INDUSTRIAL CROPS AND PRODUCTS
·
2025
·
IF 6.2
Qishan Xie,Jiawei Yang,Jianwei Wang,Lufan Yang,Bingye Yang,Han Yan,Aiguo Wang,Xiang Zhang,Ying Cui,Shengfeng Wang,Xuan Chen,Xinyi Zhang,Penghui Lyu,Yanling Zhang
Early aging is critical for colour formation in tobacco leaves, yet the underlying metabolic mechanisms remain elusive. This study integrated image processing with untargeted and targeted LC-MS to construct a metabolic network characterising colour evolution in flue-cured tobacco (cv. Cuibi-1, CB-1 ) during early aging (0–120 days). Results indicated that leaf colour significantly brightened during the first 30 days, followed by deepening and reddening. Specifically, L* and b* values showed an initial increase followed by a decrease, whereas the a* value exhibited a sustained upward trend. The constructed metabolic network was anchored in saccharide metabolism, connecting downstream phenolic, flavonoid, sphingolipid, and terpenoid pathways. Sixteen differentially accumulated metabolites (DAMs) were identified across categories including alcohols, flavonoids, lignans, nucleotides, phenolic acids, saccharides, and xanthophylls. These DAMs exhibited distinct change patterns and significant correlations with colour parameters (L* and a*, r ranging from −0.88 to −0.58 and 0.56–0.74, respectively; P < 0.05). For the first time, this study elucidated the metabolic mechanisms governing colour changes in CB-1 tobacco leaves during early aging for the first time, providing novel insights for assessing aging progression and maintaining high-value raw material quality.
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FREE RADICAL BIOLOGY AND MEDICINE
·
2019
·
IF 5.657
Zhen Wang,Shi-peng Wang,Qun Shao,Pei-feng Li,Yue Sun,Lan-zi Luo,Xiu-qing Yan,Zi-yi Fan,Juan Hu,Jing Zhao,Peng-zhou Hang,Zhi-min Du
Brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TrkB) pathway is associated with ischemic heart diseases (IHD). 7,8-dihydroxyflavone (7,8-DHF), BDNF mimetic, is a potent agonist of TrkB. We aimed to investigate the effects and the underlying mechanisms of 7,8-DHF on cardiac ischemia . Myocardial ischemic mouse model was induced by ligation of left anterior descending coronary artery . 7,8-DHF (5 mg/kg) was administered intraperitoneally two days after ischemia for four weeks. Echocardiography , HE staining and transmission electron microscope were used to examine the function, histology and ultrastructure of the heart. H9c2 cells were treated with hydrogen peroxide (H 2 O 2 ), 7,8-DHF or TrkB inhibitor ANA-12. The effects of 7,8-DHF on cell viability , mitochondrial membrane potential (MMP) and mitochondrial superoxide generation were examined. Furthermore, mitochondrial fission and protein expression of mitochondrial dynamics (Mfn2 [mitofusin 2], OPA1 [optic atrophy 1], Drp1 [dynamin-related protein 1] and Fis-1 [fission 1]) was detected by mitotracker green staining and western blot , respectively. 7,8-DHF attenuated cardiac dysfunction and cardiomyocyte abnormality of myocardial ischemic mice. Moreover, 7,8-DHF increased cell viability and reduced cell death accompanied by improving MMP, inhibiting mitochondrial superoxide and preventing excessive mitochondrial fission of H 2 O 2 -treated H9c2 cells. The cytoprotective effects of 7,8-DHF were antagonized by ANA-12. Mechanistically, 7,8-DHF repressed OMA1-dependent conversion of L-OPA1 into S-OPA1, which was abolished by Akt inhibitor . In conclusion, 7,8-DHF protects against cardiac ischemic injury by inhibiting the proteolytic cleavage of OPA1. These findings provide a novel pharmacological effect of 7,8-DHF on mitochondrial dynamics and a new potential target for IHD.
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PubMed
高影响因子
EXPERIMENTAL ANIMALS
·
2021
·
IF 2.319
Lili TAN,Limin LIU,Jian YAO,Chenghao PIAO
Myocardial ischemia-reperfusion (I/R) injury is a common complication following reperfusion therapy that involves a series of immune or apoptotic reactions. Studies have revealed the potential roles of miRNAs in I/R injury. Herein, we established a myocardial I/R model in rats and a hypoxia/reoxygenation (H/R) model in H9c2 cells and investigated the effect of miR-145-5p on myocardial I/R injury. After 3 h or 24 h of reperfusion, LVESP, EF, and FS were obviously decreased, and LVEDP was increased. Meanwhile, I/R induced an increase in myocardial infarction area. Moreover, a decrease in miR-145-5p and increase in NOH-1 were observed following I/R injury. With this in mind, we performed a luciferase reporter assay and demonstrated that miR-145-5p directly bound to NOH-1 3’ UTR. Furthermore, miR-145-5p mimics decreased the levels of TNF-α, IL-1β, and IL-6 via OGD/R stimulation. Upregulation of miR-145-5p increased cell viability and reduced apoptosis accompanied by downregulation of Bax, cleaved caspase-3, cleaved PARP and upregulation of Bcl2. In addition, miR-145-5p overexpression increased SOD activity and reduced ROS and MDA content under OGD/R stress. Notably, NOH-1 could significantly abrogate the above effects, suggesting that it is involved in miR-145-5p-regulated I/R injury. In summary, our findings indicated that miR-145-5p/NOH-1 has a protective effect on myocardial I/R injury by inhibiting the inflammatory response and apoptosis.
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PubMed
高影响因子
Molecular Medicine Reports
·
2022
·Vol. 26
·期 6
·1-11
·
IF 3.423
Wenjuan Guo,Xiaodi Wang,Fang Liu,Shuo Chen,Shuai Wang,Qingrui Zhang,Lan Yuan,Shiyu Du
Ulcerative colitis (UC) is a significant burden on human health, and the elucidation of the mechanism by which it develops has potential for the prevention and treatment of UC. It has been reported that acteoside (ACT) exhibits strong anti‑inflammatory activity. In the present study, it was hypothesized that ACT may exert a protective effect against UC. The effects of ACT on inflammation, oxidative stress and apoptosis were evaluated using dextran sulphate sodium (DSS)‑treated mice and DSS‑treated human colorectal adenocarcinoma Caco‑2 cells, which have an epithelial morphology. The results demonstrated that the ACT‑treated mice with DSS‑induced UC exhibited significantly reduced colon inflammation, as demonstrated by a reversal in body weight loss, colon shortening, disease activity index score, inflammation, oxidative stress and colonic barrier dysfunction. Further in vivo experiments demonstrated that ACT inhibited DSS‑induced apoptosis in colon tissues, as demonstrated by the results of the TUNEL assay and the altered protein expression levels of Bax, cleaved caspase‑3 and Bcl‑2. Furthermore, DSS significantly stimulated the protein expression levels of high mobility group box 1 protein (HMGB1), which serves a central role in the initiation and progression of UC, an effect which was markedly inhibited by ACT. Finally, DSS significantly decreased the protein expression levels of heme oxygenase‑1 (HO‑1) in colon tissues and the effect of ACT on GSH, apoptotic proteins and HMGB1 was markedly attenuated in the presence of the HO‑1 inhibitor tin protoporphyrin. In conclusion, ACT ameliorated colon inflammation through HMGB1 inhibition in a HO‑1‑dependent manner.
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PubMed
高影响因子
ORGANIC & BIOMOLECULAR CHEMISTRY
·
2015
·Vol. 13
·期 26
·7257-7264
·
IF 3.562
Juan Xiao,Chunmei Jin,Zhixue Liu,Shujing Guo,Xiaochuan Zhang,Xin Zhou,Xue Wu
1-Benzyl-3-(substituted aryl)-5-methylfuro[3,2-c]pyrazole (YC-1) is a well-known synthetic compound with various satisfactory pharmacological activities, such as the activation of soluble guanylate cyclase (sGC) and the inhibition of hypoxia-induced factor-1α (HIF-1α). Recently, YC-1 has been demonstrated to have a potent activity on anti-fibrotic activity. However, the mechanism underlying its anti-fibrotic activity is still largely unknown. To this end, we presented here the design and synthesis of YC-1 and its novel derivatives, as well as the evaluation of their anti-fibrotic effects on activated human hepatic stellate cells (HSCs) LX-2. Moreover, the possible underlying mechanism of anti-fibrotic activity was also investigated for the first time by means of a CCK-8 assay, cell apoptosis analysis, and western blot analysis. Our study revealed that YC-1 and its derivatives suppressed activated LX-2 cell viability and induced cell apoptosis in a time- and dose-dependent manner. Western blot data demonstrated that these derivatives not only decreased the expression of α-smooth muscle actin (α-SMA), but also increased the expression of caspase-3, resulting in cell apoptosis. These findings strongly indicated that YC-1 and its derivatives, especially AC, could significantly inhibit LX-2 cell activation and induce LX-2 cell apoptosis by inhibiting α-SMA protein expression and promoting caspase-3 expression, respectively. In summary, our findings suggested that YC-1 derivatives might be potential agents for hepatic fibrosis therapy.
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Frontiers in Pharmacology
·
2020
·
IF 4.225
Huang Mei-Zhou,Zhang Zhen-Dong,Yang Ya-Jun,Liu Xi-Wang,Qin Zhe,Li Jian-Yong
Aspirin eugenol ester (AEE) is a new potential pharmaceutical compound possessing anti-inflammatory, anti-cardiovascular disease, and antioxidative stress activity. The pharmacological activities of AEE are partly dependent on its regulation of cell apoptosis. However, it is still unclear how AEE inhibits cell apoptosis on the basis of its antioxidative stress effect. This study aimed to reveal the vascular antioxidative mechanism of AEE in response to H2O2-induced oxidative stress in HUVECs and paraquat-induced oxidative stress in rats. In the different intervention groups of HUVECs and rats, the expression of ASK1, ERK1/2, SAPK/JNK, and p38 and the phosphorylation levels of ERK1/2, SAPK/JNK, and p38 were measured. The effects of ASK1 and ERK1/2 on the anti-apoptotic activity of AEE in the oxidative stress model were probed using the corresponding inhibitors ASK1 and ERK1/2. The results showed that in the HUVECs, 200 μM H2O2 treatment significantly increased the phosphorylation of SAPK/JNK and the level of ASK1 but decreased the phosphorylation of ERK1/2, while in the HUVECs pretreated with AEE, the H2O2-induced changes were significantly ameliorated. The findings were observed in vitro and in vivo. Moreover, inhibition of ASK1 and ERK1/2 showed that ASK1 plays a vital role in the protective effect of AEE on H2O2-induced apoptosis. All findings suggested that AEE protects the vascular endothelium from oxidative injury by mediating the ASK1 pathway.
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高影响因子
Experimental and Therapeutic Medicine
·
2017
·Vol. 14
·期 4
·2937-2942
·
IF 1.261
Lixiao Pan,Fengyun Yang,Caixia Lu,Changxin Jia,Qing Wang,Kexue Zeng
The purpose of this investigation was to determine the effects of sevoflurane on rats with ischemic brain injury and to determine the potential role of the TREK-1 channel in this process. Normal rats were randomly divided into three groups: Sham operation, sevoflurane anesthesia or chloral hydrate anesthesia group, an additional group of TREK-1 knockout rats were also studied. Semi-quantitative PCR and western blot analysis confirmed the lack of TREK-1 expression in the brain of TREK-1 knockout rats. The thread-tie method was used to establish middle cerebral artery occlusion (MCAO) model to induce cerebral ischemic brain injury. All rates were treated for 4 days prior to ischemia (for 2 h) followed by a 24 h reperfusion period. Physiological indexes of rats in each group both prior to and after surgery showed no statistical difference (P>0.05). Neurological function was scored both before (no statistical difference) and after surgery where it was found to be significantly better (lower score) in the sevoflurane anesthesia group than in chloral hydrate anesthesia and TREK-1 knockout groups (P<0.01). The area of cerebral infarction was measured by triphenyl tetrazolium chloride staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay to detect the apoptosis of brain cells. TTC staining showed different degrees of cerebral infarction in the various groups; the area of cerebral infarction in sevoflurane anesthesia group was significantly lower than that in chloral hydrate anesthesia and TREK-1 knockout groups (P<0.01). TUNEL assay showed that the number of TUNEL-positive cells was significantly lower in sevoflurane anesthesia group than in TREK-1 knockout and chloral hydrate anesthesia groups (P<0.01). In conclusion, results from this investigation showed that sevoflurane can protect the nerve function of rats with cerebral ischemic brain injury possibly by affecting the expression of proteins involved in the TREK-1 signaling pathway.
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CRYSTAL GROWTH & DESIGN
·
2025
·
IF 3.4
Hongyu Wang,Fumin Wang,Kaiwei Wang,Xubin Zhang,Changhao Bing,Xiaolu Fan,Tongxue Zhang,Syed Mujtaba ul Hassan
Developing an approach for the efficient synthesis of TS-1 zeolites with desirable morphologies and tunable coordination environments for Ti active sites is a pivotal challenge in the design of high-performance catalysts and zeolite crystal engineering. Herein, we report a cost-effective and efficient additive, guanidinoacetic acid (GAA), and conduct a systematic study on the synthesis of plate-like TS-1 zeolites using GAA as an additive. Introducing GAA during hydrothermal synthesis not only modulates the morphology of TS-1 crystals but also permits GAA to adequately chemically interact with titanium precursors to form hexa-coordinated Ti species. TS-1 zeolites with a controllable b-axis thickness in the range of 80–110 nm, and abundant framework Ti and hexa-coordinated Ti species are successfully achieved by optimizing the synthetic parameters. Through SEM, FT-IR, XPS, TEM, and XRD analysis, the mechanism of GAA altering crystal growth is mainly to inhibit the growth of the (010) plane. A b-axis-oriented TS-1 zeolite enriched with hexa-coordinated Ti species displays better catalytic performance in the 1-hexene epoxidation reaction than the conventional TS-1 zeolite containing only framework Ti species (35 vs 24%). This can be ascribed to the more active hexa-coordinated Ti species and shorter diffusion distance. This synthetic strategy provides a way to change the zeolite morphology and tune the number and distribution of Ti species in TS-1 zeolites.
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Journal of Energy Storage
·
2025
·
IF 9.8
Zhongkai Zheng,Zhubin Yao,Xunan Xie,Guoqing Zhang,Xinxi Li,Xiaoqing Yang
Organic phase change materials (PCMs) are highly flammable, presenting substantial safety risks in battery thermal management (BTM) applications. In this study, based on the nucleophilic addition reaction, a novel flame-retarded PCM is synthesized via a reaction between 3-isocyanatopropyltrimethoxysilane and 1-hexadecanol (HD). The latent heat of the obtained silyl-modified HD (SiHD) is up to 115.1 J·g −1 , and its peak phase transition temperature region is approximately 30–45 °C. Moreover, the silyl groups endow the SiHD with significantly enhanced flame-retarded properties. After incorporating expanded graphite (EG) as both supporting and thermal conductive frameworks, the SiHD/EG composite PCM possesses a thermal conductivity of 1.85 W·m −1 ·K −1 and an excellent anti-leakage performance. During the BTM tests, the maximum temperature difference of the battery module with SiHD/EG is reduced by approximately 23 %, and the maximum temperature is decreased by about 3 °C in comparison to those with traditional flame-retarded PCMs. Additionally, in extreme overheating conditions, the resultant SiHD/EG can effectively delay thermal propagation, thereby postponing the occurrence of thermal runaway.
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高影响因子
ARCHIV DER PHARMAZIE
·
2025
·Vol. 358
·期 12
·e70155
·
IF 3.6
Xinli Wang,Xia Wang,Xuejing Su,Zexin Wang,Yongxiao Sun,Lijun Xie,Xiaoyan Lin
The development of theranostic probes with tumor-specific targeting and high therapeutic efficacy remains a pivotal challenge in precision oncology. Herein, we have successfully developed a new cyclooxygenase-2 (COX-2)-targeted probe compound 2 derived from Rofecoxib. Compound 2 facilitated tumor visualization by a sixfold fluorescence enhancement upon COX-2 binding, while it exhibited minimal background fluorescence under physiological conditions. Moreover, compound 2 monotherapy achieved 53% tumor regression ( p < 0.01). When combined with a programmed cell death protein 1 (PD-1) inhibitor (RMP1-14), concurrent blockade of the COX-2/prostaglandin E2 (PGE2) and PD-1/programmed death-ligand 1 (PD-L1) axes achieved 95% tumor regression ( p < 0.001). Compound 2 involves activating fluorescence by targeting tumor markers COX-2 as well as enhancing therapeutic efficacy. We believe this approach could provide insights for advancing cancer diagnosis and treatment technologies.
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JOURNAL OF INDUSTRIAL AND ENGINEERING CHEMISTRY
·
2025
·
IF 6
Hengyang Liu,Wanyuan Li,Yong Xu,Enzhu Hu,Guangchao Qin,Kunhong Hu
A 1 T/2H-MoS 2 (THM) lubricant additive was synthesized via a solvothermal method to improve the lubrication of poly-alpha-olefin (PAO) and reduce the negative influence of diesel carbon soot (CS). The THM was then modified with Cu to further enhance the wear resistance. The average interlayer spacing of MoS 2 in THM and the Cu-modified THM (CTHM) was 0.99 nm, significantly larger than the 0.63 nm of 2H-MoS 2 nanoparticles. In PAO, CTHM demonstrated a 45 % improvement in friction reduction and a 77 % increase in wear resistance compared to 2H-MoS 2 . While the friction reduction of CTHM was similar to that of THM, CTHM exhibited 36 % superior wear resistance. In CS-contaminated PAO, CTHM outperformed 2H-MoS 2 with a 37 % reduction in friction and a 29 % enhancement in wear resistance. The Cu modification reduced the oxidation of CTHM and the conversion of 1 T-MoS 2 to 2H-MoS 2 in the tribofilm, contributing to improved wear resistance. The CS contamination negatively influenced the lubrication by accelerating MoS 2 oxidation, catalyzing the transition from 1 T-MoS 2 to 2H-MoS 2 , and inhibiting Cu incorporation into the tribofilm. Nonetheless, the effect of CS on CTHM and THM was less severe than on 2H-MoS 2 . This work provides an alternative method to alleviated the antagonism between MoS 2 and CS.
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JOURNAL OF THE EUROPEAN CERAMIC SOCIETY
·
2023
·
IF 5.7
Zhihua Tian,Bingzhen Yan,Fushuo Wu,Jingwen Tang,Xueqin Xu,Jian Liu,Peigen Zhang,ZhengMing Sun
Herein, high-purity Ti 2 (In x Al 1- x )C ( x = 0–1) solid solutions were successfully synthesized. The crystal structure and actual composition of solid solutions were confirmed using XRD, SEM, and TEM analyses, and their formation mechanism was revealed by thermal analysis. On the In-rich side ( x ≥ 0.5), primary Ti 2 InC first formed and then acted as a crystalline seed for the subsequent solid solutions, resulting in a cluster-like morphology. The lattice constants of Ti 2 (In x Al 1- x )C were found to well follow Vegard’s law. The examined properties of Ti 2 (In x Al 1- x )C also greatly depended on their A-site compositions. Ti 2 AlC exhibited the highest hardness and elastic moduli, while the best corrosion resistance was achieved at Ti 2 InC, and all Ti 2 (In x Al 1- x )C displayed active dissolution in 0.5 M HCl solution. Thus, adjusting the In/Al ratio at A-site can yield a desired set of performances, which provides a good example for regulating the performance of MAX phases via A-site solid solution strategy.
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