextranated conjugate were further characterized by TEM, DLS, and DSC. The DSC analysis revealed that dextranation can markedly enhance the thermal stability of the recombinant protein. To empower the conjugate with highly potent cytotoxicity, the resulting Dex–rLDP was then assembled with the active enediyne (AE) chromophore of LDM to generate an enediyne-energized conjugate, namely Dex–rLDP–AE. In vitro MTT assay clearly indicated that the cytotoxicity of Dex–rLDP–AE was at least an order of magnitude higher than that of free LDM. At tolerable doses, Dex–rLDP–AE markedly suppressed the growth of human carcinoma xenografts and transplantable murine hepatoma. Notably, selective accumulation and retention of the fluorescently labeled Dex–rLDP within the tumor was detected by in vivo fluorescence imaging in tumor-bearing mice. The observed results indicate that this cross-linking strategy offers important implications for controlled and targeted drug delivery to solid tumors, and the enediyne-energized dextran–apoprotein conjugate is a potentially promising candidate for tumor targeted therapy.
    No preview · Article · Jul 2014
  • Bin Li · Yan-Bo Zheng · Dian-Dong Li · Yong-Su Zhen
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    ABSTRACT: We have chemically synthesized NGR-LDP-PYM, a novel CD13/aminopeptidase (APN)-targeting and hydrolase-resistant conjugate by cross-linking of the antitumor antibiotic pingyangmycin (bleomycin A5 , PYM) to an engineered NGR motif-integrated apoprotein (NGR-LDP) with a noncleavable linker. This protein-drug conjugate not only basically retains the original properties of PYM but also can specifically deliver PYM to the CD13/APN-expressing tumor cells. Furthermore, the resulting conjugate exhibits more resistance to hydrolysis of recombinant human bleomycin hydrolase than parental PYM. These results may be useful for improving the therapeutic efficacy of PYM and have implications in the treatment of PYM-refractory and CD13/APN-overexpressing tumors. © 2014 Wiley Periodicals, Inc. and the American Pharmacists Association J Pharm Sci.
    No preview · Article · Apr 2014 · Journal of Pharmaceutical Sciences
  • Rui-Juan Gao · Chun-Yan Zhao · Dian-Dong Li · Yong-Su Zhen
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    ABSTRACT: This study is to optimize the preparation process of fusion protein Fv-LDP which was expressed in the form of inclusion body and consisted of lidamycin apoprotein LDP and single-chain Fv antibody (scFv) directed against type IV collagenase. The preparation and the dissolution of inclusion body, the immobilized metal affinity chromatography of the target protein and the renaturization by stepwise dialysis were optimized by single-factor analysis or orthogonal design. In addition, the refolded fusion protein Fv-LDP was refined by Sephadex G-75 chromatography followed by fluorescence-activated cell sorter (FACS)-based saturation binding assay to measure its antigen-binding activity. After optimization of the process, the purity of fusion protein Fv-LDP existed in the inclusion body was 63.9% and the corresponding solubility was 95.7%; Under denaturing conditions, the purity of fusion protein Fv-LDP was more than 95% after the purification process. The percentage of monomeric fusion protein Fv-LDP was 60% after the refolding process, while it was further refined to 85% which was 5.6-fold higher than that of the initial refolding condition. The refined fusion protein Fv-LDP could bind to human lung adenocarcinoma PAa cells and human hepatoma BEL-7402 cells with the dissociation constants (Kd) of 0.176 micromol x L(-1) and 0.904 micromol x L(-1), respectively. The preparation process of fusion protein Fv-LDP has been successfully optimized, which provides the experimental basis for the production and future development of fusion protein Fv-LDP, and might serve as a relatively practical system for the preparation of other scFv-based proteins expressed in the form of inclusion body.
    No preview · Article · Oct 2013 · Yao xue xue bao = Acta pharmaceutica Sinica
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    ABSTRACT: Salidroside (SAL) is one of main active components of Rhodiola rosea L and possesses diverse pharmacological effects. However, the direct role of SAL in bone metabolism remains elusive. In this study, effects of SAL on osteoblast differentiation of murine pluripotent mesenchymal cell line C3H10T1/2 and osteoblastic cell line MC3T3-E1 were examined. We first identified SAL as a potential BMP2 activator in a cell-based screening assay. SAL (0.5-10 μM) could slightly promote the proliferation and greatly increase the alkaline phosphatase (ALP) activity in both cells. Furthermore, SAL increased the mRNA expressions of osteoblast marker genes in either C3H10T1/2 or MC3T3-E1 cells after treatment for different time. Moreover, the mineralization of C3H10T1/2 cells assayed by Alizarin Red S staining was dose-dependently increased by SAL. Mechanistically, SAL increased the mRNA level of genes involved in the regulation of BMP signaling pathway, including BMP2, BMP6 and BMP7, and enhanced the phosphorylation of Smad1/5/8 and ERK1/2. The osteogenic effect of SAL was abolished by BMP antagonist noggin or by BMP receptor kinase inhibitor dorsomorphin. Further in vivo study demonstrated that SAL reversed bone loss in ovariectomized rats. Collectively, our findings indicate that SAL regulates bone metabolism through BMP signaling pathway.
    No preview · Article · Sep 2013 · Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association
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    ABSTRACT: LPS stimulation of macrophages production of IFN-beta plays a key role in innate immunity defending the microbial invasion. In this study, the effect of S632A3 promoting LPS-induced IFN-beta production and the underlying mechanism were investigated, mRNA level was measured by real-time PCR, cytokine production was determined by ELISA, GSK-3beta activity was investigated by kinase assay, protein phosphorylation and expression were evaluated by Western blotting. The results revealed that S632A3 significantly augmented IFN-beta production by LPS-stimulated macrophages. S632A3 inhibition of the activation of GSK-3beta, reduced the threonine 239 phosphorylation of transcription factor c-Jun but increased the total level of c-Jun in LPS-stimulated macrophages. Moreover, small interfering RNA-mediated knockdown of c-Jun level abrogated the ability of S632A3 to augment IFN-beta. The study thus demonstrates S632A3 being a new anti-inflammation lead compound and provides a molecular mechanism by which S632A3 promoted LPS-induced IFN-beta production in macrophages through inhibiting the activation of GSK-3beta.
    No preview · Article · Jul 2013 · Yao xue xue bao = Acta pharmaceutica Sinica
  • Chun-Sheng Li · Hong-Bin Deng · Dian-Dong Li · Zhao-He Li
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    ABSTRACT: To provide a better service for senior health care, we summarized screening studies of traditional Chinese anti-aging materia medica (TCAM). We collected and analyzed literature of TCAM screening studies using the lifespan test and animal models of aging from 1984 to 2012. We found 26 screening methods for TCAM, and 153 single herbs or active ingredients of TCAM that have been screened out during the past 28 years. The cell lifespan test, the fruit fly lifespan test, and D-galactose aging model were the most widely used and intensively studied screening methods. However, the method for establishing the D-galactose aging model needs to be standardized, and the D-galactose aging model cannot completely be a substitute for the normal aging mouse model. Great success has been achieved in screening studies in TCAM. To further improve screening studies in TCAM, we suggest that the D-galactose aging model be incorporated into the lifespan test in the New Drugs of Traditional Chinese Medicine Research Guide.
    No preview · Article · Apr 2013 · Chinese Journal of Integrative Medicine
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    ABSTRACT: Na(+)/K(+)-ATPase targeted cancer therapy has attracted increasing interests of oncologists in lung cancer field. Although multiple anti-cancer mechanisms of cardiac glycosides as Na(+)/K(+)-ATPase inhibitors are revealed, the role of autophagy and related molecular signaling pathway for the class of compounds in human non-small cell lung cancer (NSCLC) cells has not been systematically examined. We herein investigated the anti-cancer effects of two representative cardiac glycosides, digoxin and ouabain, in A549 and H460 cell lines. Both agents caused significant growth inhibition at nanomolar level. The cardiac glycosides were found to induce moderate G(2)/M arrest but not apoptosis at IC(50) level in the NSCLC cell lines. Moreover, autophagy was markedly induced by both agents, as evidenced by the time- and dose-dependent increase of LC3-II, up-regulation of Atg5 and Beclin1, as well as by the observations through acridine orange staining, transmission electron microscopy and quantification of GFP-LC3 fluorescence. Importantly, AMP-activated protein kinase (AMPK) pathway was activated, resulting in mammalian target of rapamycin (mTOR) deactivation during autophagy induction. Moreover, extracellular-signal-regulated kinase 1/2 (ERK1/2) activation was simultaneously found to be involved in the autophagy regulation. Co-treatment with respective inhibitors or siRNAs could either block the autophagic phenotypes and signals, or significantly increase the cellular viability, indicating the drugs-induced autophagy plays tumor-suppressing role. This work provides first evidence showing that the cardiac glycosides induce autophagy in human NSCLC cells through regulation of both mTOR and ERK1/2 signaling pathways. The autophagy may at least partially account for the growth inhibitory effects of the compounds in human NSCLC cells.
    No preview · Article · Jun 2012 · The international journal of biochemistry & cell biology
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    ABSTRACT: Although salidroside and salidroside-like compounds are considered as most critical constitutes needed and responsible for multiple therapeutic benefits of Rhodiola rosea L., including anti-aging, direct demonstration regarding the role of salidroside in anti-aging process is still deficient. In this study, we selected the H(2)O(2)-induced premature senescence model in human fetal lung diploid fibroblasts to investigate the protection of salidroside against aging in vitro and associated molecular mechanisms. We found that salidroside considerably reversed senescence-like phenotypes in the oxidant challenged model, including alterations of morphology, cell cycle, SA-β-gal staining, DNA damage, as well as related molecules expression such as p53, p21 and p16. The protection occurred in a dose-dependent manner, with 5μM offering best efficacy. The proposed antioxidant property of the compound was confirmed in this cellular system, and thus at least partially accounted for the protection of the compound against premature senescence. Similar protection of salidroside against replicative senescence was observed as well. Interestingly, the regulation of senescence-related molecules by salidroside involved ROS-irrelevant mechanisms in both models. This finding presents salidroside as an attractive agent with potential to retard aging and attenuate age-related diseases in humans.
    No preview · Article · Oct 2010 · Mechanisms of ageing and development
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    ABSTRACT: To investigate the protective effects of putative AGEs (advanced glycation endproducts) inhibitor salidroside against aging in an accelerated mouse aging model induced by D-galactose. A group of 5-month-old C57BL/6J mice were treated daily with D-galactose, D-galactose combined with salidroside, salidroside alone, and control buffer for 8 weeks. At the end of the treatment, serum AGEs levels, neurological activities, expression of glial fibrillary acidic protein (GFAP) and neurotrophin-3 (NT-3) in the cerebral cortex, as well as lymphocyte proliferation and IL-2 production were determined. D-galactose induced mouse aging model was developed as described before. As expected, salidroside blocked D-galactose induced increase of serum AGEs levels. It also reversed D-galactose induced aging effects in neural and immune system, as evidenced by improving motor activity, increasing memory latency time, and enhancing lymphocyte mitogenesis and interleukin-2 (IL-2) production. Furthermore, elevated expression of GFAP and NT-3 in the aged model mice was also reduced upon salidroside treatment. Salidroside inhibits AGEs formation in vivo, which at least partially contributes to its anti-aging effect in D-galactose induced aging model.
    No preview · Article · Apr 2010 · Biomedical and Environmental Sciences
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    ABSTRACT: Lidamycin, an enediyne antibiotic, leads to apoptosis and mitotic cell death of human tumor cells at high and low concentrations. The reason why tumor cells have distinct responses to lidamycin remains elusive. This study was to elucidate if cellular prosurvival molecules are involved in these responses. Cleavage of chromatin and DNA was observed by chromatin condensation and agarose gel electrophoresis. Accumulation of rhodamine 123 in lidamycin-treated cells was assayed by flow cytometry. Cell multinucleation was detected by staining with Hoechst 33342. Western blot and senescence-associated beta-galactosidase (SA-beta-gal) staining were used to analyze protein expression and senescence-like phenotype, respectively. SIRT1 deacetylase remained unchanged in 0.5 nmol/L lidamycin whereas cleavage occurred when apoptosis was induced by lidamycin. Increased FOXO3a, SOD-1 and SOD-2 expression and transient phosphorylation of ERK were detected after exposure of human hepatoma BEL-7402 cells to 0.5 nmol/L lidamycin. High expressions of SIRT1 and Akt were found in colon carcinoma HCT116 p53 knock-out cells exposed to lidamycin. Degradation of PARP and p53 by lidamycin as a substitute for SIRT1 and Akt was confirmed with caspase inhibitor Q-VD-OPh and proteasome inhibitor MG132. Resistance to lidamycin-induced DNA cleavage was observed in breast cancer doxorubicin-resistant MCF-7 cells. This was not induced by P-glycoprotein as no accumulation of rhodamine 123 was detected in the resistant cells following exposure to lidamycin. In contrast to sensitive MCF-7 cells, a lower multinucleation rate for the resistant cells was measured following exposure to equal concentrations of lidamycin. Cellular prosurvival molecules, such as SIRT1, Akt, SOD-1, SOD-2 and other unknown factors can influence the action of lidamycin on human tumor cells.
    Preview · Article · Jul 2009 · Biomedical and Environmental Sciences
  • Yong Li · Rong Xu · Xiu-min Zhang · Dian-dong Li · Qi-yang He
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    ABSTRACT: The mechanism of apoptosis induced by SIRT1 deacetylase inhibitors in both human breast cancer MCF-7 and MCF-7 doxorubicin-resistant cells was studied. MTT assay was used to detect growth-inhibitory effect on the cells. Protein expression was detected by Western blotting. Chromatin condensation was detected by a fluorescent microscope after Hoechst 33342 staining. Cell cycle distribution was analyzed with flow cytometry. Apoptotic cells were detected with Annexin V staining. Nicotinamide (NAM) and Sirtinol, two SIRT1 deacetylase inhibitors, exhibited the similar growth-inhibitory effects on MCF-7/DOX cells and MCF-7 cells, but no potentiation of DOX activities. The arrest at G2/M phase was detected by flow cytometry in both MCF-7 and MCF-7/DOX cells after NAM treatment. Activation of caspase pathway in MCF-7 cells, such as the cleavages of PARP, caspase-6, -7, -9, were observed after exposure to NAM 50 mmol x L(-1), accompanied by the occurrence of chromatin condensation and Annexin V positive cells. However, the cleavages of PARP, caspase-6 and -7 in MCF-7/DOX cells delayed after exposure to NAM for 24 h and obviously increased at 48 h with appearance of chromatin condensation and Annexin V positive cells. SIRT1 deacetylase inhibitors show no cross resistance to MCF-7 drug-resistant cells, and the similar growth-inhibitory actions of them to MCF-7 sensitive and drug-resistant cells by which it is mediated by activation of apoptotic caspase pathway.
    No preview · Article · Nov 2008 · Yao xue xue bao = Acta pharmaceutica Sinica
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    ABSTRACT: To study whether Lycium barbarum glycopeptide 3 (LBGP3) affects T cell apoptosis in aged mice. LBGP3 was purified with DEAE cellulose and Sephadex columns. Apoptotic "sub-G1 peak" was detected by flow cytometry and DNA ladder was resolved by agarose gel electrophoresis. Levels of IFN-gamma and IL-10 were measured with specific kits and mRNA expression was detected by RT-PCR. Apoptosis-related proteins of FLIP, FasL, and Bcl-2 were determined by Western blotting. LBGP3 was purified from Fructus Lycii water extracts and identified as a 41 kD glycopeptide. Treatment with 200 microg/mL LBGP3 increased the apoptotic rate of T cells from aged mice and showed a similar DNA ladder pattern to that in young T cells. The reversal of apoptotic resistance was involved in down-regulating the expression of Bcl-2 and FLIP, and up-regulating the expression of FasL. Lycium barbarum glycopeptide 3 reverses apoptotic resistance of aged T cells by modulating the expression of apoptosis-related molecules.
    Preview · Article · Jul 2008 · Biomedical and Environmental Sciences

  • No preview · Article · Jan 2008
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    ABSTRACT: To investigate the effect of lidamycin (LDM) on telomerase activity in human hepatoma BEL-7402 cells under the condition of LDM inducing mitotic cell death and senescence. Chromatin condensation was detected by co-staining with Hoechst 33342 and PI. Cell multinucleation was observed by Giemsa staining and genomic DNA was separated by agarose gel electrophoresis. Fluorescent intensity of Rho123 was determined for mitochondrial membrane potential. MTT assay and SA-beta-gal staining were employed to analyze the senescence-like phenotype. The expression of proteins was analyzed by Western blot. Telomerase activity was assayed by telomerase PCR-ELISA. Mitotic cell death occurred in LDM-treated cells characterized by unique and atypical chromatin condensation, multinucleation and increased mitochondrial membrane potential. However, no apoptotic bodies or DNA ladders were found. In addition, apoptosis-related proteins remained nearly unaltered. Senescence-like phenotype was identified by increased and elongated size of cells, growth retardation, enhanced SA-beta-gal activity and the changes of senescence-related protein expression. Telomerase activity markedly decreased (P<0.01) in LDM-treated hepatoma BEL-7402 cells. Mitotic cell death and senescence could be triggered simultaneously or sequentially after exposure of hepatoma BEL-7402 cells to LDM. The decrease in telomerase activity may play a key role in the defective mitosis and aging morphology. Further investigation of detailed mechanism is needed.
    No preview · Article · Jun 2007 · Biomedical and Environmental Sciences
  • Qiang Qiu · Zhen Wang · Jian-ming Jiang · Dian-dong Li
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    ABSTRACT: Although enediyne antibiotic lidamycin ( LDM) is a potent inducer of apoptosis, the underlying mechanisms of its apoptotic functions remain to be explored. Here, we aim to elucidate its possible mechanisms in mitochondria initiated apoptotic pathway involved in human BEL-7402 and MCF-7 cells. Cytochrome c released from mitchondria to cytosol fraction was detected by Western blotting. p53 and Bax, Bcl-2 expressions were detected by Western blotting and RT-PCR. MTT assay was used to detect cytotoxicity of LDM with or without caspase inhibitor z-VAD-fmk. After the BEL-7402 cells were exposed to 0. 1 micromol x L(-1) LDM within 6 h, the increase of cytochrome c in the cytosol and decrease in the mitochondria were observed when compared with untreated cells. The expression of Bax, an important proapoptotic member of the Bcl-2 family, increased gradually in the BEL-7402 cells after exposure to LDM of 0. 1 micromol x L (-1) for 2, 6, and 9 h, separately, while Bcl-2 increased at 2 and 6 h, and decreased at 9 h after LDM treatment. Enhanced protein expressions were parallel with respective increased mRNA level for Bax only, but not p53. Caspase inhibitor may inhibit partially the killing effects induced by LDM. Therefore we conclude that the rapid activation of mitochondrial pathway induced by LDM in tumor cells might contribute to its highly potent cytotoxicities.
    No preview · Article · Mar 2007 · Yao xue xue bao = Acta pharmaceutica Sinica
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    ABSTRACT: To investigate the role of D-galactose, especially in the structural and functional changes of the immune system in aging. Serum levels of advanced glycation end-products (AGE) were determined by ELISA method. Ultra-structures of thymus and spleen were detected by transmission electron microscopy. MTT method was used to determine the lymphocyte proliferation. IL-2 activity was determined by bioassay. Northern blot was used to detect the IL-2 mRNA levels. Serum AGE levels of D-galactose- (P < 0.01) and AGE-treated (P < 0.05) mice (n = 8) were increased significantly. The ultra-structures of thymus and spleen in D-galactose- and AGE-treated mice showed regressive changes similar to those in the aged control group. The lymphocyte mitogenesis and IL-2 activity of spleen were also decreased significantly (P < 0.01, n = 8). The change of IL-2 activity shown by Northern blot resulted from the change of mRNA expression. The AGE plus aminoguanidine group, however, showed no significant change in these parameters in comparison with the young control group (P < 0.01 or P < 0.05, n = 8). D-galactose and AGE lead to a mimic regression change of aging in the immune system in vivo.
    Preview · Article · Dec 2006 · Biomedical and Environmental Sciences
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    ABSTRACT: A new antibiotic, S632A3, was isolated from a cultured broth of Streptomyces hygroscopicus S632. It was purified by column chromatography on silica gel, Sephadex LH-20 and HPLC. Structural studies by analysis of 1H NMR and 13C NMR, MS, UV and IR spectra in comparison with those of S632A2 clarified that S632A3 is an isomer of 9-methylstreptimidone. In addition, this antibiotic showed potent biological activity including differentiation induction effects on HL-60 cell and antitumour activity in vivo.
    No preview · Article · Jan 2006 · Journal of Asian Natural Products Research
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    Chun-Lei Cheng · Tian-Qin Gao · Zhen Wang · Dian-Dong Li
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    ABSTRACT: The insulin/insulin-like growth factor 1 (IGF-1) signaling pathway is evolutionary conserved in diverse species including C.elegans, saccharomyces cerevisiae, Drosophila melanogaster, rodents and humans, which is involved in many interrelated functions that are necessary for metabolism, growth and reproduction. Interestingly, more and more research has revealed that insulin/IGF-1 signaling pathway plays a pivotal role in the regulation of longevity. Generally, disruption of the power of this pathway will extend longevity in species ranging from C.elegans to humans. The role of insulin/IGF-1 in longevity is probably related to stress resistance. Although the underlying mechanisms of longevity are not fully understood, the Insulin/IGF-1 signaling pathway has attracted substantial attention and it will be a novel target to prevent or postpone age-related diseases and extend life span. In this review, we mainly focus on the similar constitution and role of insulin/IGF-1 signaling pathway in C.elegans, saccharomyces cerevisiae, rodents and humans.
    Preview · Article · May 2005 · World Journal of Gastroenterology
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    Jian-Ming Jiang · Zhen Wang · Dian-Dong Li
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    ABSTRACT: To investigate whether two kinds of in vitro prepared advanced glycation end products (AGEs), Glu-BSA and Gal-BSA, could change oxidation stress and anti-oxidation abilities in astrocytes, and thus might contribute to brain injury. Changes of GSH, MDA, SOD, MAO-B, nitric oxide were measured after AGEs treatment. Both 0.1 g/L Glu-BSA and Gal-BSA could slightly decrease GSH level, while 1 g/L of them significantly decreased GSH level by 35% and 43% respectively. The MDA levels of both 1 g/L AGEs treated groups (306 +/- 13 and 346 +/- 22) were higher than that of the normal group (189 +/- 18), which could be inhibited by free radical scavenger NAC. The SOD activities of both 1 g/L AGEs treated groups (67.0 +/- 5.2 and 74.0 +/- 11.0) were lower than that of the normal group (85.2 +/- 8.0). Both 0.1 g/L AGEs could slightly increase the activity of MAO-B, while 1 g/L of them could increase MAO-B activity by 1.5 and 1.7 folds respectively. Both AGEs stimulation could produce NO level by 1.7 and 2 folds respectively. Enhanced levels of astrocytic oxidation stress and decrease of antioxidation abilities may contribute to, at least partially, the detrimental effects of AGEs in neuronal disorders and aging brain.
    Preview · Article · Apr 2004 · Biomedical and Environmental Sciences
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    ABSTRACT: To analyze the effects of aging or advanced glycation on gene expression in the cerebrum and spleen of female C57BL/6J mice. The gene expression profile was determined by using cDNA expression arrays containing 588 cDNA. Aging and advanced glycation resulted in differential gene expression patterns of cerebrum and spleen compared with young mice. Among the 80 genes detected in cerebrum, 43 exhibited a change in mRNA ratios with aging or treatment. Thirty-four changes (79%) were common in aged and D-galactose treated mice, whereas the cerebrum from aged and AGE-lysine treated mice showed common changes in expression of 38 genes (88%). Of the 86 genes detected in spleen, 29 (34%) displayed an age-related decrease in expression, whereas 3 (3%) displayed an increase in expression levels with aging. Eighteen genes from the detectable genes exhibited expression changes in both cerebrum and spleen of mice. The gene expression profiles of D-galactose and AGE-lysine treated mice resemble those of aged mice. Use of cDNA hybridization arrays may provide a promising tool to explore the mechanism of aging at a molecular level.
    No preview · Article · Jan 2004 · Biomedical and Environmental Sciences