Time filter

Source Type

Li X.,Huazhong University of Science and Technology | Li W.,Huazhong University of Science and Technology | Gao Z.,Huazhong University of Science and Technology | Gao Z.,Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica | And 2 more authors.
Biochimie | Year: 2016

The role of iron in the etiology of diabetes complications is not well established. Thus, this study was performed to test whether the iron-induced increase of oxidative/nitrative damage is involved in SERCA2a-related diabetic heart complication. Four randomly divided groups of rats were used: normal control group; iron overload group; diabetes group, and diabetic plus iron overload group. Iron supplementation stimulated cardiomyocyte hypertrophy and led to an increase in cardiac protein carbonyls, nitrotyrosine (3-NT) formation, and iNOS protein expression, thus resulting in abnormal myocardium calcium homeostasis of diabetic rats. The levels of SECA2a oxidation/nitration were significantly increased in the iron overload diabetic rats, along with a decrease in SECA2a expression and activity. In order to elucidate the possible role of iron in SERCA2a dysfunction, the effects of iron (Fe3+ or hemin) on peroxynitrite (ONOO-) induced SERCA2a oxidation and nitration were further investigated in vitro. It was found that tyrosine nitration played more important role in SERCA2a inactivation than thiol oxidation. These results present a potential mechanism in which iron exacerbates the diabetes-induced oxidative/nitrative modification of SERCA2a, which may cause functional deficits in the myocyte associated with diabetic cardiac dysfunction. Our findings may help to further understand the role of iron in the pathogenesis of diabetic complications. © 2016 Elsevier B.V. and Société Française de Biochimie et Biologie Moléculaire (SFBBM).


Li X.,Huazhong University of Science and Technology | Li X.,Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica | Li H.,Huazhong University of Science and Technology | Li H.,Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica | And 7 more authors.
Biochimie | Year: 2012

Excessive tissue iron levels are associated with the increase of oxidative/nitrative stress which contributes to tissue damage that may elevate the risk of diabetes. Therefore, we investigated the effects of iron on diabetes-associated liver injury and whether iron-related tyrosine nitration participated in this process. Rats were randomly divided into four groups: control, iron overload (300 mg/kg iron dextran, i.p.), diabetic (35 mg/kg of streptozotocin i.p. after administration of a high-fat diet) and diabetic simultaneously treated with iron. Iron supplement markedly increased diabetes-mediated liver damage and hepatic dysfunction by increasing liver/body weight ratio, serum levels of aspartate and alanine aminotransferase, and histological examination, which were correlated with elevated levels of lipid peroxidation, protein carbonyls and tyrosine nitration, oxidative metabolism of nitric oxide, and reduced antioxidant capacity. Consequently, the extent of oxidized/nitrated glucokinase was markedly increased in the iron-treated diabetic rats that contribute to a decrease in its expression and activity. Further studies revealed a significant contribution of iron-induced specific glucokinase nitration sites to its inactivation. In conclusion, iron facilitates diabetes-mediated elevation of oxidative/nitrative stress, simultaneously impairs liver GK, and can be a link between enzymatic changes and hepatic dysfunction. These findings may provide new insight on the role of iron in the pathogenesis of diabetes mellitus. © 2012 Elsevier Masson SAS. All rights reserved.


Zhao J.,Huazhong University of Science and Technology | Zhao J.,Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica | Wang P.,Huazhong University of Science and Technology | Wang P.,Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica | And 4 more authors.
Chemical Research in Toxicology | Year: 2015

Amyloid β peptide (Aβ) aggregation is considered to be a crucial pathological biomarker of Alzheimers disease (AD). It was found that Aβ and heme can form an Aβ-heme complex, which results in increased heme pseudoperoxidase activity. Recently, we found that increasing pseudoperoxidase activity induces elevated tyrosine nitration on Aβ in the presence of nitrite and hydrogen peroxide. However, the nature of tyrosine nitration of Aβ and its physiologic significance are still unknown. In this study, we revealed that Aβ1-40 can be nitrated in vitro by binding to heme in the presence of nitrite and hydrogen peroxide. Moreover, we found that tyrosine nitration had little effect on Aβ1-40s binding activity with heme. A TMB assay also revealed that the peroxidase activity of the heme-Aβ1-40Y10(3N)T (tyrosine 10 was replaced with 3-nitrtotyrosine in Aβ1-40) complex was moderately increased compared with that of the heme-Aβ1-40 complex. Furthermore, Thioflavin T fluorescence and transmission electron microscopic characterization indicated that tyrosine nitration significantly decreased the aggregation of Aβ1-40. In addition, a cytotoxicity test verified that wild-type Aβ1-40 was more cytotoxic than that of Aβ1-40Y10(3N)T. These results suggest that nitration of Aβ1-40 might be an Aβ detoxicant process and a compensatory reaction to nitrative stress. Our findings may lead to a detailed understanding of the function of Aβ1-40 and may be helpful in preventing and curing AD. © 2014 American Chemical Society.


Yuan C.,Huazhong University of Science and Technology | Yuan C.,Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica | Yi L.,Huazhong University of Science and Technology | Yi L.,Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica | And 10 more authors.
Journal of Biological Inorganic Chemistry | Year: 2012

Amyloid beta (Aβ) peptide accumulation has been demonstrated to play a central role in Alzheimer's disease (AD). Substantial evidence indicates that protein nitrotyrosination contributes to Aβ-dependent neurotoxicity; however, the molecular mechanism is unknown. Recent research has shown that Aβ complexes with heme to form Aβ-heme, and increases the pseudo-peroxidase activity of heme. We found that Aβ-heme uses H #2O 2 and NO 2 - to cause nitration of enolase and synaptic proteins more effectively than heme. Thus, the increased peroxidase activity of Aβ-heme may be the molecular link between excess Aβ and the widespread protein nitration in AD. Interestingly, the site of enolase nitration that was catalyzed by Aβ-heme is different from that induced by heme. Moreover, the secondary structural perturbations of Aβ-heme-treated and heme-treated enolase are also different. These observations suggest that Aβ-heme targets specific amino acid sequences in enolase. Furthermore, our data show that Aβ-heme peroxidase activity is independent of the aggregation state of Aβ, suggesting an important role of soluble Aβ in addition to Aβ aggregates and oligomers in AD pathogenesis. © SBIC 2011.


Liu H.,Huazhong University of Science and Technology | Liu H.,Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica | Bian W.,Huazhong University of Science and Technology | Liu S.,Huazhong University of Science and Technology | And 2 more authors.
Biological Trace Element Research | Year: 2012

Osteoporosis is a bone disease that leads to an increased risk of fracture. Oxidative stress may play a major role in the development of osteoporosis in part by inhibiting osteoblastic differentiation of bone marrow stromal cells (MSCs). Some evidence suggested that antioxidant selenium could prevent osteoporosis, but the underlying mechanism remains unclear. In this work, the effect of sodium selenite on H2O2-induced inhibition of osteoblastic differentiation of primary rat bone MSCs and the related mechanisms were examined. Pretreatment with selenite inhibited the adverse effect of H2O2 on osteoblastic differentiation of MSCs, based on alkaline phosphatase activity, gene expression of type I collagen and osteocalcin, and matrix mineralization. In addition, selenite pretreatment also suppressed the activation of extracellular signal-regulated kinase (ERK) induced by H2O2. The above effects were mediated by the antioxidant effect of selenite. Selenite enhanced the gene expression and activity of glutathione peroxidase, reversed the decreased total antioxidant capacity and reduced glutathione, and suppressed reactive oxygen species production and lipid peroxidation level in H2O2-treated MSCs. These results showed that selenite protected MSCs against H 2O2-induced inhibition of osteoblastic differentiation through inhibiting oxidative stress and ERK activation, which provided, for the first time, the mechanistic explanation for the negative association of selenium status and risk of osteoporosis in terms of bone formation. © 2012 Springer Science+Business Media, LLC.


Ye Y.,Huazhong University of Science and Technology | Fu F.,Huazhong University of Science and Technology | Li X.,Huazhong University of Science and Technology | Yang J.,Huazhong University of Science and Technology | And 2 more authors.
Journal of Cellular Biochemistry | Year: 2016

Atherosclerosis and related cardiovascular diseases (CVD) represent one of the greatest threats to human health worldwide. The protection of vascular smooth muscle cells (VSMCs) from apoptosis in the plaque has become an important therapeutic target for atherosclerotic plaque stabilization. A significant association of selenoprotein S (SelS) gene polymorphism with atherosclerotic CVD has been reported in epidemiologic studies, but the underlying mechanism remains unknown. In this paper, SelS expression in the thoracic aorta and its role in the protection of VSMCs from apoptosis have been studied. Western blot analysis showed that SelS was highly expressed in rat thoracic aorta. SelS gene silence by small interference RNA (siRNA) rendered VSMCs more sensitive to hydrogen peroxide- or tunicamycin- induced injury and apoptosis, as determined by MTT assay, Hoechst staining, and annexin V/propidium iodide staining. SelS silence aggravated hydrogen peroxide-induced oxidative stress and phosphorylation of p38 MAPK and c-Jun N-terminal kinase (JNK) in VSMCs. Furthermore, SelS silence enhanced endoplasmic reticulum (ER) stress induced by hydrogen peroxide or tunicamycin, as showed by the increased protein levels of ER chaperone 78 kDa glucose-regulated protein (GRP78), ER stress transducer phosphorylated protein kinase RNA like ER kinase (PERK), and the proapoptotic transcription factor C/EBP homologous protein (CHOP). In conclusion, the present study suggested that SelS highly expressed in the blood vessel might protect VSMCs from apoptosis by inhibiting oxidative stress and ER stress. Our finding provided mechanistic insights for the potential preventive role of SelS in atherosclerotic CVD. © 2015 Wiley Periodicals, Inc.


Huang X.,Huazhong University of Science and Technology | Huang X.,Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica | Huang X.,Wuhan Huanghelou Flavor and Fragrance Company | Yi L.,Huazhong University of Science and Technology | And 5 more authors.
Analytical Letters | Year: 2012

A simple micellar electrokinetic chromatography (MEKC) method was developed for determination of citronellal, citral (Z; E), α-pinene, limonene, linalool, and eugenol in plant essential oils (EOs). A buffer consisting of 20 mM Na2B4O7, 50 mM SDS, 20% (v:v) methanol adjusted to pH 9.5 was found to provide a very efficient and stable electrophoretic system for the analysis. The validation of the method included linearity, LODs, LOQs, precision (intra - and inter - day variation of migration time and peak area), and recovery. Seven terpenoids presented good linearity (R2 > 0.9960) within the test ranges; LODs (S/N = 3) and LOQs (S/N = 10) were 0.2-1.8 μg/mL and 0.8-5.9 μg/mL, respectively. The precision and accuracy were satisfactory, with the overall intra- and inter-day variation (for migration time and peak area, RSD%) being less than 7.0%, and recoveries of this method were greater than 91% at spiked levels. The proposed method was successfully applied to the determination of seven terpenoids in clove oil, litsea cubeba oil, and citronella oil, respectively. © 2012 Copyright Taylor and Francis Group, LLC.


Huang X.-W.,Huazhong University of Science and Technology | Huang X.-W.,Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica | Huang X.-W.,Wuhan Huanghelou Flavor and Fragrance Company | Feng Y.-C.,Huazhong University of Science and Technology | And 5 more authors.
Journal of Essential Oil Research | Year: 2013

Clove oil and citronella oil from China were selected to evaluate their potential as skin-care ingredients. The gas chromatography-mass spectrometry (GC-MS) results showed that the main component of clove oil was eugenol, while citronellal was the main compound of citronella oil. Clove oil exhibited prominent free radical scavenging activities (ic 50: 58 μg/mL for O2 -· and 8.5 μg/mL for ABTS+·) and strong inhibitory effect on lipid peroxidation, whilst citronella oil showed weaker antioxidative activities (ic 50: 150 μg/mL for O2 -· and 500 μg/mL for ABTS+·) and lipid peroxidation inhibitory efficiency. In addition, both oils revealed dose-dependence in protecting bovine serum albumin against UV-TiO2-NO2 - induced protein oxidation and tyrosine nitration injury. This study suggests that both clove oil and citronella oil could be used as new source of skin-care ingredient in the cosmetic industry. © 2013 Taylor and Francis.


Huang X.-W.,Huazhong University of Science and Technology | Huang X.-W.,Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica | Huang X.-W.,Wuhan Huanghelou Flavor and Fragrance Company | Feng Y.-C.,Huazhong University of Science and Technology | And 5 more authors.
Journal of Essential Oil Research | Year: 2013

Litsea cubeba essential oil (LCEO) is widely used as a flavor enhancer in cosmetics and as a folk skin-care agent in southern China. The objective of this paper is to investigate whether LCEO has biological activities that might be useful in modern skin-protection formulations. The present study results revealed that citral (57.4%) was a major component, while LCEO exhibited a potent inhibitory effect on tyrosinase (IC50 values 100 μg/mL), good antioxidative activities (IC50: 17.75 mg/mL for ABTS+., 10.2 mg/mL for O2-), and apparent protective effect against UV- TiO2-NO2--induced protein oxidation at 0.01 mg/mL and tyrosine nitration at 0.1 mg/mL. Additionally, the biological activities of LCEO were compared with that of its main constituents. The results demonstrated that any individual major component was not the unique contributor to the high activity of LCEO. Based on these results, we suggested that LCEO could serve as a new natural skin-whitening agent. © 2013 Taylor and Francis.


Yi L.,Huazhong University of Science and Technology | Li H.,Huazhong University of Science and Technology | Li H.,Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica | Deng Q.,Huazhong University of Science and Technology | Yuan Z.,Huazhong University of Science and Technology
Biomedical Chromatography | Year: 2010

A very recent epidemiological study provided strong support for nobiletin (NOB) as a potential candidate chemopreventive agent against cancer. From the pharmacology point of view, drug-protein interactions are determining factors in therapeutic, pharmacodynamic and toxicological drug properties. In this work, for the first time, detection of NOB at near-physiological conditions was accomplished by means of capillary electrophoresis-frontal analysis (CE-FA), and then the binding constants of NOB with bovine serum albumin (BSA) at the same conditions were determined. Complexation of NOB-BSA led to a decrease of the height for free NOB with increasing concentration of BSA. These results revealed the presence of a single class of binding site on BSA, and provided the binding constant of 10 3/M, showing the strong affinity of NOB for BSA. Furthermore, circular dichroism spectra showed that, when the molar ratio of NOB to BSA was up to 2:1, NOB did not affect the overall protein conformation significantly and the protein thus retained a native-like structure. These results may provide important information for preclinical studies of nobiletin in pharmaceutical research. Copyright © 2010 John Wiley & Sons, Ltd.

Loading Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica collaborators
Loading Hubei Key Laboratory of Bioinorganic Chemistry and Materia Medica collaborators