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Frontiers in Cell and Developmental Biology · 2020 · IF 5.186

BM-MSC Transplantation Alleviates Intracerebral Hemorrhage-Induced Brain Injury, Promotes Astrocytes Vimentin Expression, and Enhances Astrocytes Antioxidation via the Cx43/Nrf2/HO-1 Axis

Chen Xiao,Liang Huaibin,Xi Zhiyu,Yang Yong,Shan Huimin,Wang Baofeng,Zhong Zhihong,Xu Canxin,Yang Guo-Yuan,Sun Qingfang,Sun Yuhao,Bian Liuguan

Intracerebral hemorrhage (ICH) is a particularly severe form of stroke, and reactive astrogliosis is a common response following injury to the central nervous system (CNS). Mesenchymal stem cells (MSCs) are reported to promote neurogenesis and alleviate the late side effects in injured brain regions. Gap junctions (Gjs) are abundant in the brain, where the richest connexin (Cx) is Cx43, most prominently expressed in astrocytes. Nuclear factor erythroid 2-related factor 2 (Nrf2) is an essential transcription factor regulating antioxidant reactions. Here, we aimed to explore whether bone marrow MSCs (BM-MSCs) could alleviate brain injury and protect astrocytes from apoptosis, by regulating Cx43 and Nrf2. We validated the effect of BM-MSC transplantation in an ICH model in vivo and in vitro and detected changes using immunofluorescence, as well as protein and mRNA expression of glial fibrillary acidic protein (GFAP), vimentin (VIM), Cx43, Nrf2, and heme oxygenase-1 (HO-1). Our results showed that BM-MSC transplantation attenuated brain injury after ICH and upregulated VIM expression in vivo and in vitro. Additionally, Cx43 upregulation and Nrf2 nuclear translocation were observed in astrocytes cocultured with BM-MSC. Knockdown of Cx43 by siRNA restrained Nrf2 nuclear translocation. Cx43 and Nrf2 had a connection as determined by immunofluorescence and coimmunoprecipitation. We demonstrated that astrocytes undergo astroglial-mesenchymal phenotype switching and have anti-apoptotic abilities after BM-MSC transplantation, where Cx43 upregulation triggers Nrf2 nuclear translocation and promotes its phase II enzyme expression. The Cx43/Nrf2 interaction of astrocytes after BM-MSC transplantation may provide an important therapeutic target in the management of ICH.

研究领域: 神经科学 · 干细胞研究 · 神经病学 · 分子生物学
✓ 已验证 DOI PubMed 高影响因子
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Journal of Cleaner Production · 2026 · IF 10.7

Revisit the improvement of coagulation pretreatment on ozonation performance: The critical roles of HO• and O3 for effluent organic matter transformation and micropollutant degradation

Rui Hu,Hao-Tong Zheng,Boxi Tang,Jialing Tu,Yu-Hong Cui,Xuedong Zhai,Gang Wen,Zheng-Qian Liu

Effluent organic matter (EfOM) from municipal wastewater treatment plants is an emerging concern because of its refractory and potential risk to ecological environment. Herein, this investigation comprehensively evaluated the effects of HO • and O 3 exposures on EfOM transformation and micropollutant degradation under different pre-coagulation operating conditions during ozonation. Compared to coagulation and ozonation alone, coupling two processes could effectively reduce total organic carbon, color and UV 254 of effluent. Fe-based coagulant was easier to combine with OH − to generate floc in bulk than Al-based coagulant for EfOM capture, which could decrease total scavenging capacities of effluents as well as increase the exposures of O 3 and HO • during ozonation, enhancing ozonation efficiency for EfOM degradation. EfOM from membrane bioreactor treatment was more difficult to capture during pre-coagulation but more easily degraded during ozonation than that from conventional activated sludge treatment due to its lower molecular weight distribution and higher contents of humic-like and tryptophan-like substances. Parallel factor analysis shows that coagulation combined with ozonation breaks the fluorescent groups of humic-like and tryptophan-like substances effectively. Molecular weight distribution determination indicates that coupling two processes could more effectively remove humic-like substances, organic colloids and polysaccharides compared to coagulation or ozonation alone. Furthermore, micropollutants with higher energy of highest occupied molecular orbital were degraded more efficiently during ozonation. The investigation reveals that O 3 utilization efficiency for micropollutant degradation can be significantly improved by pre-coagulation, offering new ideas for reducing energy consumption during advanced ozonation treatment and ensuring the safety of effluent and sustainable water reuse.

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ANALYTICAL AND BIOANALYTICAL CHEMISTRY · 2025 · IF 3.8

Bioanalysis of monodisperse HO-PEG8-OH polymers in MCF-7 cells by UHPLC-MS/MS coupled with μ-SPE to improve greenness and sensitivity

Yu Luyao,Liu Meichen,Niu Ziyi,Zhang Jiarui,Deng Yue,Zhou Xinyue,You Jiansong,Xue Hongyu,Yin Lei,Shi Meiyun

Monodisperse polyethylene glycol (PEG) derivatives offer significant advantages over conventional polydisperse PEGs for biomedical applications due to their precisely defined molecular structures. This study establishes an eco-efficient, selective, and sensitive analytical assay integrating microscale solid-phase extraction (μ-SPE) with ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS) to investigate the cellular uptake of HO-PEG 8 -OH polymers in MCF-7 cells. The method achieved greater than 91% recovery from 20 μL lysates using M-PEG 6 -OH as the internal standard, with validated linearity (10–1000 ng/mL, R  > 0.997), accuracy (relative error <  ± 7.49%), and precision (RSD < 7.50%). The novelty of the assay is the harmonization of analytical performance with green analytical chemistry principles. The validated method provides a robust platform for studying monodisperse PEG derivatives while addressing growing demands for sustainable analytical technologies. Green analytical chemistry metric assessments confirmed the environmental sustainability of the method. Cellular pharmacokinetic analysis revealed time-/concentration-dependent uptake kinetics of HO-PEG 8 -OH polymers in MCF-7 cells, showing 3.2-fold accumulation between 0.5 and 48 h exposure. These findings offer important insights for PEG-based drug delivery system optimization and establish a new standard for environmentally conscious bioanalytical method development. Graphical

CAS / MDL: 64-18-6
✓ 已验证 产品关联 DOI PubMed 高影响因子
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Inorganic Chemistry Frontiers · 2025 · IF 6.4

Reactive flux assisted metal oxide–boron–sulfur routine for syntheses of CsRESiS4 (RE = Sm, Gd–Ho): featuring nonlinear optical activity and wide band gaps

Zhen-Cheng Wu,Fang-Xu Tian,Rui Xiao,Mao-Yin Ran,Wenlong Liu,Wen-Tong Chen,Sheng-Ping Guo

The study of infrared nonlinear optical (NLO) materials with wide band gaps and high laser induced damage thresholds (LIDTs) is an urgent and challenging topic. Here, we report the NLO properties of CsRESiS4 (RE = Sm, Gd–Ho), which were synthesized by the reactive flux CsCl assisted RExOy–B–S routine. The structure of CsRESiS4, [CsS7] pentagonal bipyramids are orderly arranged to populate the interlayer space created by [RES7] monocapped triangular prisms consolidated [SiS4] tetrahedra. They all exhibit wide band gaps of 3.51–3.95 eV, high LIDTs of 3.6–5.5 × AGS, and NLO activity, with CsHoSiS4 possessing the largest band gap among rare-earth chalcogenides. The theoretical calculation results indicate that [RES7] monocapped triangular prisms are the main source of NLO activity and have a wide band gap. This work provides an effective case for exploring wide band gap infrared NLO materials.

CAS / MDL: 7440-42-8 7704-34-9
研究领域: 材料科学 · 凝聚态物理 · 无机化学 · 光学材料 · 功能晶体
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CERAMICS INTERNATIONAL · 2023 · IF 5.2

Efficient upconversion and downshifting luminescence of CaIn2O4: Yb3+/Tm3+/RE3+ (RE=Er/Ho) phosphor: Temperature sensing performance in the visible and near-infrared range

Hang Liu,Ziyi Zhang,Jian Liu,Kailin Wang,Yuhong Zhang

In this paper, the upconversion(UC) and downshifting(DS) luminescence and thermal sensing performances of the CaIn 2 O 4: RE 3+ /Tm 3+ /Yb 3+ (RE=Er, Ho) phosphors are investigated in detail. The bright UC emission bands from 450 to 900 nm and the DS luminescence bands from 1000 to 1700 nm are obtained under 980 nm excitation. The typical near infrared(NIR) emisson band(∼1550 nm) of Er 3+ ions and the NIR emission band(∼1200 nm) of Ho 3+ ions are gained. The temperature sensing features of CaIn 2 O 4: RE 3+ /Tm 3+ /Yb 3+ (RE=Er, Ho) phosphors are investigated with the luminescence intensity ratio (LIR) technique. The results indicate that the maximum relative sensitivity (S Rmax ) of CaIn 2 O 4: Er 3+ /Tm 3+ /Yb 3+ sample reaches 1.576% K -1 at 313 K, and the S Rmax of CaIn 2 O 4: Ho 3+ /Tm 3+ /Yb 3+ sample reaches 0.797% K -1 at 353 K in UC range. In addition, the higher temperature measuring sensitivities have been obtained in NIR-II region with the DS luminescence of CaIn 2 O 4: RE 3+ /Tm 3+ /Yb 3+ phosphors. The above results indicate that the CaIn 2 O 4: RE 3+ /Tm 3+ /Yb 3+ phosphors show bright emission bands in visible and NIR-II, and higher sensitivity for temperature measurement. The CaIn 2 O 4: RE 3+ /Tm 3+ /Yb 3+ phosphors present great application in optical temperature measurement.

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Iranian Journal of Basic Medical Sciences · 2023 · IF 2.2

Protective effects of baicalin against L-glutamate-induced oxidative damage in HT-22 cells by inhibiting NLRP3 inflammasome activation via Nrf2/HO-1 signaling

Junyuan Li,Gang Wang,Yehao Zhang,Xiaodi Fan,Mingjiang Yao

Objective(s): To explore the ability and underlying molecular mechanisms involved in the protective effects of Baicalin (BA) against L-Glutamate-induced mouse hippocampal neuron cell line HT-22. Materials and Methods: The cell injury model of HT-22 cells was induced by L-glutamate, and cell viability and damage were detected by CCK-8 and LDH assays. Generation of intracellular reactive oxygen species (ROS) was measured by DCFH-DA in situ fluorescence method. The SOD activity and MDA concentration in the supernatants were determined by WST-8 and colorimetric method, respectively. Furthermore, Western blot and real-time qPCR analysis were utilized to detect the expression levels of the Nrf2/HO-1 signaling pathway and NLRP3 inflammasome proteins and genes. Results: L-Glutamate exposure induced cell injuries in HT-22 cells, and the concentration of 5 mM L-Glutamate was chosen to be the modeling condition. Co-treatment with BA significantly promoted cell viability and reduced LDH release in a dose-dependent manner. In addition, BA attenuated the L-Glutamate-induced injuries by decreasing the ROS production and MDA concentration, while increasing the SOD activity. Moreover, we also found that BA treatment up-regulated the gene and protein expression of Nrf2 and HO-1, and then inhibited the expression of NLRP3. Conclusion: Our study found that BA could relieve oxidative stress damage of HT-22 cells induced by L-Glutamate, and the mechanism might be related to the activation of Nrf2/HO-1 and inhibition of NLRP3 inflammasome.

CAS / MDL: 67-68-5
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BIOCHEMICAL PHARMACOLOGY · 2023 · IF 5.8

Phenolic compound SG-1 from Balanophora harlandii and its derivatives exert anti-influenza A virus activity via activation of the Nrf2/HO-1 pathway

Runhong Zhou,Jianan Hu,Jingnan Qiu,Shengsheng Lu,Haixing Lin,Ruifeng Huang,Shaofen Zhou,Guoqing Huang,Jian He

Influenza A virus (IAV) is one of the leading causes of respiratory illness and continues to cause pandemics around the world. Against this backdrop, drug resistance poses a challenge to existing antiviral drugs, and hence, there is an urgent need for developing new antiviral drugs. In this study, we obtained a phenolic compound SG -7, a derivative of natural compound 2-hydroxymethyl-1,4-hydroquinone, which exhibits inhibitory activity toward a panel of influenza viruses and has low cellular toxicity. Mechanistic studies have shown that SG -7 exerts its anti-IAV properties by acting on the virus itself and modulating host signaling pathways. Namely, SG -7 targets the HA2 subunit of hemagglutinin (HA) to block the fusion of viral-cellular membranes and inhibits IAV-induced oxidative stress and overexpression of pro-inflammatory factors by activating the Nrf2/HO-1 pathway and reducing NF-κB activation. In addition, SG -7 can enhance type I IFN antiviral response by inducing Nrf2 expression. Importantly, SG-7 showed the ability to inhibit viral replication in the lungs of IAV-infected mice and reduce their mortality. Therefore, SG-7 may be a promising lead compound for anti-influenza drug development .

CAS / MDL: 131707-23-8
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INTERNATIONAL IMMUNOPHARMACOLOGY · 2018 · IF 3.118

Rosmarinic acid protects mice from lipopolysaccharide/d-galactosamine-induced acute liver injury by inhibiting MAPKs/NF-κB and activating Nrf2/HO-1 signaling pathways

Zheng Li,Haihua Feng,Yue Wang,Bingyu Shen,Ye Tian,Lin Wu,Qiaoling Zhang,Meiyu Jin,Guowen Liu

Rosmarinic acid (RA) has antioxidation, anticancer, antibacterial, anti-inflammatory and various biological functions. In our study, we aim to evaluate effects of RA on acute liver injury caused by LPS and d -galactosamine ( d -GalN) and its underlying molecular mechanism in mice. Our findings showed that RA could protect C57BL/6 mice from LPS/ d -GalN-induced acute liver injury, which not only reflected on declining aspartate aminotransferase (AST) and alanine aminotransferase (ALT) of the serum, but also restrained the phosphorylation of nuclear factor-kappa B (NF-κB), extracellular signal-regulated kinase (ERK1/2) and p38 protein expression and the content of tissue myeloperoxidase (MPO) elevation. Moreover, RA could enhance the level of glutathione-dependent peroxidase (GSH-PX). Furthermore, RA promoted that nuclear factor erythroid-2-related factor 2 (Nrf2) transported into nucleus, and then up-regulated heme oxygenase 1 (HO-1), glutamate-cysteine ligase catalytic (GCLC), glutamate cysteine ligase modifier (GCLM) and quinone oxidoreductase (NQO1). These results indicated that RA could protect the mice from acute liver injury induced by LPS/ d -GalN.

CAS / MDL: 131-56-6
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Nutrients · 2022 ·Vol. 14 ·期 19 ·3928 · IF 6.706

Isinglass Polysaccharides Regulate Intestinal-Barrier Function and Alleviate Obesity in High-Fat Diet Mice through the HO-1/Nrf2 Pathway and Intestinal Microbiome Environment

Guopeng Li,Shugang Li,Huanhuan Liu,Lihua Zhang,Jingzhu Gao,Siteng Zhang,Yue Zou,Xiaodong Xia,Xiaomeng Ren

Plant polysaccharide intervention has shown significant potential to combat obesity. However, studies on animal polysaccharides are indeed rare. The aim of this study was to investigate the potential functions of CIP (IL) on obesity, intestinal microflora dysbiosis, and the possible protection of intestinal barrier in mice fed with high-fat diet (HFD). Our results revealed that after 13 weeks, the HFD+L (high-fat diet + 25 mg/kg CIP) group showed significantly more weight loss and fat accumulation relative to the HFD+H (high-fat diet + 50 mg/kg CIP) group. Furthermore, CIP intervention modulated lipid metabolism and mRNA levels of inflammatory mediators in liver. Overall, CIP clearly improved the intestinal barrier in HFD-fed mice. Additionally, we observed that CIP intervention improved intestinal microbiota community richness and diversity in HFD-fed mice. The CIP intervention mice group showed a relatively lowFirmicutestoBacteroidetesratio compared to the HFD group. This study concluded that CIP could be used as a functional food to prevent adipocyte accumulation, reduce systemic inflammation, and protect the intestinal barrier.Keywords:crude isinglass polysaccharides (CIP);intestinal barrier;inflammation;HO-1/Nrf2 pathway;intestinal flora

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FOOD AND CHEMICAL TOXICOLOGY · 2016 · IF 3.584

Curcumin attenuates quinocetone induced apoptosis and inflammation via the opposite modulation of Nrf2/HO-1 and NF-kB pathway in human hepatocyte L02 cells

Chongshan Dai,Bin Li,Yan Zhou,Daowen Li,Shen Zhang,Hui Li,Xilong Xiao,Shusheng Tang

The potential toxicity of quinocetone (QCT) has raised widely concern, but its mechanism is still unclear. This study aimed to investigate the protective effect of curcumin on QCT induced apoptosis and the underlying mechanism in human hepatocyte L02 cells. The results showed that QCT treatment significantly decreased the cell viability of L02 cell and increased the release of lactate dehydrogenase (LDH), which was attenuated by curcumin pre-treatment at 1.25, 2.5 and 5 μM. Compared to the QCT alone group, curcumin pre-treatment significantly attenuated QCT induced oxidative stress , mitochondrial dysfunction and apoptosis. In addition, curcumin pretreatment markedly attenuated QCT-induced increase of iNOS activity and NO production in a dose-dependent manner. Meanwhile, curcumin pretreatment markedly down-regulated the expression of nuclear factor –kB (NF-kB) and iNOS mRNAs, but up-regulated the expressions of Nrf2 and HO-1 mRNAs, compared to the QCT alone group. Zinc protoporphyrin IX , a HO-1 inhibitor, markedly partly abolished the cytoprotective effect of curcumin against QCT-induced caspase activation, NF-kB mRNA expression. These results indicate that curcumin could effectively inhibit QCT induced apoptosis and inflammatory response in L02 cells, which may involve the activation of Nrf2/HO-1 and inhibition of NF-kB pathway.

CAS / MDL: 458-37-7
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INTERNATIONAL IMMUNOPHARMACOLOGY · 2017 · IF 2.956

Protective effects of morin on lipopolysaccharide/d-galactosamine-induced acute liver injury by inhibiting TLR4/NF-κB and activating Nrf2/HO-1 signaling pathways

Ye Tian,Zheng Li,Bingyu Shen,Qiaoling Zhang,Haihua Feng

Morin , a bioactive flavonoid extracted from the bark of Moraceae plants and many medicinal herbs, has anti-inflammatory and antioxidative effects. In this research, we explored the protective effects of morin against lipopolysaccharide (LPS) and d -galactosamine (D-GalN) induced acute liver injury in mice. Mice were given an intraperitoneal injection of morin before LPS and D-GalN treatment and the HepG2 cells were only given morin to investigate its effects. The results showed that morin markedly inhibited the production of serum alanine transaminase (ALT), aspartate aminotransferase (AST), interleukin-6 (IL-6), tumor necrosis factor (TNF-α) and hepatic TNF-α, IL-6, and myeloperoxidase (MPO) induced by LPS/D-GalN. In order to evaluate morin effect in the future, we investigated the expression of nuclear factor E2 related factor 2 (Nrf2), nuclear factor-kappaB (NF-κB), toll like receptor 4 (TLR4) on liver injury. Taken together, these results suggested that morin could exert the anti-inflammatory and anti-oxidative effects against LPS/D-GalN-induced acute liver injury by activating Nrf2 signal pathways and inhibiting NF-κB activation.

CAS / MDL: 131-56-6
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CHEMICO-BIOLOGICAL INTERACTIONS · 2024 · IF 4.7

HO-1 activation contributes to cadmium-induced ferroptosis in renal tubular epithelial cells via increasing the labile iron pool and promoting mitochondrial ROS generation

Yan-Ting Lv,Tian-Bin Liu,Yue Li,Zhen-Yong Wang,Cai-Yu Lian,Lin Wang

Cadmium (Cd), a prevalent environmental contaminant, has attracted widespread attention due to its serious health hazards. Ferroptosis is a form of iron-dependent oxidative cell death that contributes to the development of various kidney diseases. However, the mechanisms underlying the occurrence of ferroptosis in Cd-induced renal tubular epithelial cells (TECs) have not been fully elucidated. Hereby, both in-vitro and in-vivo experiments were established to elucidate this issue. In this study, we found that Cd elicited accumulation of lipid peroxides due to intracellular ferrous ion (Fe 2+ ) overload and glutathione depletion, contributing to ferroptosis. Inhibition of ferroptosis via chelation of Fe 2+ or reduction of lipid peroxidation can significantly mitigate Cd-induced cytotoxicity. Renal transcriptome analysis revealed that the activation of heme oxygenase 1 (HO-1) was closely related to ferroptosis in Cd-induced TECs injury . Cd-induced ferroptosis and resultant TECs injury are significantly alleviated due to HO-1 inhibition, demonstrating the crucial role of HO-1 in Cd-triggered ferroptosis. Further studies showed that accumulation of lipid peroxides due to iron overload and mitochondrial ROS (mtROS) generation was responsible for HO-1-triggered ferroptosis in Cd-induced cytotoxicity. In conclusion, the current study demonstrates that excessively upregulating HO-1 promotes iron overload and mtROS overproduction to trigger ferroptosis in Cd-induced TECs injury, highlighting that targeting HO-1-mediated ferroptosis may provide new ideas for preventing Cd-induced nephrotoxicity .

CAS / MDL: 10108-64-2 15442-64-5
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