Lipids in Health and Disease
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2025
·Vol. 24
·期 1
·1-15
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IF 4.2
An He,Cheng Dong-liang,Xia Xian-ru,Li Xian-dong,Ruan Zhi-hua,Peng Chun-yan
Background Dyslipidemia has been extensively documented as a key driver of cardiovascular pathology. Regulating lipid homeostasis holds promise for treating atherosclerosis (AS). Although the protein phosphatase 2 catalytic subunit beta (PPP2CB) is involved in post-transcriptional gene regulation, its role in AS-associated dyslipidemia is not well understood. Methods The study included both human participants and animal models. The following techniques were employed: cell culture, extraction of exosomes, preparation of pooled hyperlipidemic serum (HS), transfection, western blotting, immunofluorescence staining, quantitative reverse transcription polymerase chain reaction (qRT-PCR), co-immunoprecipitation, low-density lipoprotein cholesterol (LDL-C) uptake assay, biochemical assays, assessment of aortic atherosclerotic lesions, as well as statistical analysis. Results This study identified a marked upregulation of PPP2CB expression in peripheral blood leukocytes of AS patients, artery plaque of ApoE −/− mice given a high-fat diet, and hepatic cells exposed to hyperlipidemic stimuli. Overexpression of PPP2CB in hepatic cells exacerbated lipid accumulation and low-density lipoprotein uptake, whereas silencing PPP2CB mitigated this effect. Immunofluorescence co-localization and co-immunoprecipitation analysis confirmed a direct interaction between PPP2CB and lectin-like oxidized LDL receptor-1 (LOX-1). Notably, PPP2CB manipulation disrupted hyperlipidemia-induced LOX-1 expression. Additionally, PPP2CB-mediated lipid dysregulation was linked to the activation of the LOX-1/ mitogen-activated protein kinase (MAPK)/ extracellular signal-regulated kinase (ERK) signaling cascade. Conclusions These results unveil PPP2CB as a novel lipid regulator in the progression of pathological AS and highlight its involvement in signaling regulation during abnormal lipid metabolism. PPP2CB could be considered a promising candidate for biomarker development and therapeutic intervention in AS.
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ACS Applied Materials & Interfaces
·
2025
·
IF 8.2
Xuecheng Yang,Xiaoyu Zhang,Ge Yu,Yubin Ma,Xin Li,Yiyang Guo,Shuping Wang,Dan Ge,Changying Xue,Kun Jin,Bingbing Sun
Amyloid-β (Aβ) fibrillation is a spontaneous, thermodynamic process governed by nucleation and elongation. While many studies have explored the ability of engineered nanomaterials (ENMs) to modulate Aβ fibrillation, such as inhibitors, promoters, and dual-modulators, the key physicochemical property of ENMs that determines this behavior remains unclear. In this study, we developed a comprehensive library of ENMs with well-controlled physicochemical properties, including surface charges, morphologies, and hydrophilicity, to systematically investigate their effects on Aβ40 fibrillation. We identified hydrophilicity as the primary determinant of ENM-mediated modulation, rather than surface charge or morphology. Thioflavin T (ThT) kinetics assays indicated that hydrophilic ENMs exhibited bidirectional modulation, both promoting and inhibiting fibrillation depending on concentration. This bidirectional effect results from a competition between accelerated nucleation and decelerated elongation. While hydrophobic ENMs exhibited only unidirectional inhibition from the initial nucleation phase, two-dimensional-NMR (2D-NMR) mechanism studies indicated that this difference resulted from specific interactions with Aβ40 residues. Hydrophilic ENMs targeted hydrophilic residues involved in elongation, including Arginine R5, Glycine G9, G25, G33, G37, and G38, Lysine K28, and Alanine A30, while hydrophobic ENMs bound to hydrophobic residues critical for nucleation, such as I31. These findings provide mechanistic insight into NP–peptide interactions and lay a foundation for the rational design of nanomaterials to modulate amyloid fibrillation.
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FREE RADICAL BIOLOGY AND MEDICINE
·
2025
·
IF 8.2
Xiaomeng Ji,Jingquan Dong,Wenting Zhu,Shasha Zhang,Yaru Chen,Xiao Liu,Yan Cao,Panpan Zhao,Zibo Dong
Background Sepsis-associated encephalopathy (SAE) represents one of the most common neurological complications observed in sepsis patients, contributing to both increased mortality and long-term cognitive impairment. Microglial mitochondrial reactive oxygen species (mtROS) overproduction and NLR family pyrin domain-containing 3 (NLRP3) inflammasome activation were key pathological drivers of SAE. Although PIM-1, a serine/threonine kinase, was known to regulate both mtROS generation and NLRP3 signaling, its specific contribution to SAE remained poorly defined. Methods This study established a SAE mouse model using cecal ligation and puncture (CLP) surgery, and screened the differentially expressed gene PIM-1 through immunohistochemistry, GEO database analysis, and etc. An in vitro model was established using Lipopolysaccharide + Adenosine(LPS + ATP) Triphosphate stimulated Mouse Microglia (BV-2), and the regulation mechanism of PIM-1 was analyzed through siRNA interference, RNA-seq, and etc. Potential drug Urolithin B (UB) targeting PIM-1 inhibition was screened through molecular docking, and its inhibitory effect on PIM-1 and therapeutic potential in SAE were evaluated through thermal stability experiments, behavioral experiments, etc. Results PIM-1 was upregulated in SAE, which was associated with brain damage. PIM-1 knockdown suppressed microglial activation and reduced inflammatory cytokines release. Further investigation indicated that PIM-1 modulated mtROS generation and facilitated NLRP3 inflammasome activation. Notably, pharmacological inhibition of PIM-1 by UB alleviated SAE both in vivo and in vitro , resulting in improved neuronal damage and cognitive impairment. Conclusion PIM-1 played a critical role in SAE progression, potentially through its mediation of microglial activation and neuroinflammation via the mtROS/NLRP3 axis. Notably, pharmacological inhibition of PIM-1 with urolithin B significantly alleviated SAE.
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MICROPOROUS AND MESOPOROUS MATERIALS
·
2024
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IF 4.8
Ying Zhang,Qinqin Wang,Mingyuan Zhu,Bin Dai
The prevailing Zn/AC catalysts was plagued by limited lifetime and difficulties in regeneration for acetylene acetoxylation. In order to exploring renewable catalyst for acetylene acetoxylation, Zn/S-1 catalyst was synthesized using Silicalite-1(S-1) as support. The catalytic performance of Zn/S-1 was compared with Zn/AC catalyst using active carbon as support. The CH 3 COOH conversion of Zn/S-1 catalyst only decreased 15 % after running 225 h, much better than the 66 % of Zn/AC after 154 h. TG analysis revealed that the improved stability of Zn/S-1 catalyst was attributed to its better resistance for carbon deposition with the presence of S-1 support. A series of characterizations and DFT results elucidated that the Lewis acid sites of S-1 support and Zn component serve as dual active sites, which enhanced the adsorption of CH 3 COOH and inhibited the carbon deposition. In addition, the deactivated Zn/S-1 catalyst could be regenerated by calcination in air atmosphere due to the thermal stability of S-1, and the regenerated Zn/S-1 catalyst showed similar catalytic activity with the fresh catalyst.
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PHYSICS LETTERS A
·
2024
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IF 2.3
Ting-ting Yan,Ran Jiang,Dong-yang Xi,Long Ma,Dan-dan Zhang,Yi-fei Xu
This study investigated the structural stability of 1-methylhydantoin (1-MH, C 4 H 6 N 2 O 2 ) Form-I at room temperature using Raman spectroscopy and a diamond anvil cell (DAC) for high-pressure experiments. Two phase transitions were identified at pressures of 0.6–1.7 GPa and 3.4–6.7 GPa. After complete release of pressure, the spectrum aligned with the Raman spectrum at ambient pressure, indicating reversibility of the phase transition. Analysis of Hirshfeld surface energy and fingerprints was conducted to assess changes in intermolecular interactions, revealing that the phase transitions are associated with rearrangements in the hydrogen-bonded network.
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BIOTECHNOLOGY LETTERS
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2019
·Vol. 41
·期 6
·789-799
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IF 2.154
Wang Xiuwen,Cheng Yang,Jin Qingzhe,Wei Wei,Wang Xingguo
Objectives To investigate the lipase-catalyzed synthesis of high purity sn -1/3 and sn -2 monoacylglycerols (1/3-MAG and 2-MAG) of different fatty acids (FAs). Results The 1/3-MAGs of three FAs (16:0, 17:0, 16:1) were synthesized using lipase-catalyzed esterification of glycerol with FAs. The 2-MAGs were obtained from the ethanolysis of synthetic triacylglycerols using sn -1,3 regiospecific lipase. The effects of lipase types, substrate ratio, temperature, reaction time and lipase load on the MAG conversion were studied. Under the optimal conditions, high purities (96.74%, 95.44%, 92.96%) with acceptable isolated yields (51.00%, 54.28%, 46.00%) were obtained for 1/3-16:0-MAG, 1/3-17:0-MAG, and 1/3-16:1-MAG, respectively. For 2-16:0-MAG, 2-17:0-MAG, and 2-16:1-MAG, the purities were 92.64, 95.04, and 96.48%, with isolated yields of 50.64, 52.16, and 26.12%, respectively. The molecular structures of the synthetic compounds were confirmed by 1 H NMR, and MS and the melting points were characterized by DSC. Conclusions High purity MAG isomers can be synthesized via lipase-catalyzed reactions to be building blocks for production of functional lipids, the melting points of which are largely governed by the hydrophobic interactions among the alkanyl chains.
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JOURNAL OF SURGICAL RESEARCH
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2021
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IF 2.192
Shaohang Cheng,Runxiao Lv,Jing Xu,Abdul Razaq Hirman,Lili Du
ABSTRACT Background Stem cell-based regenerative therapy is a novel approach to severe damaged skin. Perinatal tissues such as placenta are considered as promising alternatives. The present study aimed to investigate the effect of insulin-like growth factor-1 (IGF-1)-expressing placenta-derived mesenchymal stem cells (hPMSCs) on healing of burn wounds. Materials and methods hPMSCs were isolated from human placenta, and IGF-1 was transducted into hPMSCs via lentivirus . Flow cytometry and MTT assay were performed to assess cell apoptosis and viability, respectively. Immunostaining of CK19 and ki67 was for evaluating epithelial differentiation ability and cell proliferation . For in vivo studies, we established a mouse model of scalding and performed local administration of IGF-1-expressing hPMSCs via subcutaneous injection . Wound histology was analyzed with H&E staining. The expression of fibrogenic cytokines was detected by western blot. The production of pro-inflammatory factors was measured by ELISA. Results Overexpression of IGF-1 promoted cell proliferation and epithelial differentiation of hPMSCs in vitro and in vivo . Mice with burn injury displayed increased wound contraction and healing rates following treatment with IGF-1-expressing hPMSCs. There was less inflammatory infiltration and reduced collagen disposition in the presence of IGF-1 at the wound site. Administration of IGF-1-expressing hPMSCs suppressed inflammation by decreasing the levels of pro-inflammatory cytokines including tumor necrosis factor-α, interleukin-1β, and interleukin-6. Besides, IGF-1 increased VEGF expression, and decreased TGF-β1, collagen I and collagen III expressions in vivo . Conclusions IGF-1-expressing PMSCs promotes cell proliferation and epithelial differentiation, inhibits inflammation and collagen deposition, and thus contributes to wound healing.
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BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
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2018
·
IF 3.679
Yu Zhang,Yudan Zhao,Zhuoyi Wang,Hao Gong,Liang Ma,Dongsheng Sun,Chen Yang,Yang Li,Biao Cheng,Robert B. Petersen,Fengchao Jiang,Gongping Liu,Kun Huang
Protein misfolding and aggregation are associated with amyloidosis. The toxic aggregation of amyloid-β 1–42 (Aβ42) may disrupt cell membranes and lead to cell death and is thus regarded as a contributing factor in Alzheimer's disease (AD). 1,4-naphthoquinone (NQ) has been shown to exhibit strong anti-aggregation effects on amyloidogenic proteins such as insulin and α-synuclein; however, its high toxicity and poor solubility limit its clinical application. Menadione sodium bisulfite (MSB, also known as vitamin K3), is used clinically in China to treat hemorrhagic diseases caused by vitamin K deficiency and globally as a vitamin K supplement. We hypothesized that MSB could inhibit amyloid formation since its backbone structure is similar to NQ. To test our hypothesis, we first investigated the effects of MSB on Aβ42 amyloid formation in vitro . We found that MSB inhibited Aβ42 amyloid formation in a dose dependent manner, delayed the secondary structural conversion of Aβ42 from random coil to ordered β-sheet, and attenuated the ability of Aβ42 aggregates to disrupt membranes; moreover, the quinone backbone rather than lipophilicity is esstial for the inhibitory effects of MSB. Next, in cells expressing a pathogenic APP mutation (Osaka mutation) that results in the formation of intraneuronal Aβ oligomers, MSB inhibited the intracellular aggregation of Aβ. Moreover, MSB treatment significantly extended the life span of Caenorhabditis elegans CL2120, a strain that expresses human Aβ42. Together, these results suggest that MSB and its derivatives may be further explored as potential therapeutic agents for the prevention or treatment of AD.
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JOURNAL OF ELECTRONIC MATERIALS
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2025
·Vol. 54
·期 10
·8561-8569
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IF 2.5
Dong Tianhao,Cui Yongpeng,Wei Lianghuan,Zhu Shengjie,Si Jianxiao
CaM(M = Cu, Ag)Sb Zintl-phase compounds have ignited tremendous research activities due to their promising thermoelectric properties. In this work, a series of CaCu 1− x Ag x Sb (x = 0, 0.2, 0.4, 0.6, 0.7, 0.8, 0.9, 1) samples have been synthesized and investigated. The continuous structure transition from the hexagonal CaCuSb to the orthorhombic CaAgSb is characterized as the composition regulation on Cu/Ag ratios. Lattice bonding hardens and the electrical band structure changes as a result of this transition. The lattice thermal conductivity of CaCu 0.2 Ag 0.8 Sb, which benefitted from the structure transition, showed a minimum value of 1.05 W m −1 K −1 at 323 K. At the same time, the Seebeck coefficient was improved as a result of the rise in effective mass. The findings show that the CaMSb compounds have flexible structural tunability for thermoelectric applications if the hole concentration can be further optimized. Graphical
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Journal of the Taiwan Institute of Chemical Engineers
·
2025
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IF 6.3
Yunxiang Du,Zhuoyue Lan,Wanting Yang,Xiong Li,Yunchuan Li,Hang Li,Zhiyu Pu,Letian Hu
Background Conventional chalcopyrite depressants face environmental and selectivity challenges in copper-molybdenum separation. This study introduces 1-thioglycerol (1-TG), an eco-friendly organic depressant, demonstrating exceptional selectivity for chalcopyrite. Methods The depression performance of 1-TG was evaluated through flotation experiments. Its selective adsorption mechanism was elucidated using surface characterization techniques, including contact angle, SEM-EDS, LEIS, FTIR, XPS and molecular dynamics simulations. Significant findings 1-TG achieved efficient separation of molybdenite from chalcopyrite. For the synthetic mixed ore at pH 5 with 25 mg/L 1-TG, recoveries of Cu and Mo were 6.01% and 89.53%. Mechanistic studies demonstrated that 1-TG selectively chemisorbs on chalcopyrite surfaces through coordinating with metal sites, effectively masking adsorption sites and reducing surface hydrophobicity. The -SH groups in 1-TG promoted selective adsorption, as confirmed by surface analyses. This non-toxic depressant functions effectively at low dosages, offering a sustainable alternative to conventional toxic inhibitors like cyanides. The findings provide fundamental insights into green reagent design and advance eco-friendly strategies for sulfide mineral separation, addressing critical environmental and efficiency challenges in copper-molybdenum processing.
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FUEL
·
2025
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IF 7.5
Xuemeng Yang,Jiadong Wang,Subing Fan,Qingxiang Ma,Xinhua Gao,Jianli Zhang,Tian-Sheng Zhao
The derivatives of primary Fischer-Tropsch synthesis (FTS) products are indispensable to the sustainable FTS run. For the one-pot conversion of FTS-based 1-octene to nonanol, nitrogen-doped cobalt oxides were obtained through hydrothermal synthesis followed by ammonia atmosphere thermal treatment (AATT) at 325 °C with varying treatment time. The AATT significantly affected the phase structure and the surface element valence states of the synthetic samples. The resulting (Co 3 O 4 ) x N showed high catalytic activity toward the reaction of 1-octene with CO + H 2 to nonanol through a successive hydroformylation-hydrogenation process, with conversion of 98 % and selectivity of close to 80 %. The crucial role of the CoO phase and the enhanced adsorption of the reactant molecules by the induced oxygen vacancy (O v ) were discussed based on multiple physicochemical properties characterization and activity evaluation.
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HUMAN GENE THERAPY
·
2025
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IF 4
Ting Liu,Zhuo Li,Yun Sun,Dan Chen
Myocardial fibrosis represents a maladaptive response to some pathological stimulus affecting the heart's functions, predisposing to arrhythmia and ultimately heart failure (HF). Stathmin 1 (Stmn1) is a core protein in regulating the formation of the mitotic spindle. Although the dysregulation of Stmn1 has been confirmed to be related to the occurrence of kidney or liver fibrosis, the role of Stmn1 in HF remains obscure. In this study, bioinformatic analysis (GSE150736) of myocardial tissues from HF patients suggested that Stmn1 was significantly upregulated compared with healthy controls. The consistent results were also observed in the heart tissues of the rat model of HF. Furthermore, we demonstrated that Adenovirus-mediated overexpression of Stmn1 in the peri-infarct border zone area significantly improved cardiac fibrosis and collagen deposition, as evidenced by the decreased expression of transforming growth factor-beta1 (TGF-β1), collagen IV, and alpha-smooth muscle actin in heart tissues. In vitro, overexpression of Stmn1 reduced the production and deposition of collagen in cardiac fibroblasts (CFs) induced by TGF-β1, and thus inhibited the activation of CFs into myofibroblasts. Mechanistically, upregulation of Stmn1 significantly suppressed the phosphorylation of p38 both in vivo and in vitro. Moreover, we demonstrated that Stmn1 was transcriptionally regulated by the cohesin and CCCTC-binding factor (Ctcf) and functionally mediated the cardioprotective effects of Ctcf. Collectively, this work established Stmn1 as a promising therapeutic target for myocardial fibrosis in HF.
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