PREPARATIVE BIOCHEMISTRY & BIOTECHNOLOGY
·
2025
·
IF 1.9
Shuhan Yang,Shouqi Zhao,Yingying Ning,Dan Zhao
Previous studies have shown that co-culture methods can enhance exopolysaccharide production, no studies have reported this enhancement in co-cultures between Weissella confusa and Candida shehatae. This study developed an efficient co-culture system combining W. confusa XG-3 and C. shehatae (1:1 ratio), and employed response surface methodology to optimize both exopolysaccharide yield and properties. The initial co-culture produced 56.82 ± 0.12 g/L exopolysaccharide, a 1.63-fold increase over single culture. Optimization (sucrose: 105.97 g/L; yeast extract: 5.81 g/L; peptone: 6.24 g/L) further increased the yield to 115.66 g/L, a 2.04-fold improvement. The co-cultured exopolysaccharide had high water solubility (60.45 ± 0.70%) and water holding capacity (614.74 ± 9.26%). The co-cultured EPS showed significant antioxidant activity. At 5 mg/mL, the scavenging rates of ABTS, DPPH, hydroxyl, superoxide, H2O2 and total reducing power reached the highest 52.22 ± 0.47%, 50.79 ± 2.86%, 55.80 ± 2.56%, 36.05 ± 2.07%, 66.85 ± 0.30%, and 0.39 ± 0.01. It also had a superior effect on the proliferation of several probiotics compared with commercial prebiotics and exhibited high thermostability with a degradation threshold at 292.5 °C. These results demonstrate a novel, scalable strategy for producing multifunctional EPS with broad applications in the food industry.
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Toxics
·
2025
·Vol. 13
·期 4
·274
·
IF 4.1
Jie Gu,Huilin Jin,Jun Hu,Jian Wang,Daqiang Yin
Endocrine-disrupting chemicals (EDCs) are exogenous substances discharged into the environment through human activities. 3-Isopropylphenol, a typical alkylphenol-based EDC, has been extensively studied due to its broad application and potential ecological impacts. However, the mechanism of its neurotoxicity remains unclear. In this study, the neurotoxic effects of 3-isopropylphenol were examined using the zebrafish model. We predicted its potential toxic mechanisms and action targets using network toxicology and molecular docking and verified them via RT-qPCR. Results showed that 3-isopropylphenol exposure inhibits the cAMP/PKA signaling pathway in zebrafish larvae, promoting apoptosis, impairing neural development, and suppressing locomotor behavior. These findings enhance our understanding of the toxic effects and mechanisms of 3-isopropylphenol on zebrafish larval neural development and aid in evaluating its potential ecological hazards.
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DALTON TRANSACTIONS
·
2024
·
IF 3.5
Jiayang Huang,Yao Su,Zhangjie Qian,Miaoer Wu,Yunchang Xie,Chao Zeng
The photocatalytic conversion of CO2 and H2O into useful chemicals or fuels over semiconductor photocatalysts is regarded as a promise technology to settle the problems of global warming and energy exhaustion. Whereas, the inefficient photo-absorption and slow charge dynamics limit the CO2 photoreduction efficiency. Here, a ternary heterojunction photocatalyst Cu2Cl(OH)3/In/In2O3 (Cu H IO) with intimate interface is obtained via hydrogen chemical reduction approach followed by hydrolysis reaction, where In species can be produced on the surface of In2O3 from the hydrogen chemical reaction with the calcining temperature over 500℃. The Cu H IO exhibits enhanced photocatalytic activity of CO2 conversion to the pristine In2O3, In2O3 with In species (H IO), and Cu2Cl(OH)3/In2O3 (Cu IO). On the absence of sacrificial agent or cocatalyst, the yield rate of CO and CH¬4 over Cu H IO are 4.36 and 1.09 μmol·g-1·h-1, which is 8.38-fold and 18-fold that of pristine In2O3 (0.52 and 0.06 μmol·g-1·h-1), respectively. The photocatalytic performance enhancement of Cu H IO results from the construction of the ternary heterojunction, which synchronous improve the photo-response and charge separation of In2O3. Moreover, the possible CO2 reduction pathway over Cu H IO has also been investigated and proposed. This work provides an important strategy for developing high-efficiency heterojunction photocatalyst system for solar fuel generation.
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MUSCLE & NERVE
·
2025
·Vol. 71
·期 3
·474-486
·
IF 3.1
Zhuajin Bi,Qing Zhang,Huajie Gao,Huizhen Ge,Jiayang Zhan,Mengge Yang,Bitao Bu
Introduction/Aims Tofacitinib, a first-generation Janus kinase (JAK) 1/3 inhibitor, is commonly used for treating ulcerative colitis and rheumatoid arthritis. However, its role in myasthenia gravis (MG) remains unclear. This study aimed to evaluate the immunomodulatory effects of tofacitinib on experimental autoimmune myasthenia gravis (EAMG) and peripheral blood mononuclear cells (PBMCs) from patients with MG. Methods Flow cytometry, enzyme-linked immunosorbent assay (ELISA), quantitative reverse transcription polymerase chain reaction (qRT-PCR), and Western blot were used to evaluate the effects of tofacitinib on T helper (Th) cell profiles, humoral immune responses, and the JAK-signal transducer and activator of transcription (STAT) pathway proteins. Results In vivo, tofacitinib significantly ameliorated EAMG severity in rats, reducing the proportions of Th1, Th17 and memory B cells, and anti-acetylcholine receptor (AChR) antibodies levels, while increasing the proportions of regulatory T (Treg) cells. In vitro, tofacitinib administration resulted in a significant decrease in the proportions of Th1 and IgG-secreting B cell, and a significant upregulation of Treg cells in mononuclear cells (MNCs) from EAMG rats, which was consistent with findings in PBMCs from MG patients. Further analysis revealed that tofacitinib inhibited CD4 + T cell differentiation into Th1 by decreasing phosphorylated STAT1 levels, while promoting Treg differentiation via increased phosphorylated STAT5 levels in MNCs from EAMG rats. Discussion Tofacitinib modulates Th cell profiles and humoral immune responses by targeting the JAK–STAT pathway, suggesting its potential as a therapeutic candidate for MG. Further clinical studies are warranted to evaluate the efficacy and safety of tofacitinib in MG patients.
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Chinese Journal of Integrative Medicine
·
2021
·Vol. 28
·期 11
·992-999
·
IF 1.978
Zheng Yang,Wang Lei,Wang Jia-hui,Liu Lu-lu,Zhao Tie-jian
Objective To investigate the effect of curcumol on NOD-like receptor thermoprotein domain 3 (NLRP3) inflammasomes, and analyze the mechanism underlying curcumol against liver fibrosis. Methods Thirty Kunming mice were divided into a control group, a model group and a curcumol group according to a random number table, 10 mice in each group. Mice were intraperitoneally injected with 40% carbon tetrachloride (CCl 4 :peanut oil, 2:3 preparation) at 5 mL/kg for 6 weeks, twice a week, for developing a liver fibrosis model. The mice in the control group were given the same amount of peanut oil twice a week for 6 weeks. The mice in the curcumol group were given curcumol (30 mL/kg) intragastrically, and the mice in the model and control groups were given the same amount of normal saline once a day for 6 weeks. Changes in liver structure were observed by hematoxylin and eosin (HE) and Masson staining. Liver function, liver fiber indices, and the expression of interleukin (IL)-10 and tumor necrosis factor-α (TNF-α) levels were determined by automatic biochemical analyzer and enzyme linked immunosorbent assay kit. Immunoblotting and reverse transcription-quantitative PCR (RT-qPCR) were performed to detect the expression of NLRP3 inflammasome-related molecules, TGF-β and collagen. Results HE and Masson staining results showed that the hepatocytes of the model group were arranged irregularly with pseudo-lobular structure and a large amount of collagen deposition. The mice in the curcumol group had a significant decrease in liver function and liver fibers indices compared with the model group ( P <0.05); RT-qPCR and Western blotting results reveal that, in the curcumol group, the mRNA and protein expression levels of NLRP3, IL-1 β, Caspase 1 and gasdermin D decreased significantly compared with the model group ( P <0.05); immunohistochemical results showed that in the curcumol group, the protein expression levels of NLRP3 and IL-1 β decreased significantly compared with the model group ( P <0.05). Conclusion A potential anti-liver fibrosis mechanism of curcumol may be associated with the inhibition of NLRP3 inflammasomes and decreasing the downstream inflammatory response.
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ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
·
2020
·
IF 4.872
Jinglou Chen,Jianhua Liu,Yongfang Lei,Min Liu
The environmental pollution caused by cigarette smoke (CS) seriously endangers people's health. Epigallocatechin-3-gallate (EGCG) is the most abundant catechin in green tea. In this study, rats were exposed to CS for 90 days. Kidney function was evaluated by detecting the levels of serum creatinine and blood urea nitrogen. Liver function was evaluated by detecting the activities of alanine aminotransferase and aspartate transaminase. The renal and hepatic oxidative stress and inflammation were assessed by detecting the levels of malondialdehyde, reduced glutathione , antioxidant enzymes (superoxide dismutase and glutathione peroxidase) and proinflammatory cytokines. Organ fibrosis was evaluated by observing collagen deposition via masson staining, by examining the hydroxyproline level, by measuring the mRNA levels of fibrosis-associated genes collagen (Col)-1A1 and Col-3A1, as well as by assessing the activity of profibrotic TGF-β1 pathway. Additionally, renal and hepatic epithelial-mesenchymal transition (EMT) were evaluated. It was observed that EGCG ameliorated the renal and hepatic oxidative stress, inflammation, EMT, as well as inhibited the activation of TGF-β1 signaling pathway induced by CS. These results showed that EGCG could attenuate CS-induced renal and hepatic fibrosis.
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LABORATORY INVESTIGATION
·
2022
·
IF 5.502
Ruo-Peng Liang,Xiao-Xue Zhang,Jie Zhao,Rong-Tao Zhu,Wei-Jie Wang,Qin-Wei Lu,Yu-Ling Sun
Ubiquitin-specific protease 3 (USP3), a kind of cysteine protease, is a crucial family member of deubiquitinating enzymes. USP3 is aberrantly expressed in several tumors, which may contribute to cancer progression. However, the role of USP3 in gallbladder cancer (GBC) is still unknown. In the current study, we detected the expression of USP3 in GBC tissues, measured its contribution to the cell proliferation in GBC progression, and further studied the underlying mechanism of USP3 in GBC through pyruvate kinase L/R (PKLR; a kind of glycolytic enzyme). We found that the expression of USP3 in GBC tissues were higher than that of adjacent tissues, and the protein levels of USP3 and PKLR were positively correlated. Additionally, overexpressed USP3 significantly promoted cell proliferation in vitro and tumor growth in vivo, while the silencing of USP3 inhibited proliferation and tumor growth. Glycolysis in GBC cells ws promoted by the USP3 overexpression and inhibited bye USP3 downregulation. Moreover, the loss of USP3 promoted the ubiquitination and weakened the stability of PKLR. Results of the rescue assay confirmed that PKLR knockdown suppressed USP3-induced oncogenic activity in USP3 overexpressed GBC cells. These findings imply that USP3 is an essential positive regulator in GBC progression, and USP3-PKLR plays a vital role in the progression and metabolism of GBC. Ubiquitin-specific protease 3 (USP3), a cysteine protease, is deubiquitinating enzyme. USP3 is aberrantly expressed in several types of tumors. The authors show that USP3 is an important positive regulator in gallbladder cancer progression, and that pyruvate kinase L/R plays a key role in the progression of GBC.
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POSTHARVEST BIOLOGY AND TECHNOLOGY
·
2020
·
IF 4.303
Xueyin Ru,Ning Tao,Yanyan Feng,Qingqing Li,Qingguo Wang
Enzymatic browning is one of the essential issues affecting the quality of fresh-cut produce. In this study, we identified a novel, safe, and effective anti-browning agent, 3-mercapto-2-butanol, which can prevent fresh-cut potatoes from browning for 5 d under the concentration of 25 μL L −1 at 5 °C. The inhibitory effect of 3-mercapto-2-butanol was close to sodium bisulfite. 3-Mercapto-2-butanol was further identified as a competitive inhibitor which directly inhibited the activity of polyphenol oxidase (PPO) by enzyme kinetic analysis, and the expression levels of PPO-related genes ( POT32 and POT33 ) were decreased after 3-mercapto-2-butanol treatment. Besides, the concentration of enzymatic browning substrate tyrosine (Tyr) in the potato chips was found significantly higher in 3-mercapto-2-butanol treatment group than in the control group. We speculated that 3-mercapto-2-butanol could reduce the consumption of Tyr by inhibiting the activity of PPO. Our finding not only provided a novel and safe anti-browning agent candidate (3-mercapto-2-butanol) to efficiently solve the browning issue for fresh-cut food products, but also preliminarily revealed its mechanism in browning inhibition.
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Food & Function
·
2018
·Vol. 9
·期 11
·5682-5696
·
IF 3.289
Ran Wei,Limin Mao,Ping Xu,Xinghai Zheng,Robert M. Hackman,Gerardo G. Mackenzie,Yuefei Wang
Numerous studies propose that epigallocatechin-3-gallate (EGCG), an abundant polyphenol in green tea, has anti-cancer properties. However, its mechanism of action in breast cancer remains unclear. This study investigated the capacity of EGCG to suppress breast cancer cell growth in vitro and in vivo, characterizing the underlying mechanisms, focusing on the effect of EGCG on glucose metabolism. EGCG reduced breast cancer 4T1 cell growth in a concentration- (10–320 μM) and time- (12–48 h) dependent manner. EGCG induced breast cancer apoptotic cell death at 24 h, as evidenced by annexin V/PI, caspase 3, caspase 8 and caspase 9 activation. Furthermore, EGCG affected the expression of 16 apoptosis-related genes, and promoted mitochondrial depolarization. EGCG induced autophagy concentration-dependently in 4T1 cells by modulating the levels of the autophagy-related proteins Beclin1, ATG5 and LC3B. Moreover, EGCG affected glucose, lactate and ATP levels. Mechanistically, EGCG significantly inhibited the activities and mRNA levels of the glycolytic enzymes hexokinase (HK), phosphofructokinase (PFK), and lactic dehydrogenase (LDH), and to a lesser extent the activity of pyruvate kinase (PK). In addition, EGCG decreased the expression of hypoxia-inducible factor 1α (HIF1α) and glucose transporter 1 (GLUT1), critical players in regulating glycolysis. In vivo, EGCG reduced breast tumor weight in a dose-dependent manner, reduced glucose and lactic acid levels and reduced the expression of the vascular endothelial growth factor (VEGF). In conclusion, EGCG exerts an anti-tumor effect through the inhibition of key enzymes that participate in the glycolytic pathway and the suppression of glucose metabolism.
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Experimental and Therapeutic Medicine
·
2021
·Vol. 22
·期 5
·1-9
·
IF 2.447
Wen-Hua Zhang,Yu Chen,Li-Mo Gao,Yan-Na Cao
Glaucoma is a disease involving impaired visual function accompanied by degeneration and necrosis of the optic nerve. Epigallocatechin‑3‑gallate (EGCG) exerts a neuroprotective effect against the degeneration of retinal ganglion cells. However, whether EGCG can relieve glaucoma and the possible mechanisms remain unclear. In order to determine the function of EGCG in glaucoma, an acute glaucoma rat model was established. Optic neuropathology was examined by haematoxylin‑eosin staining and immunofluorescence staining for class III‑β tubulin. The levels of inflammation‑associated cytokines, such as interleukin (IL)‑4, IL‑6, TNF‑α, IL‑1β, IL‑13 and IFN‑γ were measured by flow cytometry. T cell proliferation was assessed by the carboxyfluorescein diacetate succinimidyl ester method. Finally, the functional role of EGCG in glaucoma was explored. The levels of the inflammation‑associated proteins p‑IκBα and p‑p65 were measured by western blot analysis. The results showed that optic nerve injury occurred, and elevated levels of the inflammatory cytokines IL‑4, IL‑6, TNF‑α, IL‑1β, IL‑13 and IFN‑γ were observed in the rat model of acute glaucoma. In addition, an increased T lymphocyte proliferation rate and imbalance of Th1/Th2 cytokines were present in the models. Importantly, treatment with EGCG significantly alleviated optic nerve injury. At the molecular level, EGCG decreased the levels of inflammation‑associated cytokines, decreased the proliferation rate of T lymphocyte cells, and repaired the imbalance of Th1/Th2 cytokines. Moreover, EGCG inhibited the increase in the phosphorylation of IκBα and p65 caused by modelling and thus suppressed the activation of the nuclear factor (NF)‑κB signalling pathway. The findings of the present study indicate that EGCG could attenuate the symptoms of glaucoma and inhibit inflammatory responses by suppressing the NF‑κB signalling pathway in a rat glaucoma model.
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COLLOIDS AND SURFACES A-PHYSICOCHEMICAL AND ENGINEERING ASPECTS
·
2025
·
IF 5.4
Wangyan Lv,Yingchao Yue,Ming Nie,Changchun Zhao,Jia Wei,Jianjun Cheng
Although Ti 3 C 2 T x exhibits promising potential for corrosion protection, its susceptibility to oxidation significantly limits the practical applications. In this study, 3-aminopropyl-triethoxysilane (APTES) was employed to covalently graft onto Ti 3 C 2 T x surface, thereby preserving its layered structural integrity. Based on density-functional-theory calculations, we systematically elucidated the interaction mechanisms between amino functional group and various surface terminations of Ti 3 C 2 T x at the electronic structure level. Experimental results demonstrate that as-prepared APTES@Ti 3 C 2 T x hybrid significantly enhances the anti-corrosion performance of the epoxy coating. Electrochemical tests revealed that after 30 days of immersion in a 3.5 wt.% NaCl solution, APTES@Ti 3 C 2 T x /EP composite coating maintained a high low-frequency impedance modulus (|Z| f=0.01 Hz ) of 10 7 Ω·cm², which was one order of magnitude higher than that of the pure epoxy coating. Furthermore, the wet adhesion strength of composite coating reached 4.82 MPa, representing a 145.9% improvement compared to the control group. This study not only confirms the effectiveness of the APTES encapsulation strategy in improving the stability of MXene but also provides a new approach for designing long-scale, superior corrosion-resistant composite coatings.
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CATALYSIS LETTERS
·
2025
·Vol. 156
·期 1
·4
·
IF 2.4
Zhang Baoyu,Cui Xuchao,Liu Peng,Lv Shuheng,Zhao Jiquan,Zhang Hong-Yu,Zhang Yuecheng
Achieving cost-effective hydrogenation of 3-hydroxypyridine to 3-hydroxypiperidine is still a challenge issue. Herein, a non-noble metal core–shell structured catalyst Ni 8.0 -Co 2.0 @SiO 2 -5.0–0.10 has been prepared for the hydrogenation of 3-hydroxypyridine with a yield of 95.0%. In this study, a membrane dispersion reactor was used to prepare the core of the catalyst, followed by a hydrolysis process to construct the SiO 2 shell. This semi-continuous method enables the efficient production of core–shell catalysts, not only overcoming the low efficiency of traditional preparation methods but also enhancing catalytic performance. Characterization results indicate that the metal cores synthesized using the membrane dispersion reactor exhibit smaller particle sizes, while the SiO 2 shell effectively prevents agglomeration of the core nanoparticles. This ensures that the catalyst simultaneously achieves a minimum particle size of 9.17 nm and a maximum specific surface area of 110.31 m 2 /g. Graphical By using membrane dispersion reactor, a large number of non-noble metal nanoparticles can be prepared quickly, and then coated with a SiO2 shell exhibits remarkable hydrogenation activity, resulting in a 97.5% selectivity and 95% yield of 3-hydroxypiperidine.
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