BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
·
2022
·
IF 3.322
Wei Sun,Jing Liu,Renhao Zhao,Teng Yang,Zhichen Zheng,Tongyu Zhang,Guofeng Wang
Background and Purpose: To investigate the biological role of interferon α/β receptor 2 (IFNAR2) in type 1 diabetes (T1D). Methods First, IFNAR2 mRNA and protein expression levels in serum of T1D patients and healthy controls were detected by RT-qPCR and Western blot . For experimental studies, 80 male C57BL/6 mice were randomly divided into 4 groups with 20 mice in each group: the control group, the T1D group, the T1D + ad-con group and the T1D + ad-si-IFNAR2 group. The T1D mouse model was generated by multiple intraperitoneal injections of small doses of streptozotocin (STZ). Body weight and blood glucose levels were measured weekly until 6 weeks. After 6 weeks, all mice were sacrificed and the levels of insulin (Ins), tumor necrosis factor α (TNF-α), interleukin 4 (IL-4), IL-6, and type I interferon γ (IFN-γ), IFNAR2 protein expression, the number of dendritic cells (DCs), and changes in islet β cells were assessed. Results IFNAR2 mRNA and protein expression levels in serum of T1D patients were significantly higher than those in healthy controls ( P < 0.05). Furthermore, IFNAR2 protein expression, number of DCs, and IFNAR2 mRNA, blood glucose, TNF-α, and IFN-γ levels were significantly upregulated in T1D mice compared with the control group ( P < 0.05), while weight, and Ins, IL-6, and IL-4 levels were decreased ( P < 0.05). However, knockdown of IFNAR2 reversed these trends. There was no significant difference in markers between the T1D + ad-con group and the T1D group ( P > 0.05). Conclusions Knockdown of IFNAR2 reduced the inflammatory response and improved islet function of T1D mice.
研究领域:
免疫学
·
糖尿病
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分子生物学
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DOI
PubMed
高影响因子
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
·
2021
·Vol. 99
·期 12
·
IF 2.273
Weimin Xu,Peng Wang,Dalong Wang,Ke Liu,Shuaishuai Zhang,Wei Zhao,Guoqing Liu
The aim of the present study was to investigate the protective effect of S-ketamine (S-KET) against carbon tetrachloride (CCl4) – induced liver damage and oxidative stress, as well as to elucidate the related underlying mechanisms. Blood was collected to measure biochemical parameters (alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), total bilirubin (TB) and γ-glutamyltransferase (γ-GT)) and the liver was harvested for histopathological analysis of enzymes related to the antioxidant response (malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GSH-PX)). Liver cell apoptosis was evaluated using the TUNEL assay. In addition, the expression levels of apoptosis-related proteins and the nuclear factor erythroid 2–related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway were detected by Western blot analysis to explore potential mechanisms. S-KET protected the liver from CCl4-induced damage. The changes to the liver biochemical parameters (increased ALT, AST, ALP, TB, and γ-GT) and oxidative stress-related indicators (increased MDA; depleted SOD, GSH, and GSH-PX) induced by CCl4 were inhibited by S-KET. S-Ket also inhibited CCl4-induced cell apoptosis, the changes in expression of related proteins, and blocked CCl4-induced liver injury and oxidative stress via activation of the Nrf2/HO-1 signaling pathway. S-KET effectively protected the liver by inhibition of CCl4-induced damage via upregulation the Nrf2/HO-1 signaling pathway.
研究领域:
药理学
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肝病学
·
分子生物学
·
毒理学
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DOI
PubMed
高影响因子
Advanced Science
·
2025
·
IF 14.1
Ling-Na Zhao,Rui-Ling Wang,Ran-Xin Liu,Meng-Ru Zheng,Li Zhao,Bao-Feng Li,Jia-Le Li,De-Shen Liu,Xiao-Xia He,Qin-Bao Peng,Kai Li,Tian-Xiao Lin,Ying-Ying Liu,Sheng-Ping He,Jun Lu,Shao-Yi Zheng,Xiu Liu,Fang-Ze Huang
Atherosclerosis (AS) is a major cause of cardiovascular diseases, driven by chronic inflammation and macrophage polarization toward a proinflammatory phenotype. Pyruvate carboxylase (PC), a mitochondrial enzyme involved in glucose metabolism, is implicated in various metabolic disorders; however, its role in AS remains unclear. This study aims to investigate the role and mechanism of PC on macrophages in AS. PC is upregulated in macrophages of humans and mice with AS. Myeloid cell-specific PC knockout mice are generated to investigate the effects of PC deletion on atherosclerotic plaque formation. Myeloid cell-specific PC deficiency mitigates high-fat diet-induced atherosclerotic lesions in apolipoprotein E knockout mice and mice injected with adeno-associated virus- PCSK9 DY . PC deletion enhances mitochondrial respiration and reduces glycolytic activity, thereby reducing reactive oxygen species overproduction and mitochondrial damage in macrophages. PC activates the hypoxia-inducible factor-1 (HIF-1) signaling pathway through macrophage metabolic reprogramming. PC induces nuclear translocation of HIF-1α in atherosclerotic aortic roots by preventing HIF-1α from proteasome degradation. HIF-1α stabilizer reverses the anti-inflammatory effect of macrophage-PC ablation in atherogenesis; however, inhibiting HIF-1α suppresses the proinflammatory macrophage phenotype induced by PC overexpression. This study indicates that macrophage PC aggravates AS through macrophage metabolic reprogramming, promoting inflammatory responses in macrophages through the HIF-1 signaling pathway.
研究领域:
心血管疾病
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免疫学
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代谢
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分子生物学
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产品关联
DOI
PubMed
高影响因子
COLLOIDS AND SURFACES B-BIOINTERFACES
·
2025
·
IF 5.6
Peixuan Zou,Yusong Pan,Wenjie Luo,Run Huang,Xiuling Lin,Yinghai Xie
Chemo-photothermal synergistic therapy is an effective method for tumor treatment. Herein, the CuS/HKUST-1@PDA drug carrier was successfully prepared by a simple combination of in-situ partial vulcanization and in-situ polymerization technologies. The micro-structure, morphology, and functional groups of the prepared samples were characterized by XRD, SEM, TEM, BET, and FTIR technologies. The drug loading experiment verified that the CuS/HKUST-1@PDA possesses an excellent doxorubicin (DOX) drug loading capacity, whose drug loading capacity is as high as 88.7 %. The drug release indicated that CuS/HKUST-1@PDA drug carrier inherited pH-responsive drug release behavior, which it can release DOX in acidic conditions resembling the tumor microenvironment, while effectively containing the drug within the PDA coating under neutral conditions. The CuS/HKUST-1@PDA drug carrier demonstrated outstanding biocompatibility, sustaining cell viability above 80 % across a concentration range of 1.5–15 μg/mL. Moreover, the drug carrier realized chemo-Photothermal synergistic therapy triggered by near-infrared light in tumor treatment, reducing tumor cell viability to 28 % during in vitro cellular experiments. The innovative design and effective tumor treatment ability of the CuS/HKUST-1@PDA drug carrier highlight its significant potential in anticancer therapy.
研究领域:
材料科学
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肿瘤学
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纳米医学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF VIROLOGY
·
2018
·Vol. 92
·期 17
·
IF 4.368
Cong-Cong Wu,Xuan Jiang,Xian-Zhang Wang,Xi-Juan Liu,Xiao-Jun Li,Bo Yang,Han-Qing Ye,Thomas Harwardt,Man Jiang,Hui-Min Xia,Wei Wang,William J. Britt,Christina Paulus,Michael Nevels,Min-Hua Luo
The mechanisms underlying neurodevelopmental damage caused by virus infections remain poorly defined. Congenital human cytomegalovirus (HCMV) infection is the leading cause of fetal brain development disorders. Previous work has linked HCMV infection to perturbations of neural cell fate, including premature differentiation of neural progenitor cells (NPCs). Here, we show that HCMV infection of NPCs results in loss of the SOX2 protein, a key pluripotency-associated transcription factor. SOX2 depletion maps to the HCMV major immediate early (IE) transcription unit and is individually mediated by the IE1 and IE2 proteins. IE1 causes SOX2 downregulation by promoting the nuclear accumulation and inhibiting the phosphorylation of STAT3, a transcriptional activator of SOX2 expression. Deranged signaling resulting in depletion of a critical stem cell protein is an unanticipated mechanism by which the viral major IE proteins may contribute to brain development disorders caused by congenital HCMV infection.IMPORTANCE Human cytomegalovirus (HCMV) infections are a leading cause of brain damage, hearing loss, and other neurological disabilities in children. We report that the HCMV proteins known as IE1 and IE2 target expression of human SOX2, a central pluripotency-associated transcription factor that governs neural progenitor cell (NPC) fate and is required for normal brain development. Both during HCMV infection and when expressed alone, IE1 causes the loss of SOX2 from NPCs. IE1 mediates SOX2 depletion by targeting STAT3, a critical upstream regulator of SOX2 expression. Our findings reveal an unanticipated mechanism by which a common virus may cause damage to the developing nervous system and suggest novel targets for medical intervention.
研究领域:
病毒学
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神经科学
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发育生物学
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细胞生物学
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DOI
PubMed
高影响因子
DYES AND PIGMENTS
·
2022
·
IF 5.122
Hui Zhang,Shuhui Bo,Ji Zhang,Yuhui Ao,Ming Li
Developing new organic second-order nonlinear optical chromophores with a new electron donor is crucial for enhancing performance of electro-optic (EO) materials. A series of new second-order nonlinear optical chromophores (J1, JS and JO) with new electron donor 1-Oxajulolidine have been designed and synthesized. Ref1, Ref2 and Ref3 with N, N-diethylaniline (DEA), 4-anisole and julolidine as electron donor had also been synthesized for comparison. The result of TGA and DSC tests suggested that the decomposition temperature of the chromophores was higher than 260 °C. As the UV–vis absorption spectra of chromophores in solution, maximum absorption ( λ max ) of the chromophores J1 with 1-Oxajulolidine group presented red-shift compared to Ref1 and Ref2, but blue-shift to Ref3. Nevertheless, chromophore with 1-Oxajulolidine presented more obvious solvatochromic behavior from dioxane to dichloromethane . Density functional theory had been used to calculate HOMO-LUMO energy gaps and β of these chromophores. The r 33 values of guest-host EO polymers Ref1/APC , J1/APC , JS/APC and JO/APC with a loading density of 10 wt% were obtained as 7.5, 9.6, 15.3 and 13.5 pm V −1 , respectively. The above result clearly indicated that r 33 of J1/APC (9.6 pm V −1 ) was 27% higher than that of Ref1/APC (7.5 pm V −1 ). The electro-optic coefficient of JS with the same conjugate bridge and acceptor was higher than that of FTC in the same doping concentration. As revealed by the above results, the introduction of the polycyclic structure of 1-Oxajulolidine, containing two electron-rich atoms (N and O) , could efficiently enhance the electro-optical performance. Furthermore, λ max of JS in doped film showed blue-shift compared with FTC which exhibited a promising potential for tackling nonlinearity and transparency trade-off in second-order nonlinear optical (NLO) materials.
研究领域:
材料科学
·
光学
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DOI
高影响因子
ChemElectroChem
·
2019
·Vol. 6
·期 17
·4681-4688
·
IF 3.975
Yu Huang,Rengui Xiao,Zhiming Ma,Weichen Zhu
Graphical In sync : The 1-ethyl-3-methylimidazolium trifluoromethanesulfonate (EMImTfO) dual-graphite battery exhibits a high discharge plateau above 3.0 V, which originates from the synchronized de-intercalations of EMIm + and TfO − from the graphite cathode and anode, respectively. The battery can light up a red LED with 3.0 V standard voltage. In this work, a novel dual-graphite battery (DGB) based on a pure 1-ethyl-3-methylimidazolium trifluoromethanesulfonate (EMImTfO) ionic liquid electrolyte is constructed. Within a charge/discharge voltage range of 1.0–3.9 V and at a current of 400 mA g −1 , batteries with dual-natural-graphite electrodes exhibit a high discharge plateau above 3.0 V with an initial discharge capacity of 46.2 mAh g −1 , delivering a capacity retention of 71.0 % after 100 cycles. Comparative studies between the natural graphite and the synthetic graphite (KS6) electrodes are also conducted. Charge-discharge tests reveal that the dual natural-graphite battery presents a higher discharge voltage plateau and better retention than the dual KS6-graphite battery. To confirm the principle of the dual-graphite systems, a cyclic voltammetry test is conducted. The results demonstrate that the EMIm + cation exhibits an even more stable intercalation/de-intercalation behavior than the TfO − anion. Further tests, including ex situ X-ray diffraction and ex situ Raman spectroscopy, are performed to reveal the mechanism of TfO − and EMIm + intercalation into graphite, both demonstrating a reversible process.
研究领域:
电化学
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电池技术
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材料科学
·
能源存储
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DOI
高影响因子
Human Cell
·
2022
·Vol. 35
·期 5
·1424-1439
·
IF 4.374
Liu Wen,Li Guojuan,Li Jing,Chen Wei
The long-term treatment of glucocorticoids is a common cause of osteoporosis (OP). This study concentrated on inquiring into the regulatory role and potential mechanisms of TRG-AS1 on dexamethasone (Dex)-induced OP in rats. We adopted Dex to treat rat osteoblasts and rats to simulate in-vitro and in-vivo OP models, respectively. Gain-of-function assays of TRG-AS1, miR-802 and CAB39 were constructed in rat osteoblasts to make certain the influence of TRG-AS1, miR-802 and CAB39 on differentiation, proliferation and apoptosis of rat osteoblasts. TRG-AS1 and CAB39 were down-regulated in the Dex-induced OP model in rats, in contrast to miR-802. Overexpression of TRG-AS1 restrained Dex-induced inhibition of osteogenic differentiation, promoted CAB39/AMPK/SIRT-1 and inhibited NF-κB, while overexpression of miR-802 bridled the inhibitory effect of TRG-AS1 on OP. miR-802 was targeted by TRG-AS1, and inhibited CAB39. Inhibition of either AMPK or SIRT-1 abated the osteogenic differentiation-promoting effect of CAB39. Animal experiments displayed that overexpressing TRG-AS1 alleviated Dex-induced OP in rats. In conclusion, up-regulation of TRG-AS1 protected against glucocorticoid-induced OP in rats by modulating the miR-802-mediated CAB39/AMPK/SIRT-1/NF-κB axis.
研究领域:
分子生物学
·
药理学
·
骨科
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DOI
PubMed
高影响因子
Journal of Analysis and Testing
·
2024
·
IF 5.5
Xiao Qi,Liu Shuai,Wang Yali,Li Huihao,Yang Mingli,Fang Yi,Chen Sijing,Huang Shan
Human T-cell lymphophilic virus type 1 (HTLV-1), the known retrovirus causing cancer in humans, is closely associated with adult T-cell leukemia/lymphoma and HTLV-1 associated myelopathy/tropical spastic paraparesis. Due to its ability to evade the host's defense mechanisms, early tracking of HTLV-1 becomes crucial. In this study, we integrate λ-Exonuclease (λ-Exo)-assisted target recycling with a terminal deoxynucleotidyl transferase (TdT)-mediated template-free DNA extension process to develop an electrochemical analysis platform for the specific and sensitive detection of HTLV-1 DNA. During the λ-Exo-assisted target recycling, HTLV-1 DNA is recognized by hairpin DNA (Hp-DNA), forming double-stranded DNA (dsDNA) through DNA hybridization. The dsDNA, featuring blunt 5' terminal phosphorylation, is cleaved by λ-Exo, generating abundant short output sequence (sDNA). HTLV-1 DNA is released, initiating a cyclic hybridization-cleavage process. Subsequently, thiol-labelled capture DNA (CP-DNA) assembled on gold electrode surface captures a substantial amount of the generated sDNA, forming CP-DNA-sDNA nanostructures. When TdT and dNTPs are present on the electrode surface, the 3'-OH terminal of sDNA extends to generate long single-stranded DNA (ssDNA) structure. Methylene blue (MB) is selected as the electrochemical signal molecule. MB not only binds with ssDNA but also interacts specifically with dsDNA, resulting in a significantly enhanced electrochemical signal on modified electrode surface. The detection limit of HTLV-1 DNA is as low as 19 amol/L ( S / N = 3) when the two signal amplification strategies are combined. The analysis platform exhibits excellent analytical performance and holds promise as a novel tool for the early tracing and diagnosis of HTLV-1 DNA.
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产品关联
DOI
高影响因子
JOURNAL OF CHEMICAL SCIENCES
·
2020
·Vol. 132
·期 1
·1-14
·
IF 1.406
Cheng Si Yuan,Yang Xi Nan,Tao Zhu,Wei Lian Tong,Zhao Wei Wei,Jiang Dao Fa,Jin Yan Mei,Gao Jie,Ma Pei Hua
Abstract The host–guest binding characteristics of cyclopentanocucurbit[6]uril (CyP 6 Q[6]) and cyanine dye trans -4-[4-(dimethylamino)styryl]-1-methylpyridinium iodide ( t -DSMI) have been studied. The results show that CyP 6 Q[6] and t -DSMI form a 1:1 inclusion system, generating strong fluorescence. On this basis, the fluorescent probe t -DSMI@CyP 6 Q[6] has been constructed, and its anion recognition ability has been investigated. In a neutral environment, BF 4 − , H 2 PO 4 − , and I − elicit obvious specific responses from the probe, since they have stronger binding forces. This probe shows greater sensitivity than the previously reported probe t -DSMI@HMeQ[6]. Graphic abstract Since the complex formed by CyP 6 Q[6] and t -DSMI can produce strong fluorescence at pH > 4.6, t -DSMI@CyP 6 Q[6] was constructed to recognize the anions at pH ≅ 5. The results show that in a near neutral environment, BF 4 − , H 2 PO 4 − , and I − elicit obvious specific responses from the probe.
研究领域:
分析化学
·
材料科学
·
化学传感器
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DOI
高影响因子
DRUG DELIVERY
·
2023
·
IF 6
Ru Wang,Nuannuan Li,Tianyu Zhang,Yiying Sun,Xiaoyan He,Xiaoyan Lu,Liuxiang Chu,Kaoxiang Sun
Mitoxantrone (MX) can induce the immunogenic-cell death (ICD) of tumor cells and activate anti-tumor immune responses. However, it can also cause high expression of indole amine 2, 3-dioxygenase (IDO) during ICD, leading to T-cell apoptosis and a weakened immune response. An IDO inhibitor, 1-methyl tryptophan (1-MT), can inhibit the activity of IDO caused by MX, resulting in enhanced chemo-immunotherapy. Here, MX-1-MT was connected by ester bond which could be broken in an acidic tumor microenvironment. MX-1-MT was combined with polyethylene glycol (PEG) via a disulfide bond which could be reduced by glutathione overexpressed in tumors, thereby accelerating drug release at target sites. Folic acid-modified distearoyl phosphoethanolamine-polyethylene glycol (DSPE-PEG-FA) was introduced to form targeting micelles. The micelles were of uniform particle size, high stability, and high responsiveness. They could be taken-up by drug-resistant MCF-7/ADR cells, displayed high targeting ability, and induced enhanced cytotoxicity and ICD. Due to 1-MT addition, micelles could inhibit IDO. In vivo studies demonstrated that micelles could accumulate in the tumor tissues of nude mice, resulting in an enhanced antitumor effect and few side-effects.
研究领域:
药学
·
癌症研究
·
纳米技术
·
免疫学
·
药物递送系统
✓ 已验证
DOI
PubMed
高影响因子
CATALYSIS LETTERS
·
2022
·Vol. 153
·期 2
·348-363
·
IF 2.936
Chu Jidong,Ge Zhijin,Peng Jiahui,Hu Hui,Guo Shujuan,Chen Xiaohui
The efficient and economic heteroatom-implanting method for MWW-type zeolite has been the focus of attention and needs further exploration. Ti incorporated MWW zeolite was synthesized by sequential treatment of boron-containing zeolite precursor. The catalysts were applied to the epoxidation of 1-hexene. The implanting titanium process was conducted under a mild condition with Ti(SO 4 ) 2 /NH 4 HF 2 /HNO 3 solution, and the product Ti-MWW precursors have framework titanium alone, the novel method is named as refluxing and implanting titanium method which integrates acid treatment and titanium incorporation into one step and reduces the consumption of time of this process into 1 h. A density functional theory was conducted to explain the formation mechanism of interlayer-expanded structure of Ti-MWW zeolite. Subsequently, Ti-MWW precursors were treated in modified reagent solution to obtain larger pore structure, which increase the conversion of 1-hexene from 20.45 to 62.96%. The catalytic performance of Ti-MWW zeolite in this work are superior to Ti-MWW zeolite synthesized by traditional dry-gel conversion method the conversion of 1-hexene of which was 4.2%. This novel method is a promising approach for the synthesis of high catalytic performance heteroatomic zeolite. Graphical abstract
研究领域:
材料科学
·
化学工程
·
催化
·
无机化学
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DOI
高影响因子
危险品化学品经营许可证（带存储）