Publications by authors named "Hui-Li Wang"

98 Publications

Dihydromyricetin attenuates heat stress-induced apoptosis in dairy cow mammary epithelial cells through suppressing mitochondrial dysfunction.

Ecotoxicol Environ Saf 2021 May 3;214:112078. Epub 2021 Mar 3.

Jiangsu Key Laboratory for Food Quality and Safety-State Key Laboratory Cultivation Base, Ministry of Science and Technology, Jiangsu Academy of Agricultural Sciences, Nanjing 210014, China; Key Laboratory of Crop and Animal Integrated Farming, Ministry of Agriculture, Jiangsu Academy of Agricultural Sciences, Nanjing 210014, China. Electronic address:

It is well known that the dairy cow production is very sensitive to environmental factors, including high temperature, high humidity and radiant heat sources. High temperature-induced heat stress is the main environmental factor that causes oxidative stress and apoptosis, which affects the development of mammary glands in dairy cows. Dihydromyricetin (DMY) is a nature flavonoid compound extracted from Ampelopsis grossedentata; it has been shown to have various pharmacological functions, such as anti-inflammation, antitumor and liver protection. The present study aims to evaluate the protective effect of DMY on heat stress-induced dairy cow mammary epithelial cells (DCMECs) apoptosis and explore the potential mechanisms. The results show that heat stress triggers heat shock response and reduces cell viability in DCMECs; pretreatment of DCMECs with DMY (25 μM) for 12 h significantly alleviates the negative effects of heat stress on cells. DMY can provide cytoprotective effects by suppressing heat stress-caused mitochondrial membrane depolarization and mitochondrial dysfunction, Bax and Caspase 3 activity, and modulation of oxidative enzymes, thereby preventing ROS production and apoptosis in DCMECs. Importantly, DMY treatment could attenuate heat stress-induced mitochondrial fragmentation through mediating the expression of mitochondrial fission and fusion-related genes, including Dynamin related protein 1 (Drp1), Mitochondrial fission 1 protein (Fis1), and Mitofusin1, 2 (Mfn1, 2). Above all, our findings demonstrate that DMY could protect DCMECs against heat stress-induced injury through preventing oxidative stress, the imbalance of mitochondrial fission and fusion, which provides useful evidence that DMY can be a promising therapeutic drug for protecting heat stress-induced mammary glands injury and mastitis.
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http://dx.doi.org/10.1016/j.ecoenv.2021.112078DOI Listing
May 2021

S-allyl cysteine ameliorates heat stress-induced oxidative stress by activating Nrf2/HO-1 signaling pathway in BMECs.

Toxicol Appl Pharmacol 2021 Apr 25;416:115469. Epub 2021 Feb 25.

Jiangsu Key Laboratory for Food Quality and Safety-State Key Laboratory Cultivation Base, Ministry of Science and Technology, Jiangsu Academy of Agricultural Sciences, Nanjing 210014, China. Electronic address:

Heat stress-induced oxidative stress in bovine mammary epithelial cells (BMECs) threatens the normal growth and development of bovine mammary tissue, resulting in lower milk production of dairy cows. The aim of the present study is to investigate the protective effects of S-allyl cysteine (SAC), an organosulfur component extracted from aged garlic, on heat stress-induced oxidative stress and apoptosis in BMECs and to explore its underlying mechanisms. Our results showed that heat stress treatment considerably decreased cell viability, whereas SAC treatment dose-dependently restored cell viability of BMECs under heat-stress conditions. In addition, SAC protected BMECs from heat stress-induced oxidative damage by inhibiting the excessive accumulation of reactive oxygen species (ROS) and increasing the activity of antioxidant enzymes. It also inhibited heat stress-induced apoptosis by reducing the ratio of Bax/Bcl-2 and blocking proteolytic the cleavage of caspase-3 in BMECs. Interestingly, we found that the protective effect of SAC on heat stress-induced oxidative stress and apoptosis was dependent on the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway. SAC promoted the Nrf2 nuclear translocation in heat stress-induced BMECs. The results were also validated by Nrf2 and Keap1 knockdown experiments further demonstrating that Nrf-2 was indeed involved in the protective effect of SAC on heat stress-induced oxidative damage and apoptosis. In summary, our results showed that SAC could protect BMECs from heat stress-induced injury by mediating the Nrf2/HO-1 signaling pathway, suggesting that SAC could be considered as a therapeutic drug for attenuating heat stress-induced mammary gland diseases.
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http://dx.doi.org/10.1016/j.taap.2021.115469DOI Listing
April 2021

Effect of extruded starches on the structure, farinograph characteristics and baking behavior of wheat dough.

Food Chem 2021 Jun 12;348:129017. Epub 2021 Jan 12.

Engineering Research Center of Bio-process, Ministry of Education, Hefei University of Technology, 193 Tunxi Road, Hefei, Anhui 230009, PR China; School of Food and Biological Engineering, Hefei University of Technology, 193 Tunxi Road, Hefei, Anhui 230009, PR China. Electronic address:

Extruded wheat starch (ES) was obtained by a single-screw extruder to determine its effect on the farinograph, structural properties and baking behaviors of wheat dough. XRD analysis showed that increasing extrusion temperature made the crystalline peaks less pronounced due to the partial gelatinization. In terms of FTIR results, the molecular order of extruded starch was lower than that of native starch. The dough development time was decreased from 3.2 min to 2.7 min while the stability time was increased from 14.4 min to 15.5 min, as 70 ES were added. It was accompanied with increasing levels of α-helix and β-turn transferred from the decreased content of random coil and β -sheet. These effects in bread were to increase loaf volume and reduced loaf hardness. These results indicated that extruded starch had a good potential for producing a high-quality bread.
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http://dx.doi.org/10.1016/j.foodchem.2021.129017DOI Listing
June 2021

Synergistic effect of hypocrellin B and curcumin on photodynamic inactivation of Staphylococcus aureus.

Microb Biotechnol 2021 03 19;14(2):692-707. Epub 2021 Jan 19.

School of Food and Bioengineering, Hefei University of Technology, Hefei, 230009, China.

Antimicrobial photodynamic inactivation (aPDI) serves as a new approach to control the growth of foodborne bacteria. It remains elusive if the photodynamic efficacy of hypocrellin B (HB) can be potentiated by joint action with curcumin. In this study, we measured the survival rate of Staphylococcus aureus strains under the varying photodynamic conditions. According to our data, a maximum of 5-6 log decrease of bacterial survival can be achieved under the tested conditions (500 nM, 9 J cm ). Regarding the bactericidal mechanisms, HB-based aPDI disrupted the membrane integrity of staphylococcal cells, probably owing to the stimulated reactive oxygen species (ROS). In addition, aPDI disrupted the enzymatic activities of bacterial antioxidant proteins and caused the leakage of multiple intracellular substances. The HB-mediated photodynamic efficacy was potentiated by the addition of curcumin with a sublethal dose. This dual-photon synergy arose from unique aPDI conditions (100 nM each and 9 J cm ). The synergistic action might be accounted for by the increased type I/type II ratio of ROS, as evidenced by the effect of different quenchers. Finally, the joint use of photosensitizers reduced the microbial contamination of the tested apple while maintaining its quality. In summary, photodynamic inactivation based on dual photons showed synergistic activity in controlling the growth of Staphylococcal aureus, which provided a novel approach to maintain food safety.
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http://dx.doi.org/10.1111/1751-7915.13734DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7936292PMC
March 2021

Nuclear accumulation of histone deacetylase 4 (HDAC4) by PP1-mediated dephosphorylation exerts neurotoxicity in Pb-exposed neural cells.

Neurotoxicology 2020 12 17;81:395-405. Epub 2020 Oct 17.

School of Food and Biological Engineering, Hefei University of Technology, No. 193 of Tunxi Road, Baohe District, 230009, Hefei, China. Electronic address:

Lead (Pb) is an environmental contaminant that primarily affects the central nervous system, particularly the developing brain. Recently, increasing evidence indicates the important roles of histone deacetylases (HDACs) in Pb-induced neurotoxicity. However, the precise molecular mechanisms involving HDAC4 remains unknown. The purpose of this study was to investigate the role of HDAC4 in Pb-induced neurotoxicity both in vivo and in vitro. In vitro study, PC12 cells were exposed to Pb (10 μM) for 24 h, then the mRNA and protein levels of HDAC4 were analyzed. In vivo study, pregnant rats and their female offspring were treated with lead (50 ppm) until postnatal day 30. Then the pups were sacrificed and the mRNA and protein levels of HDAC4 in the hippocampus were analyzed. The results showed that HDAC4 was significantly increased in both PC12 cells and rat hippocampus upon Pb exposure. Blockade of HDAC4 with either LMK-235 (an inhibitor of HDAC4) or shHDAC4 (HDAC4-knocking down plasmid) ameliorated the Pb-induced neurite outgrowth deficits. Interestingly, HDAC4 was aberrantly accumulated in the nucleus upon Pb exposure. By contrast, blocking the HDAC4 shuffling from the cytosol to the nucleus with ΔNLS2-HDAC4 (the cytosol-localized HDAC4 mutant) was able to rescue the neuronal impairment. In addition, Pb increased PP1 (protein phosphatase 1) expression which in turn influenced the subcellular localization of HDAC4 by dephosphorylation of specific serine/threonine residues. What's more, blockade of PP1 with PP1-knocking down construct (shPP1) ameliorated Pb-induced neurite outgrowth deficits. Taken together, nuclear accumulation of HDAC4 by PP1-mediated dephosphorylation involved in Pb-induced neurotoxicity. This study might provide a promising molecular target for medical intervention with environmental cues.
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http://dx.doi.org/10.1016/j.neuro.2020.10.006DOI Listing
December 2020

Transferrin1 modulates rotenone-induced Parkinson's disease through affecting iron homeostasis in Drosophila melanogaster.

Biochem Biophys Res Commun 2020 10 14;531(3):305-311. Epub 2020 Aug 14.

School of Food and Biological Engineering, Hefei University of Technology, Hefei, Anhui, 230009, China. Electronic address:

Mitochondrial dysfunction and oxidative stress are pathophysiologic mechanisms implicated in Parkinson's disease (PD). In recent years, environmental toxins are employed to increase oxidative stress mediated neuropathology and sporadic PD. Disruption of iron homeostasis has been implicated in PD patients for many years, but the functional role of iron in sporadic PD pathogenesis is still not well clarified in vivo. To address this question, we set out to investigate the effect of iron on a Drosophila rotenone model of sporadic PD. Iron homeostasis is maintained by many transporters. We found that inhibition of transferrin1 (Tsf1) expression in the central nervous system (CNS) results in reduced iron levels in brains and significantly ameliorates the neurodegenerative phenotypes of rotenone exposure Drosophila; moreover, the rotenone induced reactive oxygen species (ROS) levels in the brain, the damaged complex I activity and the decreased ATP generation were dramatically rescued by Tsf1 knockdown. Further study indicated that all the rescue effects of Tsf1 knockdown on sporadic PD could be inhibited by malvolio (Mvl) overexpression, an iron transporter responsible for iron uptake. These results imply that Tsf1 knockdown in the CNS could attenuate rotenone toxicity by decreasing the ROS levels in brains through reducing iron levels, and manipulation of iron transporters in brains may provide a novel therapeutic strategy for sporadic PD.
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http://dx.doi.org/10.1016/j.bbrc.2020.07.025DOI Listing
October 2020

Heat stress induces apoptosis through disruption of dynamic mitochondrial networks in dairy cow mammary epithelial cells.

In Vitro Cell Dev Biol Anim 2020 Apr 6;56(4):322-331. Epub 2020 May 6.

Jiangsu Key Laboratory for Food Quality and Safety-State Key Laboratory Cultivation Base, Ministry of Science and Technology, Jiangsu Academy of Agricultural Sciences, Nanjing, 210014, China.

Heat stress-induced reductions in milk yield and the dysfunction of mammary glands are economically important challenges that face the dairy industry, especially during summer. The aim of the present study is to investigate the effects of heat stress on mitochondrial function by using dairy cow mammary epithelial cells (DCMECs) as an in vitro model. Live cell imaging shows that the mitochondria continually change shape through fission and fusion. However, heat stress induces the fragmentation of mitochondria, as well as the decreased of ATP level, membrane potential, and anti-oxidant enzyme activity and the increased of respiratory chain complex I activity. In addition, the cytosolic Ca concentration and cytochrome c expression (Cyto-c) were increased after heat stress treatment. Both qRT-PCR and western blot analysis indicate that mitofusin1/2 (Mfn1/2) and optic atrophy protein-1 (Opa-1) are downregulated after heat stress, whereas dynamin-related protein 1 (Drp1) and fission 1 (Fis-1) are upregulated, which explains the observed defect of mitochondrial network dynamics. Accordingly, the present study indicated that heat stress induced the dysfunction of DCMEC through disruption of the normal balance of mitochondrial fission and fusion.
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http://dx.doi.org/10.1007/s11626-020-00446-5DOI Listing
April 2020

Combined exposure of lead and cadmium leads to the aggravated neurotoxicity through regulating the expression of histone deacetylase 2.

Chemosphere 2020 Aug 23;252:126589. Epub 2020 Mar 23.

School of Food and Biological Engineering, Hefei University of Technology, 193 Tunxi Road, Hefei, Anhui, 230009, PR China. Electronic address:

Lead (Pb) and cadmium (Cd) are common heavy metals in the environment, exerting detrimental effects on central nervous system. Although increasing evidence demonstrated the Pb and Cd-induced neurotoxicity, the exact epigenetic mechanisms induced by combined exposure (co-exposure) of Pb and Cd are still unclear. In this study, the neurotoxicity of individual exposure and co-exposure to Pb and Cd in vivo (150 ppm and 5 ppm respectively) and in vitro (10 μM and 0.1 μM respectively) was investigated. The results showed that neurite outgrowth was inhibited by either individual or combined exposure to Pb/Cd, whereas the co-exposure aggravated the inhibitory effect in PC12 cells. The results of Morris Water Maze (MWM), Y maze and Golgi-Cox staining showed that either Pb or Cd alone exposure damaged the ability of learning and memory and decreased the dendritic spine density in both the hippocampal CA1 and DG area of Sprague---Dawley (SD) rats, and that the co-exposure aggravated the damages. Subsequently, histone deacetylase (HDAC) 2 was significantly increased in both hippocampal tissues and PC12 cells co-exposed to Pb and Cd, and the treatment of trichostatin A (TSA) and HDAC2-knocking down construct (shHDAC2) could markedly prevent neurite outgrowth impairment in PC12 cells. In summary, HDAC2 plays essential regulatory roles in neurotoxicity induced by the co-exposure to Pb and Cd, providing a potential molecular target for neurological intervention.
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http://dx.doi.org/10.1016/j.chemosphere.2020.126589DOI Listing
August 2020

EGCG ameliorates neuronal and behavioral defects by remodeling gut microbiota and TotM expression in Drosophila models of Parkinson's disease.

FASEB J 2020 04 10;34(4):5931-5950. Epub 2020 Mar 10.

School of Food and Bioengineering, Hefei University of Technology, Hefei, China.

Parkinson's disease (PD) is the second most common neurodegenerative disease. Eigallocatechin-3-gallate (EGCG), the major polyphenol in green tea, is known to exert a beneficial effect on PD patients. Although some mechanisms were suggested to underlie this intervention, it remains unknown if the EGCG-mediated protection was achieved by remodeling gut microbiota. In the present study, 0.1 mM or 0.5 mM EGCG was administered to the Drosophila melanogaster with PINK1 (PTEN induced putative kinase 1) mutations, a prototype PD model, and their behavioral performances, as well as neuronal/mitochondrial morphology (only for 0.5 mM EGCG treatment) were determined. According to the results, the mutant PINK1 flies exhibited dopaminergic, survival, and behavioral deficits, which were rescued by EGCG supplementation. Meanwhile, EGCG resulted in profound changes in gut microbial compositions in PINK1 flies, restoring the abundance of a set of bacteria. Notably, EGCG protection was blunted when gut microbiota was disrupted by antibiotics. We further isolated four bacterial strains from fly guts and the supplementation of individual Lactobacillus plantarum or Acetobacter pomorum strain exacerbated the neuronal and behavioral dysfunction of PD flies, which could not be rescued by EGCG. Transcriptomic analysis identified TotM as the central gene responding to EGCG or microbial manipulations. Genetic ablation of TotM blocked the recovery activity of EGCG, suggesting that EGCG-mediated protection warrants TotM. Apart from familial form, EGCG was also potent in improving sporadic PD symptoms induced by rotenone treatment, wherein gut microbiota shared regulatory roles. Together, our results suggest the relevance of the gut microbiota-TotM pathway in EGCG-mediated neuroprotection, providing insight into indirect mechanisms underlying nutritional intervention of Parkinson's disease.
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http://dx.doi.org/10.1096/fj.201903125RRDOI Listing
April 2020

Long-term probiotic intervention mitigates memory dysfunction through a novel H3K27me3-based mechanism in lead-exposed rats.

Transl Psychiatry 2020 01 22;10(1):25. Epub 2020 Jan 22.

Engineering Research Center of Bio-process, Ministry of Education, Hefei University of Technology, Hefei, China.

Chronic lead exposure is associated with the development of neurodegenerative diseases, characterized by the long-term memory decline. However, whether this pathogenesis could be prevented through adjusting gut microbiota is not yet understood. To address the issue, pregnant rats and their female offspring were treated with lead (125 ppm) or separately the extra probiotics (10 organisms/rat/day) till adulthood. For results, memory dysfunction was alleviated by the treatment of multispecies probiotics. Meanwhile, the gut microbiota composition was partially normalized against lead-exposed rats, which in turn mediated the memory repairment via fecal transplantation trials. In the molecular aspect, the decreased H3K27me3 (trimethylation of histone H3 Lys 27) in the adult hippocampus was restored with probiotic intervention, an epigenetic event mediated by EZH2 (enhancer of zeste homolog 2) at early developmental stage. In a neural cellular model, EZH2 overexpression showed the similar rescue effect with probiotics, whereas its blockade led to the neural re-damages. Regarding the gut-brain inflammatory mediators, the disrupted IL-6 (interleukin 6) expression was resumed by probiotic treatment. Intraperitoneal injection of tocilizumab, an IL-6 receptor antagonist, upregulated the hippocampal EZH2 level and consequently alleviated the memory injuries. In conclusion, reshaping gut microbiota could mitigate memory dysfunction caused by chronic lead exposure, wherein the inflammation-hippocampal epigenetic pathway of IL-6-EZH2-H3K27me3, was first proposed to mediate the studied gut-brain communication. These findings provided insight with epigenetic mechanisms underlying a unique gut-brain interaction, shedding light on the safe and non-invasive treatment of neurodegenerative disorders with environmental etiology.
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http://dx.doi.org/10.1038/s41398-020-0719-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7026181PMC
January 2020

Dietary intake of polyunsaturated fatty acids alleviates cognition deficits and depression-like behaviour via cannabinoid system in sleep deprivation rats.

Behav Brain Res 2020 04 6;384:112545. Epub 2020 Feb 6.

Engineering Research Center of Bio-process, Ministry of Education, Hefei University of Technology, 193 Tunxi Road, Hefei, Anhui 230009, PR China; School of Food Science and Engineering, Hefei University of Technology, Hefei, Anhui 230009, PR China. Electronic address:

Sleep deprivation (SD) is a common feature in modern society. Prolonged sleep deprivation causes cognition deficits and depression-like behavior in the model of animal experiments. Endocannabinoid system are key modulators of synaptic function, which were related to memory and mood. Although the underlying mechanism remains unknown, several studies indicated the benefits of polyunsaturated fatty acids (PUFAs, linolenic acid, 39.7 %; linoleic acid, 28 %; and oleic acid, 22 %) on brain function through the endocannabinoid system. The present study aimed to evaluate the influence of dietary PUFAs on cognition deficits induced by sleep deprivation in Sprague Dawley rats. The rats were sleep deprivation continuously for 7 days and fed with PUFAs at three different dosages (2, 4 and 8 μl/g body weight) at the meantime. The effect of PUFAs on cognition was investigated by object recognition test while depressive-like behavior were detected using sucrose preference test and forced swim test. The mechanism of PUFAs was elucidated by hippocampal synaptic transmission analyses. The resluts revealed that SD led to the disorder of cognition and mood which was improved by the supplement of PUFAs. SD significantly increased the mEPSC frequency, and decreased the protein level of cannabinoid type-1 receptors (CBR). These changes were restored by supplement of PUFAs, which showed a similar level to the control group. Behaviour tests showed that the positive effects on repairing cognition and anxiety disorders were almost completely abolished when the CBR receptor antagonist rimonabant was applied to the SD rats. These findings indicated that PUFAs are a factor regulating cognition deficits and depression induced by SD via cannabinoid type-1 receptors.
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http://dx.doi.org/10.1016/j.bbr.2020.112545DOI Listing
April 2020

Oxidative stress caused by lead (Pb) induces iron deficiency in Drosophila melanogaster.

Chemosphere 2020 Mar 20;243:125428. Epub 2019 Nov 20.

School of Food and Biological Engineering, Hefei University of Technology, Hefei, Anhui, 230009, China. Electronic address:

Toxic elements exposure disturbs the homeostasis of essential elements in organisms, but the mechanism remains elusive. In this study, we demonstrated that Drosophila melanogaster exposed to Lead (Pb, a pervasive environmental threat to human health) exhibited various health defects, including retarded development, decreased survival rate, impaired mobility and reduced egg production. These phenotypes could be significantly modulated by either intervention of dietary iron levels or altering expression of genes involved in iron metabolism. Further study revealed that Pb exposure leads to systemic iron deficiency. Strikingly, reactive oxygen species (ROS) clearance significantly increased iron uptake by restoring the expression of iron metabolism genes in the midgut and subsequently attenuated Pb toxicity. This study highlights the role of ROS in Pb induced iron dyshomeostasis and provides unique insights into understanding the mechanism of Pb toxicity and suggests ideal ways to attenuate Pb toxicity by iron supplementation therapy or ROS clearance.
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http://dx.doi.org/10.1016/j.chemosphere.2019.125428DOI Listing
March 2020

Pb exposure induces an imbalance of excitatory and inhibitory synaptic transmission in cultured rat hippocampal neurons.

Toxicol In Vitro 2020 Mar 27;63:104742. Epub 2019 Nov 27.

Engineering Research Center of Bio-process, Ministry of Education, Hefei University of Technology, 193 Tunxi Road, Hefei, Anhui 230009, PR China; School of Food Science and Engineering, Hefei University of Technology, Hefei, Anhui 230009, PR China. Electronic address:

An appropriate balance of excitatory and inhibitory synapse maintains the network stability of the central nervous system. Our recent work showed lead (Pb) exposure can inhibit synaptic transmission in cultured hippocampal neurons. However, it is not clear whether Pb exposure disrupt the balance of excitatory and inhibitory synaptic transmission. Here, primary cultured hippocampal neurons from Sprague-Dawley (SD) rats were exposed to Pb (0.2 μM, 1 μM, 5 μM, respectively) from Days in Vitro (DIV) 7 to DIV 12 for 5 days and the excitatory and inhibitory synaptic transmission was examined. Patch clamp recording results showed that distinct from exposures of 0.2 μM and 5 μM, 1 μM Pb exposure significantly increased the mIPSC frequency and decreased the mEPSC frequency, leading to a uniform inhibitory outcome. Further, the number of inhibitory presynaptic puncta was significantly increased after 1 μM Pb exposure, while the number of excitatory presynaptic terminals was decreased. In addition 1 μM Pb increased the glutamic acid decarboxylase (GAD65) expression and the surface GABA receptor (GABAR) clusters. This shift might potentiate the synthesis of GABA and enhance the surface distribution of postsynaptic GABAR clusters in hippocampus neurons. Together, these data showed that Pb exposure disrupted the balance of excitatory and inhibitory synaptic transmission via abnormal GABAergic neurotransmission.
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http://dx.doi.org/10.1016/j.tiv.2019.104742DOI Listing
March 2020

Interplay of miR-137 and EZH2 contributes to the genome-wide redistribution of H3K27me3 underlying the Pb-induced memory impairment.

Cell Death Dis 2019 09 11;10(9):671. Epub 2019 Sep 11.

School of Food and Bioengineering, Hefei University of Technology, Hefei, Anhui, 230009, People's Republic of China.

Compromised learning and memory is a common feature of multiple neurodegenerative disorders. A paradigm spatial memory impairment could be caused by developmental lead (Pb) exposure. Growing evidence implicates epigenetic modifications in the Pb-mediated memory deficits; however, how histone modifications exemplified by H3K27me3 (H3 Lys27 trimethylation) contribute to this pathogenesis remains poorly understood. Here we found that Pb exposure diminished H3K27me3 levels in vivo by suppressing EZH2 (enhancer of zeste homolog 2) expression at an early stage. EZH2 overexpression in Pb-treated rats rescued the H3K27me3 abundance and partially restored the normal spatial memory, as manifested by the rat performance in a Morris water maze test, and structural analysis of hippocampal spine densities. Furthermore, miR-137 and EZH2 constitute mutually inhibitory loop to regulate the H3K27me3 level, and this feedback regulation could be specifically activated by Pb treatment. Considering genes targeted by H3K27me3, ChIP-chip (chromatin immunoprecipitation on chip) studies revealed that Pb could remodel the genome-wide distribution of H3K27me3, represented by pathways like transcriptional regulation, developmental regulation, cell motion, and apoptosis, as well as a novel Wnt9b locus. As a Wnt isoform associated with canonical and noncanonical signaling, Wnt9b was regulated by the opposite modifications of H3K4me3 (H3 Lys4 trimethylation) and H3K27me3 in Pb-exposed neurons. Rescue trials further validated the contribution of Wnt9b to Pb-induced neuronal impairments, wherein canonical or noncanonical Wnt signaling potentially exhibited destructive or protective roles, respectively. In summary, the study reveals an epigenetic-based molecular change underlying Pb-triggered spatial memory deficits, and provides new potential avenues for our understanding of neurodegenerative diseases with environmental etiology.
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http://dx.doi.org/10.1038/s41419-019-1912-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6739382PMC
September 2019

Blocking ROR1 enhances the roles of erlotinib in lung adenocarcinoma cell lines.

Oncol Lett 2019 Sep 22;18(3):2977-2984. Epub 2019 Jul 22.

School of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu, Sichuan 611137, P.R. China.

Treatment strategies involving tyrosine kinase inhibitors (TKIs) for patients with non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) mutations have advanced significantly; however, challenges still remain regarding the development of resistance. It has been reported that receptor tyrosine kinase-like orphan receptor 1 (ROR1) acts as a hepatocyte growth factor receptor (MET) and c-Src substrate, and that the extracellular domain of ROR1 is associated with EGFR to sustain EGFR-ERBB3-PI3K signaling. Our previous study reported that blocking ROR1 significantly decreased the activity of key signal molecules in the AKT/mammalian target of rapamycin (mTOR) signaling pathway, which was associated with a significant increase of apoptosis and significant decrease of proliferation of lung adenocarcinoma cells. The present study hypothesized that inhibiting ROR1 could potentially prevent erlotinib resistance in NSCLC cell lines. Investigations were performed with two erlotinib-resistant cell lines XLA-07 and NCI-H1975, and an erlotinib-acquired-resistant cell line PC-9erlo, which was developed from its parental cell line PC-9. It was identified that the inhibition of ROR1 via small interfering RNA treatment significantly improved the anti-proliferation and apoptosis-inducing roles of erlotinib in TKI-resistant tumor cells. This was in accordance with the activity of key molecules of the AKT/mTOR signaling pathway, including glycogen synthase kinase-3α/β (GSK-3α/β), phosphatase and tensin homolog (PTEN), AKT, mTOR and ribosomal protein S6 kinase β-1 (p70S6K). The current data suggest that targeting ROR1 is a potential novel treatment strategy for patients with ROR1-positive NSCLC, particularly those with acquired resistance to EGFR-TKI.
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http://dx.doi.org/10.3892/ol.2019.10643DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6704288PMC
September 2019

The impact of sodium carbonate on physico-chemical properties and cooking qualities of starches isolated from alkaline yellow noodles.

Int J Biol Macromol 2019 Sep 2;137:697-702. Epub 2019 Jul 2.

Engineering Research Center of Bio-process, Ministry of Education, Hefei University of Technology, 193 Tunxi Road, Hefei, Anhui 230009, PR China; School of Food and Biological Engineering, Hefei University of Technology, 193 Tunxi Road, Hefei, Anhui 230009, PR China. Electronic address:

The physicochemical and cooking properties of wheat starch isolated from alkaline yellow dough treated with sodium carbonate (NaCO 0-3.2 g/100 g) were investigated. With increasing NaCO addition, swelling power increased from 7.28 to 10.70 g/g. X-ray diffraction showed no changes in crystalline patterns while the relative crystallinity decreased from 30.11% to 23.13%. Differential scanning calorimetry results suggested that alkaline salt shifted the gelatinization peak of starch to higher temperatures. The values of pasting viscosity and pasting temperature in alkali-treated starch increased and decreased, respectively. Farinograph results revealed the strengthened structure of dough with alkali-treated starch that was manifested by an increase in the dough development time and dough stability time. Cooking loss and rehydration values of noodles prepared from alkali-treated starch increased by 42% and 36%, respectively. The results suggested that NaCO affected starch crystalline structure, swelling power, gelatinization, pasting properties, starch-gluten interactions and cooking characteristics of noodle products.
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http://dx.doi.org/10.1016/j.ijbiomac.2019.07.008DOI Listing
September 2019

Performance of median kriging with robust estimators of the variogram in outlier identification and spatial prediction for soil pollution at a field scale.

Sci Total Environ 2019 May 21;666:902-914. Epub 2019 Feb 21.

Guangxi Forestry Research Institute, Nanning 530002, China.

Median kriging with robust estimators of the variogram has been proposed in literature to reduce the influences of outliers in spatial data of soil pollution, because median kriging can utilize outliers in spatial prediction and robust estimators can overcome the bias caused by outliers. However, performance of the method at a field scale remains unknown. This study compared the method in two case studies of soil Pb pollution with two other commonly used methods for outlier identification, including box-plot and standardized kriging prediction error (SKPE), and with two classical geostatistical approaches for spatial prediction, including kriging with and without outliers. One case was based on data with 359 samples collected in an area of 14.5km in Jura, Swiss. The other was based on data with 242 samples collected in an area of 2.8km in Zhuzhou, China. Results showed that the method identified both global and local outliers, while the method did not identify all global outliers based on the box-plot. For the Jura data which were more seriously affected by outliers than the Zhuzhou data, the method identified 49 outliers, sharing 39 with SKPE which identified a total of 46 outliers. For the Zhuzhou data, the method found just three outliers, much fewer than the 12 outliers identified by SKPE. In the case of Jura, kriging prediction with outliers winsorized by the method was negligibly more accurate than prediction without outliers identified by SKPE, e.g., 0.15% in terms of root mean square error (RMSE). However, in the case of Zhuzhou, the former prediction was slightly less accurate than the latter, e.g., 2.39% in terms of RMSE. This study suggested that the method performed well for data which were seriously affected by outliers, but not so well for data slightly affected by outliers.
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http://dx.doi.org/10.1016/j.scitotenv.2019.02.231DOI Listing
May 2019

Effects of stand type of artificial forests on soil microbial functional diversity.

Ying Yong Sheng Tai Xue Bao 2019 Mar;30(3):841-848

Guangxi Zhuang Autonomous Region Forestry Research Institute, Nanning 530002, China.

We explored the changes of soil microbial biodiversity in response to forest ecological restoration. Soil samples were collected from the close-to nature managed Chinese fir plantation (CF), Moso bamboo plantation (MB), and natural secondary forest (NF). Soil microbial community diversity was analyzed by Biolog-Eco micro-plate technique. The results showed that plant diversity was significantly different among the three stands. Plant diversity of NF was significantly higher than MB and CF, and MB was higher than CF. Soil pH and bulk density showed a great difference, while there was no difference of other soil physiochemical properties among the three stands. Avera-ge well color development (AWCD) of soil in various stands followed the order of NF>MB>CF, consistent with the changes of utilization of six types of carbon sources. Shannon index of NF was the highest, and the index of MB was significantly higher than that of CF. Soil physical and chemical properties in different stands were not significantly different, except soil pH and bulk density. The Shannon diversity index (H), Shannon species richness index (S), Simpson dominance index (D) and McIntosh index (U) were the highest in NF, second in MB, and the lowest in CF. Results from principal component analysis (PCA) showed that two factors from 31 carbon sources could explain 60.0% and 12.4% of the variation and that carboxylic acids, carbohydrates and its derivatives, amino acids were the main carbon sources of the two principal component factors. Correlation analysis indicated that plant species richness and Shannon diversity indexes, soil bulk density were significantly correlated to soil microbial community diversity. The microbial community of NF was more efficient in carbon utilization than that in MB and CF, while that in MB was more efficient than that of CF. Based on plant diversity and soil microbial carbon utilization, MB is much better than CF in the artificial forest restoration and improvement in South China.
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http://dx.doi.org/10.13287/j.1001-9332.201903.036DOI Listing
March 2019

Identification and Functional Characterization of a New Splicing Variant of EZH2 in the Central Nervous System.

Int J Biol Sci 2019 6;15(1):69-80. Epub 2019 Jan 6.

School of Food Science and Engineering, Hefei University of Technology, No. 193 of Tunxi Road, Baohe District, Hefei, Anhui Province, China.

EZH2 plays vital roles in epigenetic regulation, neuronal development and cancer progression. Here a novel EZH2 variant, namely EZH2-X9 (X9 for short) resulting from alternative splicing, was isolated, identified and functionally characterized. X9 was highly expressed in the brains of SD rats, indicating a potentially distinguished role in the central nervous system (CNS). Owing to a transcript profiling, X9 was enriched in multiple brain regions at very early stage of life. Immunostaining validated the presence of the protein form of X9, which was localized similarly with the wild-type form, EZH2-WT. To investigate the functional consequence of X9, genetic intervention was performed in PC-12 cell line, a classic cellular model for neuronal development. It revealed that the depletion of either variant was sufficient to impair neuronal proliferation and differentiation significantly, an evidence that roles of X9 could not be complemented by EZH2-WT. Considering epigenetic regulation, X9 lost the capability to recruit the histone mark H3K27me3, but retained the cooperation with EED, as well as the repressive aspects in governing gene expression. Nonetheless, through profiling the genes affected, it's discovered that EZH2-WT and X9 markedly differed in their regulatory targets, as X9 intended to repress cell cycle- and autophagy-related genes, like GSK and MapILC3. Overall, a novel Ezh2 variant was characterized in the mammal CNS, providing insight with the structural and functional delineation of this key developmental switch, Ezh2.
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http://dx.doi.org/10.7150/ijbs.28129DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329929PMC
January 2020

Transferrin 1 Functions in Iron Trafficking and Genetically Interacts with Ferritin in Drosophila melanogaster.

Cell Rep 2019 01;26(3):748-758.e5

State Key Laboratory of Membrane Biology, School of Life Sciences, Tsinghua University, Beijing 100084, China. Electronic address:

Iron metabolism is an essential process that when dysregulated causes disease. Mammalian serum transferrin (TF) plays a primary role in delivering iron to cells. To improve our understanding of the conservation of iron metabolism between species, we investigate here the function of the TF homolog in Drosophila melanogaster, transferrin 1 (Tsf1). Tsf1 knockdown results in iron accumulation in the gut and iron deficiency in the fat body (which is analogous to the mammalian liver). Fat body-derived Tsf1 localizes to the gut surface, suggesting that Tsf1 functions in trafficking iron between the gut and the fat body, similar to TF in mammals. Moreover, Tsf1 knockdown strongly suppresses the phenotypic effects of ferritin (Fer1HCH) RNAi, an established iron trafficker in Drosophila. We propose that Tsf1 and ferritin compete for iron in the Drosophila intestine and demonstrate the value of using Drosophila for investigating iron trafficking and the evolution of systemic iron regulation.
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http://dx.doi.org/10.1016/j.celrep.2018.12.053DOI Listing
January 2019

Pb disrupts autophagic flux through inhibiting the formation and activity of lysosomes in neural cells.

Toxicol In Vitro 2019 Mar 26;55:43-50. Epub 2018 Nov 26.

School of Food Science and Engineering, Hefei University of Technology, Hefei, Anhui 230009, PR China. Electronic address:

Lead (Pb) has long been known as a metallic toxin to exert detrimental effects on human health, particularly on the central nervous system (CNS). Misregulated autophagy was regularly associated with multiple cellular dysfunctions and human diseases. However, the role of autophagy underlying Pb-induced neurotoxicity remains to be elucidated. In this study, we demonstrated that Pb promoted the accumulation of autophagosomes in PC12 cells, and subsequent findings revealed that this autophagosome accumulation was primarily caused by the inhibition of autophagic flux. Moreover, the results showed that Pb affected autophagy course through increasing Beclin 1 and ATG5 expression levels. Specifically, by double labeling with LC3-II (a marker of autophagosome) and LAMP-1 (a marker of lysosome), Pb impaired fusion between autophagosomes and lysosomes. Additionally, Pb exposure significantly reduced the number or size of lysosomes via decreasing the level of LAMP1, which is confirmed by the LysoTracker Red staining. Furthermore, the impairment of lysosomal activity was also signaled by the altered pH value of this acidic organelle. Overall, Pb exposure led to injuries of autophagy of neural cells through inhibiting the genesis and activity of lysosomes. The data provides insight with the neurotoxicity of Pb in a novel perspective, autophagy.
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http://dx.doi.org/10.1016/j.tiv.2018.11.010DOI Listing
March 2019

Phytohormone Abscisic Acid Improves Spatial Memory and Synaptogenesis Involving NDR1/2 Kinase in Rats.

Front Pharmacol 2018 9;9:1141. Epub 2018 Oct 9.

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

The abscisic acid (ABA) is a phytohormone involved in plant growth, development and environmental stress response. Recent study showed ABA can also be detected in other organisms, including mammals. And it has been reported that ABA can improve learning and memory in rats. In this study, we attempted to investigate the effects of ABA on the alternation of dendritic spine morphology of pyramidal neurons in developmental rats, which may underlie the learning and memory function. Behavior tests showed that ABA significantly improved spatial memory performance. Meanwhile, Golgi-Cox staining assay showed that ABA significantly increased the spine density and the percentage of mushroom-like spines in pyramidal neurons of hippocampus, indicating that ABA increased dendritic spine formation and maturation, which may contribute to the improvement of spatial memory. Furthermore, ABA administration increased the protein expression of NDR1/2 kinase, as well as mRNA levels of NDR2 and its substrate Rabin8. In addition, NDR1/2 shRNA prohibited the ABA-induced increases in the expression of NDR1/2 and spine density. Together, our study indicated that ABA could improve learning and memory in rats and the effect are possibly through the regulation of synaptogenesis, which is mediated via NDR1/2 kinase pathway.
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http://dx.doi.org/10.3389/fphar.2018.01141DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6190901PMC
October 2018

Targeting ROR1 inhibits epithelial to mesenchymal transition in human lung adenocarcinoma via mTOR signaling pathway.

Int J Clin Exp Pathol 2018 1;11(10):4759-4770. Epub 2018 Oct 1.

School of Basic Medicine, Chengdu University of Traditional Chinese Medicine Chengdu, Sichuan, PR China.

The receptor tyrosine kinase-like orphan receptor 1 (ROR1) is a type I surface transmembrane protein that contributes to progression of tumor-cell growth and metastasis. We and others have shown that the roles of ROR1 include inhibiting apoptosis, potentiating EGFR signaling, and inducing proliferation in lung cancer, but the roles and mechanisms of ROR1 in lung adenocarcinoma metastasis have not been elucidated. Here we chose four lung adenocarcinoma cell lines, PC9 (erlotinib-sensitive), PC9erlo (acquired erlotinib-resistant), NCI-H358 (partial erlotinib-resistant), and NCI-H1975 (erlotinib-resistant) as cell models to simulate the clinical situation. We found that ROR1 prompted epithelial to mesenchymal transition (EMT) by increasing the expression level of a key epithelial gene, E-cadherin, while decreasing the expression level of the key mesenchymal gene vimentin. Silencing ROR1 by siRNA significantly reduced the migration and invasion of lung adenocarcinoma cells in and also significantly inhibited the phosphorylation of Akt (Ser473), mTOR (Ser2448), Raptor (Ser792) and p70S6K (Thr389) in all four cell lines. This strongly supports our proposal that ROR1 may play a central role in tumor progression and metastasis in lung adenocarcinoma through mTOR signaling, regardless of its EGFR-TKI sensitivity status.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6962910PMC
October 2018

rhPLD2 inhibits airway inflammation in an asthmatic murine model through induction of stable CD25 Foxp3 Tregs.

Mol Immunol 2018 09 30;101:539-549. Epub 2018 Aug 30.

Immunology Dept. and Center of Neuroscience, Fujian Medical University, Fuzhou, Fujian 350004, PR China. Electronic address:

Our previous studies have shown that recombinant human phospholipase D2 (rhPLD2) plays a modulator role on NF-κB and PKC signaling pathways. It also inhibits IL-5-induced inflammatory response in chronic asthmatic guinea pigs. Additionally, increasing evidence also has revealed that the adoptive transfer of induced regulatory T cells (Tregs) may be a therapeutic solution to airway allergic diseases. To investigate the epigenetic, transcriptomic and phenotypic variability of Treg population in an ovalbumin (OVA)-induced airway inflammation model derived from the induction of rhPLD2, OVA-induced asthmatic murine model is used in this study. The lung inflammation, eosinophil infiltration, the differentiation and proliferation of T helper cells and the amplification of Tregs were examined in this mouse model with and without rhPLD2 induction. Our data showed that rhPLD2 administration in asthmatic mice significantly increases CD4CD25 Foxp3 Treg cell numbers and alleviates lung inflammation. The addition of rhPLD2 in vitro enhanced the demethylation of Treg-specificdemethylated region (TSDR) in iTregs, suggesting that rhPLD2 protein may be involved in improving the quality and quantity of Treg cells that eventually significantly reduces lung inflammation in asthmatic murine model. These results suggest that rhPLD2 could have a clinical impact treating patients with allergic airway inflammation via promoting and stabilizing iTreg differentiation and function.
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http://dx.doi.org/10.1016/j.molimm.2018.07.030DOI Listing
September 2018

Pb inhibits hippocampal synaptic transmission via cyclin-dependent kinase-5 dependent Synapsin 1 phosphorylation.

Toxicol Lett 2018 Oct 16;296:125-131. Epub 2018 Aug 16.

School of Food Science and Engineering, Hefei University of Technology, Hefei, Anhui 230009, PR China. Electronic address:

Lead (Pb) exposure impairs the nervous system, of which the injury of cognitive development is obvious. But the mechanism of Pb induced disorders of neuro-transmission remain elusive. In this study, primary hippocampal neurons were exposed to Pb at the dosage of 5 μM from days in vitro (DIV) 3 to DIV14 and the electrophysiological recordings were performed at DIV14. Sprague-Dawley (SD) rat pups were exposed to Pb from parturition to weaning indirectly from their mothers whose drinking water containing 250 ppm Pb, then directly exposed to Pb at the dosage of 250 ppm from postnatal day (PND) 21 to PND30. The results showed that Pb significantly decreased the frequency of both miniature excitatory postsynaptic current (mEPSC) and miniature inhibitory postsynaptic current (mIPSC) in cultured hippocampal neurons. Paird-pulse facilitation (PPF) recordings showed there was significant increase in Pb-exposed group. The increase of the magnitude of PPF (the ratio of second to first response amplitude) further confirmed that Pb reduced presynaptic neuro-transmission. By transmission electron microscope, it found that Pb disarranged presynaptic vesicles distribution and decreased the density of presynaptic vesicles. Moreover, it was interestingly found that phosphorylation of Synapsin1, which was phosphorylated by CDK5, has been decreased upon Pb exposure. With the treatment of R-Roscovitine (Ro), an inhibitor of CDK5, it was detected that Pb induced mEPSC and mIPSC frequency reduction have been reversed. Together, our results suggested that Pb disrupted the distribution of synaptic vesicles and impaired the neurotransmitter release, which was dependent on the phosphorylation level of Synapsin 1 via CDK5. This study will help for elucidation of environmental Pb-induced neuronal disorders.
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http://dx.doi.org/10.1016/j.toxlet.2018.08.009DOI Listing
October 2018

The protective effect of polysaccharide extracted from Portulaca oleracea L. against Pb-induced learning and memory impairments in rats.

Int J Biol Macromol 2018 Nov 21;119:617-623. Epub 2018 Jul 21.

School of Food Science and Engineering, Hefei University of Technology, Hefei, Anhui 230009, PR China. Electronic address:

This paper studied the extraction of polysaccharide from Portulaca oleracea L. (POP) by hot water extraction and ethanol precipitation. Structural properties of the extracted polymers were determined. POP was composed of rhamnose, arabinose and galactose in ratios of 1: 2.34: 3.07 with a molecular weight of 1.55 × 10 Da. The neuroprotective effect of POP on Pb-induced neuronal toxicity was then evaluated in vitro and in vivo test. Treatment with POP markedly increased the survival of PC12 cells and repressed the generation of reactive oxygen species following Pb exposure. In Morris water maze analysis, Pb exposure led to an increase in escape latency and a decrease in platform crossing times of rats in the probe test, which could be attenuated by POP treatment. Additionally, the Pb-induced loss of dendritic spine was recovered after feeding rats with POP at 600 mg/kg/day. These results indicated that Pb-induced cognitive impairments could be inhibited by POP.
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http://dx.doi.org/10.1016/j.ijbiomac.2018.07.138DOI Listing
November 2018

Effect of Pb Exposure on Synaptic Scaling Through Regulation of AMPA Receptor Surface Trafficking.

Toxicol Sci 2018 09;165(1):224-231

School of Food Science and Engineering, Hefei University of Technology, Hefei, Anhui Province 230009, P.R. China.

Homeostatic synaptic plasticity (HSP) helps to stabilize the neuronal network activity, which is essential for optimal information coding. Synaptic scaling is a form of homeostatic plasticity that stabilizes neuronal firing in response to activity blockade. Lead (Pb) is a ubiquitous environmental neuro-toxicant and can impair the input-specific Hebbian type synaptic plasticity, but whether Pb exerts effects in HSP remains unknown. We previously reported that blocking L-type calcium channel induces synaptic scaling, which stimulates the synthesis of all-trans retinoic acid (RA) and the expression of GluA2-lacking α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor. Given Pb is a potent blocker of calcium channel, we hypothesized Pb may participate in synaptic scaling accompanied by RA synthesis and AMPA receptor trafficking. In this study, cultured hippocampal neurons were treated with Pb (1 μM 5 min, 15 min, 4 h, 24 h, and 10 μM 24 h) alone or in combination with tetrodotoxin (TTX, 1 μM, 24 h). The results showed that Pb alone, either at 1 μM or 10 μM, cannot induce synaptic scaling. But Pb participated in synaptic scaling when concurrent with TTX (10 μM Pb + 1 μM TTX, 24 h). Further results showed that surface heteromeric GluA1 and GluA2 AMPA receptors were increased in TTX+ Pb-induced synaptic scaling. In addition, RA was proved not to participate in TTX+ Pb-mediated synaptic scaling. Taken together, our work supported that TTX+ Pb could induce synaptic scaling and enhance synaptic accumulation of AMPAR GluA1 and GluA2 during synaptic up scaling. Our study would help for elucidation of the Pb-induced neuronal network instability mechanism.
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http://dx.doi.org/10.1093/toxsci/kfy156DOI Listing
September 2018

Effect of multiple freezing-thawing cycles on structural and functional properties of starch granules isolated from soft and hard wheat.

Food Chem 2018 Nov 15;265:18-22. Epub 2018 May 15.

School of Food Science and Technology, Jiangnan University, Wuxi 214122, Jiangsu Province, PR China. Electronic address:

Properties of starches isolated from soft and hard wheat dough after freezing/thawing (F/T) treatment were investigated. Significance of results was observed between isolated hard wheat starch (HWS) and soft wheat starch (SWS), but both cultivars showed an increase in the amounts of damaged starch and leaching proteins, lipids, and amylose with F/T cycles. The freezing-treated HWS exhibited a higher swelling power and peak, trough, breakdown and final viscosity than SWS after F/T treatment. The onset, peak and conclusion gelatinization temperatures and the enthalpy of the isolated HWS determined by differential scanning calorimetry, decreased throughout F/T cycles. Concomitantly, the bread containing freezing-treated HWS exhibited a lower bread specific volume and harder crumb firmness, which might be associated with its significant structural changes induced by F/T treatment.
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http://dx.doi.org/10.1016/j.foodchem.2018.05.065DOI Listing
November 2018

Melatonin Inhibits Reactive Oxygen Species-Driven Proliferation, Epithelial-Mesenchymal Transition, and Vasculogenic Mimicry in Oral Cancer.

Oxid Med Cell Longev 2018 21;2018:3510970. Epub 2018 Mar 21.

School and Hospital of Stomatology, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China.

Globally, oral cancer is the most common type of head and neck cancers. Melatonin elicits inhibitory effects on oral cancer; however, the biological function of melatonin and underlying mechanisms remain largely unknown. In this study, we found that melatonin impaired the proliferation and apoptosis resistance of oral cancer cells by inactivating ROS-dependent Akt signaling, involving in downregulation of cyclin D1, PCNA, and Bcl-2 and upregulation of Bax. Melatonin inhibited the migration and invasion of oral cancer cells by repressing ROS-activated Akt signaling, implicating with the reduction of Snail and Vimentin and the enhancement of E-cadherin. Moreover, melatonin hampered vasculogenic mimicry of oral cancer cells through blockage of ROS-activated extracellular-regulated protein kinases (ERKs) and Akt pathways involving the hypoxia-inducible factor 1. Consistently, melatonin retarded tumorigenesis of oral cancer . Overall, these findings indicated that melatonin exerts antisurvival, antimotility, and antiangiogenesis effects on oral cancer partly by suppressing ROS-reliant Akt or ERK signaling.
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http://dx.doi.org/10.1155/2018/3510970DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5884151PMC
September 2018

The SMYD3 VNTR 3/3 polymorphism confers an increased risk and poor prognosis of hepatocellular carcinoma in a Chinese population.

Pathol Res Pract 2018 May 17;214(5):625-630. Epub 2018 Apr 17.

Department of Oncology, Affiliated Hospital of Jining Medical University, Jining 272009, PR China.

Objective: Hepatocellular carcinoma (HCC) is one of the most lethal human malignancies in China, and the genetic link of hepatocarcinogenesis remains to be defined. Thus, we explored the role of SET and myeloid translocation protein 8, Nervy, and DEAF1 (MYND) domain containing protein 3 (SMYD3) gene polymorphism on risk and prognosis of HCC.

Methods: A total of 236 patients with HCC who received treatment in Affiliated Hospital of Jining Medical University for the first time and 230 healthy individuals were enrolled in the study. After DNA extraction for all the subjects, polymerase chain reaction (PCR) was used to amplify and sequence variable numbers of tandem repeat (VNTR) loci of SMYD3 gene. SMYD3 gene was genotyped and its frequency distribution was calculated. Age, education level, income, smoking and drinking history, HCC family history, tumor node metastasis (TNM) staging, maximum tumor diameter, lymph node metastasis (LNM) etc. were investigated. Correlation of SMYD3 gene polymorphism and other risk factors with the occurrence and prognosis of HCC was analyzed.

Results: The family history of HCC, drinking history, cirrhosis, and HBV or/and HCV infection, SMYD3 VNTR 3/3 were more frequently observed in subjects with HCC. Patients with SMYD3 VNTR 3/3 genotype, drinking-history, family history of HCC, cirrhosis and hepatitis B virus (HBV), TNM staging, maximum tumor diameter, LNM were more vulnerable to HCC. Besides, patients with SMYD3 VNTR 3/3 genotype had lower 2- and 3-year survival rate. The COX regression analysis revealed that drinking history, family history of HCC, SMYD3 VNTR 3/3 genotype, TNM staging, and LNM were all related to the prognosis of HCC.

Conclusion: This study indicates that drinking history, family history of HCC and SMYD3 VNTR 3/3, TNM staging, maximum tumor diameter, LNM might be risk factors for HCC, and SMYD3 VNTR 3/3 might contribute to a lower 2- and 3-year survival rate of patients with HCC.
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http://dx.doi.org/10.1016/j.prp.2018.04.005DOI Listing
May 2018