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RESPIRATORY PHYSIOLOGY & NEUROBIOLOGY · 2022 · IF 2.821

Branched-chain amino acid transaminase 1 inhibition attenuates childhood asthma in mice by effecting airway remodeling and autophagy

Jing Li,Meixue Chen,Lingling Lu,Jinfeng Wang,Liling Tan

Childhood asthma is a common chronic childhood disease. Branched-chain amino acid transaminase 1 (BCAT1) was reported to be upregulated in chronic airway diseases, while its role in childhood asthma is unclear. Asthma mouse models were established in neonatal mice by 10 µg ovalbumin (OVA) intraperitoneal injection and 3% OVA inhalational challenge. In OVA-challenged mice, BCAT1 levels were upregulated. BCAT1 inhibitor alleviated airway structure and inflammation by suppressing IgE, OVA-specific IgE and inflammatory cytokine release and inflammatory cell infiltration. BCAT1 inhibitor alleviated airway remodeling by inhibiting goblet cell hyperplasia, mucus secretion and the expression of α-SMA and collagen I/III. The BCAT1 inhibitor prevented OVA-enhanced autophagy by decreasing Beclin-1, Atg5 and LC3I/II and increasing p65 levels. In IL-13-stimulated BEAS-2B cells, rapamycin promoted inflammatory cytokine release and autophagy after BCAT1 inhibitor administration. Our research revealed that BCAT1 was upregulated in neonatal asthmatic mice and that a BCAT1 inhibitor might restrain airway inflammation and remodeling by decreasing autophagy, which offered a novel mechanistic understanding of childhood asthma.

✓ 已验证 DOI PubMed 高影响因子
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JOURNAL OF POLYMER RESEARCH · 2026 ·Vol. 33 ·期 11 ·435 · IF 3.5

A low viscosity poly(ethylene imine) modified by 1, 2-epoxybutane: synthesis and post-combustion CO2 capture performance

Chen Yuhuan,Zhang Yun,Chen Chunhong,Chen Jing

In the present work, a low viscosity polymer n EB-PEI 1800 ( n  = 0.22, 0.29, 0.35) is synthesized for CO 2 capture. n EB-PEI 1800 is obtained by partially modifying poly(ethylene imine) (PEI 1800 ) with 1, 2-epoxybutane (EB) and is characterized by FT-IR, elemental analysis and liquid state 13 C NMR. The physical properties, density and viscosity, of aqueous n EB-PEI 1800 solutions with weight fraction w of 30% at the temperatures ranging from (293.15 to 313.15) K are reported. Additionally, CO 2 capture performance by aqueous n EB-PEI 1800 solution is examined. CO 2 absorption loading, average absorption rate, desorption loading, average desorption rate and desorption efficiency in a variety of aqueous n EB-PEI 1800 solution ( w  = 5%, 10%, 15%, 20% and 30%) are investigated at different temperatures. The stability of PEI-based absorbent is also examined by four absorption–desorption cycles. The results reveal that modification can adjust the physical properties of n EB-PEI 1800 solutions. 0.29 EB-PEI system has the lowest viscosity and is favorable for CO 2 capture. 20% aqueous 0.29 EB-PEI solution provides excellent cycling stability and desorption performance, especially desorption efficiency, increasing by 55% compared to PEI system at 393.15 K.

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ACTA HISTOCHEMICA · 2019 · IF 1.719

High mobility group box 1 antibody represses autophagy and alleviates hippocampus damage in pilocarpine-induced mouse epilepsy model

Cui Ying,Liang Ying,Liu Yanxia,Wang Le,Cao Lili

As a neurological disorder, epilepsy has affected over 65 million people all over the world because of the unforeseeable seizures it might cause. However, in-depth understandings of the pathogenesis of epilepsy and effective treatments for the disease are still lacked. Recent discoveries suggest that autophagy, as an endogenous self-cleansing pathway in mammals, might be involved in the onset of epilepsy. Our study assumes that a non-histone DNA binding protein, high mobility group box-1 (HMGB1), formerly considered as a crucial inflammatory factor, may mediate the autophagy of neurons in epileptic mouse brain. To verify this hypothesis, pilocarpine induced epilepsy mouse model was constructed. The mice were treated with HMGB1 antibody for 4 weeks after the initial epileptic seizure . Behavioral test results suggested a recovery of learning ability and memory in epileptic mice when treated with HMGB1 antibody. Pathological changes in hippocampus were inspected under microscopes and hippocampus damages caused by seizures in mouse with epilepsy such as increased intracellular space were alleviated by HMGB1 antibody treatment. Moreover, the expressions of the proteins involved in autophagy pathways were detected by immunofluorescence staining and western blot. microtubule-associated protein 1A/1B-light chain 3 (LC3), Beclin 1, autophagy protein-5 (ATG5), and ATG7 levels were significantly decreased by HMGB1 antibody while the level of p62 was increased. TdT-mediated dUTP Nick-End Labeling (TUNEL) illustrated that cell apoptosis induced by seizures in hippocampus was mitigated by HMGB1 antibody. In conclusion, we propose that HMGB1 may induce increased autophagy in epilepsy mouse model.

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CHEMICO-BIOLOGICAL INTERACTIONS · 2019 · IF 3.407

Curcumin analogues attenuate Aβ25-35-induced oxidative stress in PC12 cells via Keap1/Nrf2/HO-1 signaling pathways

Jialin Xu,Leilei Zhou,Qi Weng,Linxia Xiao,Qingyong Li

Beta-amyloid (Aβ) has pivotal functions in the pathogenesis of Alzheimer's Disease (AD). In the present study, we adopted an vitro model that involved Aβ 25-35 -induced oxidative damage in PC12 cells. Aβ 25-35 (10 μΜ) treatment for 24 h induced significant cell death and oxidative stress in PC12 cells, as evidenced by cell viability reduction, LDH release, ROS accumulation and increased production MDA . (1E,4E)-1, 5-bis(4-hydroxy-3-methoxyphenyl) penta-1, 4-dien-3-one (CB) and (1E, 4E)-1-(3, 4-dimethoxyphenyl)-5-(4-hydroxy-3, 5-dime-thoxyphenyl) Penta-1, 4-dien-3-one (FE), two Curcumin (Cur) analogues displayed neuroprotective effects against Aβ 25-35 -induced oxidative damage and cellular apoptosis in PC12 cells. Here, we investigated three different treatment ways of CB and FE. It was interesting that post-treatment of CB and FE (restoring way) showed similar effect to the preventive way, while attenuating way did not show any protective effect. We found that low dose CB and FE increased transcriptional factor NF-E2-related factor 2 (Nrf2)/hemo oxygenase 1 (HO-1) protein expression and decreased Kelch-like ECH-associated protein 1 (Keap1) in PC 12 cells. In addition, CB and FE promoted the translation of Nrf2 into nuclear and enhanced the activity of superoxide dismutase (SOD)/catalase, which confirmed cytoprotection against Aβ 25-35 -induced oxidative damage. Moreover, CB and FE could increase Bcl-2 expression level, decrease the level of Bax and Cyt-c in Aβ 25-35 -treated PC12 cells. Ultimately, the neuroprotective effect of CB and FE provides a pharmacological basis for its clinical use in prevention and treatment of AD.

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FREE RADICAL BIOLOGY AND MEDICINE · 2021 · IF 7.376

Up-regulation of heme oxygenase-1 by celastrol alleviates oxidative stress and vascular calcification in chronic kidney disease

Xiulin Yang,An Chen,Qingchun Liang,Qianqian Dong,Mingwei Fu,Xiaoyu Liu,Siyi Wang,Yining Li,Yuanzhi Ye,Zirong Lan,Jing-Song Ou,Lihe Lu,Jianyun Yan

Vascular calcification is very commonly observed in patients with chronic kidney disease (CKD), but there is no efficient therapy available. Oxidative stress plays critical roles in the progression of vascular calcification. Celastrol (Cel), a natural constituent derived from Chinese herbals, exhibits anti-oxidative stress activity. Here, we investigated the effect of celastrol on vascular calcification using vascular smooth muscle cells (VSMCs), arterial rings and CKD rats. Alizarin red staining and gene expression analysis showed that Cel dose-dependently inhibited rat VSMC calcification and osteogenic differentiation. Similarly, ex vivo study revealed that Cel inhibited calcification of rat and human arterial rings. In addition, micro-computed tomography, alizarin red staining and calcium content analysis confirmed that Cel inhibited aortic calcification in CKD rats. Interestingly, Cel treatment increased the mRNA and protein levels of heme oxygenase-1 (HMOX-1), and reduced the levels of reactive oxygen species (ROS) in VSMCs. Furthermore, both pharmacological inhibition of HMOX-1 and knockdown of HMOX-1 by siRNA independently counteracted the inhibitory effect of Cel on vascular calcification. Moreover, knockdown of HMOX-1 prevented Cel treatment-mediated reduction in ROS levels. Finally, Cel treatment reduced Vitamin D3-induced aortic calcification in mice and this effect was blocked by HMOX-1 inhibitor ZnPP9. Collectively, our results suggest that up-regulation of HMOX-1 is required for the inhibitory effect of Cel on vascular calcification. Modulation of HMOX-1 may provide a novel strategy for the treatment of vascular calcification in CKD.

✓ 已验证 DOI PubMed 高影响因子
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iScience · 2022 · IF 6.107

Aptamer-assisted two-point immobilized agonist-bound angiotensin II type 1 receptor for a second-site modulator discovery

Jiajun Liu,Ting Li,Ge Wang,Jiahuan Chen,Qingqing Yao,Qian Li,Xinfeng Zhao

Summary Methods of immobilized proteins are challenged by the way how to capture the proteins in their intact functional states. Here we present a two-point, high-specific method for the immobilization of conformationally specific angiotensin II type 1 receptor (AT 1 R) on amino-functionalized polystyrene microspheres. We identified a selective DNA aptamer of AT 1 R by a column-based SELEX approach with micromolar affinity. Two single-stranded DNA strands were utilized to introduce the AT 1 R aptamer and angiotensin II 3-8 peptide to the microsphere surface, resulting in the two surface-positioned sites. The two-point immobilized AT 1 R exhibited enhanced ligand-binding activity and stability in comparison with that prepared by a one-positioned site. Ginsenoside Rg1 and rosmarinic acid were screened from the herbal extract and proved to bind with AT 1 R through the allosteric and orthosteric sites of the receptor, respectively. These provide a generally applicable approach for functional protein immobilization with enhanced conformation stability, ligand binding activity, and screening efficiency.

✓ 已验证 DOI PubMed 高影响因子
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Oxidative Medicine and Cellular Longevity · 2021 · IF 6.543

Vitamin D3 Protects Mice from Diquat-Induced Oxidative Stress through the NF-κB/Nrf2/HO-1 Signaling Pathway.

Haiwen Zhang,Youming Liu,Xin Fang,Lihong Gu,Caiwei Luo,Lu Chen,Qian Wang

Vitamin D 3 , as an indispensable and fat-soluble micronutrient, plays an important role in the health of humans and animals. At present, studies are focusing on the calcium absorption and immunoregulation function of vitamin D 3 ; this study was aimed at exploring the antioxidative stress ability of vitamin D 3 on diquat-induced intestinal dysfunction of ICR mice and the underlying mechanism. The results showed that oral gavage of vitamin D 3 daily significantly improved the body weight gain and immune organ index and significantly reverted the abnormal changes of ALT, AST, SOD, GSH-Px, T-AOC, and MDA in the serum and jejunum induced by diquat. The addition of vitamin D 3 also significantly reduced the concentration of DAO, D-LA, and certain proinflammatory cytokines in serum. Moreover, vitamin D 3 improved the pathological morphology of the duodenum, jejunum, colon, liver, and kidney tissues, and it also largely attenuated the degree of inflammatory infiltration of macrophages and cell apoptotic index of jejunal epithelial tissue induced by diquat. The results demonstrated that vitamin D 3 significantly recovered the intestinal barrier injury by enhancing the expression of mucins and tight junction proteins in the jejunum. In addition, the results indicated that vitamin D 3 could significantly reduce the phosphorylation level of NF- κ B (p65) and enhance the expression of Nrf2 and HO-1 in the jejunum compared with the diquat-induced group. This study suggested that oral administration of vitamin D 3 can protect mice against oxidative damage by inhibiting the phosphorylation level of NF- κ B (p65) and activating Nrf2-related signaling pathways.

✓ 已验证 DOI PubMed 高影响因子
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Experimental and Therapeutic Medicine · 2022 ·Vol. 24 ·期 1 ·1-8 · IF 2.751

The X box binding protein 1/C/EBP homologous protein pathway induces apoptosis of endothelial cells under hyperglycemia

Maoshun Tang,Yi Zheng,Jianping Li,Yuanlang Hu

Venous endothelial cell apoptosis can be induced by endoplasmic reticulum (ER) stress, thus serving an important role in the formation of deep venous thrombosis. X‑box binding protein 1 (XBP1) is a protein associated with ER. The present study aimed to explore the function of XBP1/C/EBP homologous protein (CHOP) pathway in the process of endothelial cell apoptosis under hyperglycemia. Small interfering (si)RNAs targeting XBP1 and CHOP were designed to downregulate the expression of XBP1 and CHOP in human umbilical vein endothelial cell, respectively. Flow cytometry was used to determine cell apoptosis. The expression of XBP1, glucose‑regulated protein 78 (GRP78), CHOP, Puma, cleaved caspase‑3 and Cytochrome c was evaluated by western blotting. There were seven groups of cells that were used in the present study: i) Control (5.5 mM D‑glucose); ii) hypertonic (hypertonic control, 27.8 mM mannitol and 5.5 mM D‑glucose); iii) 16.7 mM D‑glucose; iv) 33.3 mM D‑glucose; v) 33.3 mM + NC (33.3 mM D‑glucose incubated with NC); vi) 33.3 mM + si‑XBP1 (33.3 mM D‑glucose incubated with siRNA against XBP1); and vii) 33.3 mM + si‑CHOP (33.3 mM D‑glucose incubated with siRNA against CHOP). Compared with the control, the apoptosis rate of human umbilical vein endothelial cells (HUVECs) increased greatly with the increase in the concentration of D‑glucose. Compared with the 33.3 mM D‑glucose group, the HUVECs incubated with 33.3 mM D‑glucose and si‑XBP1 or 33.3 mM D‑glucose and si‑CHOP demonstrated a significantly lower apoptosis rate. Compared with the control, XBP1, GRP78, CHOP, Puma, cleaved caspase‑3 and cytochrome c were significantly upregulated in the hypertonic, 16.7 mM D‑glucose, 33.3 mM D‑glucose and 33.3 mM + negative control (NC) groups. Compared with the 33.3 mM D‑glucose group, the expression levels of XBP1, GRP78, CHOP, Puma, cleaved caspase‑3 and cytochrome c in the 33.3 mM + si‑XBP1 or 33.3 mM + si‑CHOP groups significantly decreased. High dosage of glucose induced endothelial cell apoptosis by promoting the expression of apoptotic proteins by activating endoplasmic reticulum stress. XBP1/CHOP may be a potential target for the treatment of deep vein thrombosis as one of the key pathways regulating ERS by regulating apoptosis of endothelial cells.

✓ 已验证 DOI PubMed 高影响因子
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Cell Reports · 2023 · IF 8.8

Oral feeding of nanoplastics affects brain function of mice by inducing macrophage IL-1 signal in the intestine

Qianyu Yang,Huaxing Dai,Ying Cheng,Beilei Wang,Jialu Xu,Yue Zhang,Yitong Chen,Fang Xu,Qingle Ma,Fang Lin,Chao Wang

Nanoplastics (NPs) as contaminants in food and water have drawn increasing public attention. However, little is known about how NPs shape the gut immune landscape after injection. In this study, we fabricate NPs (∼500 nm) and microplastics (MPs) (∼2 μm) and evaluate their in vivo effects by feeding them to mice. The results suggest that NPs show a better ability to induce gut macrophage activation than MPs. In addition, NPs trigger gut interleukin-1 (IL-1)-producing macrophage reprogramming via inducing lysosomal damage. More importantly, IL-1 signaling from the intestine can affect brain immunity, leading to microglial activation and Th17 differentiation, all of which correlates with a decline in cognitive and short-term memory in NP-fed mice. Thus, this study provides insight into the mechanism of action of the gut-brain axis, delineates the way NPs reduce brain function, and highlights the importance of fixing the plastic pollution problem worldwide.

✓ 已验证 DOI PubMed 高影响因子
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Polymers · 2025 ·Vol. 18 ·期 1 ·64 · IF 4.9

High-Pressure Phase Behavior of α-Olefin + n-Hexane + Ethylene/1-Octene Copolymer Systems: Experimental Study and Modeling

Ruijun Zhang,Ziyi Dong,Qiqi He,Junhua Li,Yuexin Hu,Jianhua Qian

Accurate knowledge of phase behavior in polyolefin–solvent mixtures is critical for ensuring stable operation and safe scale-up of industrial solution polymerization processes. The binary (n-hexane + ethylene/1-octene copolymer, POE96k-10) and ternary (α-olefin +n-hexane + POE96k-10) phase behaviors were investigated via a visual high-pressure cell (POE96k-10:Mw= 96 kg·mol–1,Mw/Mn= 3.87, 1-octene mole fraction = 10.31 mol%) at temperatures of 380~480 K and pressures as high as 14 MPa. To systematically analyze the effects of α-olefin mass fraction and type on phase transition, four industrially relevant α-olefins (ethylene, 1-butene, 1-hexene, and 1-octene) were investigated. The results show that the phase transition temperature and pressure for liquid–liquid and liquid–vapor transitions show an approximately linear dependence on α-olefin mass fraction. Ethylene, 1-butene, and 1-hexene lower the phase transition temperature, whereas 1-octene increases it. Ethylene exhibits a strong anti-solvent effect, significantly lowering the transition temperature while increasing the phase transition pressure. The modified Sanchez-Lacombe equation of state (MSL EOS) effectively correlates and reproduces the phase equilibrium data of the α-olefin +n-hexane + POE96k-10 ternary systems, though its accuracy decreases with increasing α-olefin chain length.

✓ 已验证 产品关联 DOI PubMed 高影响因子
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Frontiers in Microbiology · 2022 · IF 6.064

The Metabolites of Lactobacillus fermentum F-B9-1 Relieved Dextran Sulfate Sodium-Induced Experimental Ulcerative Colitis in Mice

Le Su,Feifan Ma,Zaiyong An,Xiuyu Ji,Ping Zhang,Qiulin Yue,Chen Zhao,Xin Sun,Kunlun Li,Baojun Li,Xinli Liu,Lin Zhao

Because of the increased incidence and prevalence, ulcerative colitis (UC) has become a global health issue in the world. Current therapies for UC are not totally effective which result in persistent and recurrent symptom of many patients. Lactobacillus with anti-inflammatory effects might be beneficial to the prevention or treatment for UC. Here, we examined the ameliorative effects of the metabolites of Lactobacillus fermentum F-B9-1 (MLF) in Caco-2 cells and dextran sodium sulfate (DSS)-induced UC model mice. MLF displayed intestinal barrier-protective activities in Caco-2 cells by increasing the expression of Occludin and ZO-1. They also showed anti-inflammatory potential in interleukin (IL)-1β and IL-6. In order to further examine the in vivo anti-inflammatory effect of MLF, the MLF was gavaged in the DSS-induced UC model mice. The intragastric administration of MLF effectively alleviated colitis symptoms of weight loss, diarrhea, colon shortening, and histopathological scores, protected intestinal barrier function by increasing Occludin and ZO-1, and attenuated colonic and systemic inflammation by suppressing production of IL-1β and IL-6. Finally, the use of MLF remodeled the diversity of the gut microbiota and increased the number of beneficial microorganisms. Overall, the results demonstrated that MLF relieved DSS-induced UC in mice. And MLF might be an effective therapy method to UC in the clinic in the future.

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Science of Advanced Materials · 2014 ·Vol. 6 ·期 9 ·1936-1942 · IF 2.908

A Fluorescence Assay for HIV-1 Ribonuclease H Activity and Inhibition Detection Using Graphene Oxide as Sensing Platform

Li Xiang,Ding Xuelian,Wang Gongke,Zhou Yixuan,Hou Ruipeng,Gao Shuyan,Lu Yan

In this work, we have developed a simple and highly sensitive fluorescent biosensor for the detection of HIV-1 RNase H activity and inhibition by using graphene oxide (GO) as sensing platform. In our approach, a DNA-RNA substrate was prepared which a carboxy fluorescein (FAM) was labeled at the 3 termini of single strand DNA. The FAM labeled DNA-RNA substrate preserves most of the fluorescence when mixed with GO. However, in the present of RNase H, RNase H can cleavage the RNA into fragments, resulting in the dissociation of ssDNA and mononucleotides. The fluorescence intensity was greatly quenched after the addition of GO. Because of the super quenching ability of GO, the as-proposed method provides a wide linear range from 1.0 to 26.3 units mL–1 and a low detection limit of 0.6 units mL–1 for HIV-1 RNase H activity analysis. Additionally, this approach shows potential for high-throughput screening of HIV-1 RNase H inhibitors. The method not only provides a universal platform for monitoring activity and inhibition of RNase H but also shows great potential in biological process researches, drug discovery, and clinic diagnostics.

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