FISH & SHELLFISH IMMUNOLOGY
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2022
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IF 4.622
Xiaojing Li,Ruichen Bai,Yichen Bai,Xu Shi,Yuhong Yang,Shiwen Xu
Acetochlor is a high-volume herbicide whose widespread use threatens ecosystems and affects aquaculture. Apoptosis and autophagy are important causes of hepatotoxicity caused by toxicants, which can be mediated by oxidative stress and the inhibition of PPAR/RXR pathway. However, the mechanism of acetochlor on fish hepatocyte damage still needs to be further investigated. Therefore, we treated the Ctenopharyngodon idella hepatic cell line (L8824 cells) with different concentrations (10, 20, and 40 μM) of acetochlor and/or ROS scavenger NAC (1 mM) for 24 h. The results showed that acetochlor decreased the cell viability in a dose-dependent manner. AO/EB staining and flow cytometry verified the increased apoptotic rates . Quantitative analysis of gene expression levels or protein expression levels displayed that the expression levels of Beclin1, P62, LC3B, BAX, and cleaved Casp3 were increased, and the expression of BCL2 was reduced. Besides, we detected the increased ROS contents and decreased PPAR/RXR pathway expressions after acetochlor treatment. The clearance of ROS alleviated the inhibition of the PPAR/RXR pathway and lightened apoptosis and autophagy under acetochlor stress. Overall, these results revealed that acetochlor exposure triggered BCL2/BAX/Casp3-cascaded apoptosis and Beclin1-dependent autophagy through ROS-mediated PPAR/RXR inhibition. The results partially explain the toxicological mechanism of acetochlor and provide targets for the development of its antidote.
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高影响因子
Journal of Materials Chemistry B
·
2022
·Vol. 10
·期 28
·5375-5387
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IF 7.571
Xiujun Tan,Jiayi Wu,Rui Wang,Chenglin Wang,Yimin Sun,Zhenming Wang,Ling Ye
The repair of large bone defects is an urgent problem in the clinic. Note that the disruption of redox homeostasis around bone defect sites might hinder the new bone reconstruction. The rational design of hydrogels for bone regeneration still faces the challenges of insufficient antioxidant capability and weak osteogenesis performance. Here, motivated by the versatile therapeutic functions of metal–organic cages, magnesium-seamed C-propylpyrogallol[4]arene (PgC3Mg) functionalized biodegradable and porous gelatin methacrylate (GelMA) hydrogels are constructed. The novel metal–organic cages endow hydrogels with highly bioactive characteristics and strong reactive oxygen species (ROS)-scavenging ability owing to the simultaneous release of bioactive Mg2+ ions and antioxidant phenolic hydroxyl-rich moieties. The in vitro results reveal that the PgC3Mg modified biocompatible hydrogels show higher expression of osteo-related genes and significantly eliminate the intracellular ROS levels of bone marrow-derived mesenchymal stem cells (BMSCs) against oxidative damage. Meanwhile, the bioactive and ROS scavenging hydrogels can accelerate bone regeneration in large cranial defects. Overall, this study may provide new insights into the designing of regenerative bone grafts with simultaneously enhanced osteogenic and antioxidant capabilities.
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Frontiers in Nutrition
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2022
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IF 6.59
Xiaoxiao Xu,Chuang Ma,Hang Wu,Yuanqiao Ma,Zejin Liu,Peijie Zhong,Chaolei Jin,Wenjuan Ning,Xiao Wu,Yijie Zhang,Jichang Han,Junpeng Wang
Fructose is a commonly used food additive and has many adverse effects on human health, but it is unclear whether fructose impacts pulmonary fibrosis. TGF-β1, a potent fibrotic inducer, is produced as latent complexes by various cells, including alveolar epithelial cells, macrophages, and fibroblasts, and must be activated by many factors such as reactive oxygen species (ROS). This study explored the impact of fructose on pulmonary fibrotic phenotype and epithelial-mesenchymal transition (EMT) using lung epithelial cells (A549 or BEAS-2B) and the underlying mechanisms. Fructose promoted the cell viability of lung epithelial cells, while N-Acetyl-l-cysteine (NAC) inhibited such. Co-treatment of fructose and latent TGF-β1 could induce the fibrosis phenotype and the epithelial-mesenchymal transition (EMT)-related protein expression, increasing lung epithelial cell migration and invasion. Mechanism analysis shows that fructose dose-dependently promoted the production of total and mitochondrial ROS in A549 cells, while NAC eliminated this promotion. Notably, post-administration with NAC or SB431542 (a potent TGF-β type I receptor inhibitor) inhibited fibrosis phenotype and EMT process of lung epithelial cells co-treated with fructose and latent TGF-β1. Finally, the fibrosis phenotype and EMT-related protein expression of lung epithelial cells were mediated by the ROS-activated latent TGF-β1/Smad3 signal. This study revealed that high fructose promoted the fibrotic phenotype of human lung epithelial cells by up-regulating oxidative stress, which enabled the latent form of TGF-β1 into activated TGF-β1, which provides help and reference for the diet adjustment of healthy people and patients with fibrosis.
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ACS Applied Materials & Interfaces
·
2022
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IF 10.383
Liucan Wang,Zhenqiang Wang,Yiyang Pan,Shuaishuai Chen,Xin Fan,Xiaolong Li,Guoqing Chen,Yuanhang Ma,Yujiao Cai,Jixi Zhang,Hua Yang,Weidong Xiao,Min Yu
Benefiting from the evolution of nanotechnology, the combination therapy by gene interference and reactive oxygen species (ROS) scavenging are expected, which holds great potential in inflammatory bowel disease (IBD) therapy. However, the functional integration of different therapeutic modules through interface modification of gene vectors for safe and efficient treatment is urgently needed. Herein, we present a catechol chemistry-mediated core–shell nanoplatform for ROS scavenging-mediated oxidative stress alleviation and siRNA-mediated gene interference in a dextran sulfate sodium (DSS)-induced colitis model. The nanoplatform is constructed by employing mesoporous polydopamine nanoparticles (MPDA NPs) with surface modification of amines as the porous core for TNF-α-siRNA loading (31 wt %) and exerts an antioxidant function, while PDA-induced biomineralization of the calcium phosphate (CaP) coating is used as the pH-sensitive protective shell to prevent siRNA from premature release. The CaP layer degraded under weakly acidic subcellular conditions (lysosomes); thus, the synergistic integration of catechol and cation moieties on the exposed surface of MPDA resulted in an efficient lysosomal escape. Subsequently, effective ROS scavenging caused by the electron-donating ability of MPDA and efficient knocking down (40.5%) of tumor necrosis factor-α (TNF-α) via sufficient cytosolic gene delivery resulted in a synergistic anti-inflammation therapeutic effect both in vitro and in vivo. This work establishes the first paradigm of synergistic therapy in IBD by ROS scavenging and gene interference.
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SENSORS AND ACTUATORS B-CHEMICAL
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2022
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IF 9.221
Xinran Shi,Liang Ji,Yuanyuan Hu,Jinyu Gu,Liming Wang,Wenwen Lu,Jiali Meng,Yan Du,Lingzhong Huang,Dongxia Nie,Yanyan Yu
Since adenosine triphosphate (ATP) and reactive oxygen species (ROS) are closely related to neuron functions and the pathogenesis of Alzheimer's disease , herein, the first example of using a dual-responsive zeolitic imidazolate framework-90 (ZIF-90) to fabricate a single fluorescent probe , CuNCs/ [email protected] /ZIF, was reported, which specifically and sensitively responded to intracellular level fluctuations of ATP and ROS both in neuronal and tumor cells without obvious cross-talking. Through a stepwise in situ growth method, ROS-responsive glutathione-stabilized copper nanoclusters (GSH-CuNCs) and double tagged ATP aptamer hybrid chain (P1-P2) were prepared and respectively encapsulated into the inner and outer ZIF-90. The obtained CuNCs/ [email protected] /ZIF probe as a tandem system could firstly respond to ATP in an “off-to-on” mode, in which, the quenched fluorescence of FAM by BHQ1 attached on P2 was recovered through the competitive displacement between ATP and ZIF-90, leading to the release of FAM from ZIF-90. Upon collapse of the outer ZIF-90, the strong emission of CuNCs enclosed in the inner ZIF-90 was subsequently quenched in the presence of ROS. Accompanied with high sensitivity, selectivity and accuracy, the resultant fluorescent probe exhibited good performance and properties for tracking the level variations of ATP and ROS in SH-SY5Y and Hela cells under different stimulations. This strategy highlighted the potential of the ZIF-90 based nanocomposite for multi-targets detection, and also provided a value tool for the early diagnosis of diseases.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2022
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IF 8.025
Qiuxing Liu,Xin Ding,Xiaoyu Xu,Hualu Lai,Zishan Zeng,Ting Shan,Tao Zhang,Meixu Chen,Yanjuan Huang,Zeqian Huang,Xiuling Dai,Meng Xia,Shengmiao Cui
Tumor cells with innate oxidative stress are more susceptible to exogenous ROS-mediated oxidative damage than normal cells. However, the generated ROS could be scavenged by the overexpressed GSH in cancer cells, thus causing greatly restricted efficiency of ROS-mediated antitumor therapy. Herein, using cinnamaldehyde (CA) as a ROS generator while β-phenethyl isothiocyanate (PEITC) as a GSH scavenger, we designed a tumor-targeted oxidative stress nanoamplifier to elevate intracellular ROS level and synchronously suppress antioxidant systems, for thorough redox imbalance and effective tumor cells killing. First, an amphiphilic acid-sensitive cinnamaldehyde-modified hyaluronic acid conjugates (HA-CA) were synthesized, which could self-assemble into nano-assembly in aqueous media via strong hydrophobic interaction and π-π stacking. Then, aromatic PEITC was appropriately encapsulated into HA-CA nano-assembly to obtain HA-CA/PEITC nanoparticles. Through enhanced permeability retention (EPR) effect and specific CD44 receptor-mediated endocytosis, HA-CA/PEITC nanoparticles could accumulate in tumor tissues and successfully release CA and PEITC under acidic lysosomal environment. Both in vitro and in vivo results showed that the nanoparticles could efficiently boost oxidative stress of tumor cells via generating ROS and depleting GSH, and finally achieve superior antitumor efficacy. This nanoamplifier with good biosafety provides a potential strategy to augment ROS generation and suppress GSH for enhanced oxidation therapy.
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ENVIRONMENTAL POLLUTION
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2022
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IF 9.988
Xiuying Jia,Ruopeng Yan,Huikang Lin,Zhiquan Liu,Lilai Shen,Hongmei Yang,Haoying Wu,Xiaodong Shan,Hangjun Zhang
Tetrabromobisphenol A (TBBPA), which is the most widely employed brominated flame retardant , and its alternative tetrachlorobisphenol A (TCBPA) are widely distributed in aquatic environments. In the present study, the hepatotoxicity induced by TBBPA and TCBPA was investigated in Rana nigromaculata , and the potential mechanisms were investigated with a particular focus on ROS (reactive oxygen species) -dependent mitochondria-mediated apoptosis. Healthy adult frogs were exposed to 0, 0.001, 0.01, 0.1, and 1 mg/L waterborne TBBPA and TCBPA for 14 days. The results showed that liver weight was significantly increased by 51.52%–98.99% in the 0.01, 0.1, and 1 mg/L TBBPA and TCBPA groups relative to the control. Histological examination revealed that the structure of the liver, to some extent, was influenced by TBBPA and TCBPA with nuclear shrinkage and mitochondrial swelling. Meanwhile, TBBPA and TCBPA have significantly increased the alanine transaminase level in serum and the content of ROS, while inhibiting the activity of superoxide dismutase in the liver. In addition, DNA fragments were observed in the TBBPA and TCBPA groups relative to the control. Expression of Cytochrome C was significantly increased by 1.13-, 1.38-, 1.60-, and 2.46-fold in 0.001, 0.01, 0.1, and 1 mg/L TBBPA, and by 1.26-, 1.51-, 2.14-, and 2.98- fold in 0.001, 0.01, 0.1, and 1 mg/L TCBPA, respectively, which indicated that TCBPA may be more toxic than TBBPA. Similarly, the ratio of Bax/Bcl-2 was increased in a dose-dependent manner. These results indicated that apoptosis in the ROS-dependent mitochondrial pathway mediates hepatotoxicity caused by TBBPA and TCBPA. The present study will facilitate an understanding of the toxicity mechanism of flame retardants.
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BIOMATERIALS
·
2021
·
IF 12.479
Si-Yuan Peng,Xin-Hua Liu,Qi-Wen Chen,Yun-Jian Yu,Miao-Deng Liu,Xian-Zheng Zhang
The overexpression of glutathione (GSH) in cancer cells has long been regarded as the primary obstacle for reactive oxygen species (ROS)-involved anti-tumor therapies. To solve this issue, a ferric ion and selenite-codoped calcium phosphate (Fe/Se–CaP) nanohybrid here is fabricated to catabolize endogenous GSH, instead of directly deleting it, to trigger a ROS storm for tumor suppression. The selenite component in Fe/Se–CaP can catabolize GSH to superoxide anion (O 2 •− ) and hydroxyl radicals (•OH) via cascade catalytic reactions , elevating oxidative stress while destroying antioxidant system. The doped Fe can further catalyze the soaring hydrogen peroxide (H 2 O 2 ) originated from O 2 •− to •OH via Fenton reactions. Collectively, Fe/Se–CaP mediated self-augmented catabolism dynamic therapy finally induces apoptosis of cancer cells owing to the significant rise of ROS and, combined with CaP adjuvant, evokes adaptive immune responses to suppress tumor progression, providing an innovative train of thought for ROS-involved anti-tumor therapies.
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ACS Applied Materials & Interfaces
·
2021
·
IF 9.229
Mengyao Chen,Jingxian Yang,Lulu Zhou,Xiaochun Hu,Chunhui Wang,Keke Chai,Ruihao Li,Lei Feng,Yanting Sun,Chunyan Dong,Shuo Shi
Integrating chemodynamic therapy (CDT) and photodynamic therapy (PDT) into one nanoplatform can produce much more reactive oxygen species (ROS) for tumor therapy. Nevertheless, it is still a great challenge to selectively generate sufficient ROS in tumor regions. Meanwhile, CDT and PDT are restricted by insufficient H2O2 content in the tumor as well as by the limited tumor tissue penetration of the light source. In this study, a smart pH/ROS-responsive nanoplatform, Fe2+@UCM-BBD, is rationally designed for tumor combination therapy. The acidic microenvironment can induce the pH-responsive release of doxorubicin (DOX), which can induce tumor apoptosis through DNA damage. Beyond that, DOX can promote the production of H2O2, providing sufficient materials for CDT. Of note, upconversion nanoparticles at the core can convert the 980 nm light to red and green light, which are used to activate Ce6 to produce singlet oxygen (1O2) and achieve upconversion luminescence imaging, respectively. Then, the ROS-responsive linker bis-(alkylthio)alkene is cleaved by 1O2, resulting in the release of Fenton reagent (Fe2+) to realize CDT. Taken together, Fe2+@UCM-BBD exhibits on-demand therapeutic reagent release capability, excellent biocompatibility, and remarkable tumor inhibition ability via synergistic chemo/photodynamic/chemodynamic combination therapy.
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POSTHARVEST BIOLOGY AND TECHNOLOGY
·
2021
·
IF 5.537
Kaibo Yu,Lei Zhou,Jing Xu,Fenghua Jiang,Zhiwei Zhong,Liqiang Zou,Wei Liu
The postharvest preservation of Brassica vegetables has received much attention for improving their nutritional and commercial value. In this study, carboxymethyl cellulose (CMC)-based cross-linking coating embedded with liquid paraffin was prepared to preserve fresh pakchoi ( Brassica chinensis L.) and its effects on postharvest water loss, quality and reactive oxygen species (ROS) metabolism were evaluated. Results showed that ionic cross-linking and liquid paraffin reinforced the structure compactness and water barrier property of CMC coating by uniformly distributing liquid paraffin in cross-linking network. The novel CMC-based coating effectively reduced water loss and improved appearance and nutrition of fresh pakchoi stored at 25 °C and 60 % relative humidity for 48 h. Furthermore, the coating treatment enhanced ROS scavenging capacity and reduced lipid peroxidation, which was attributed to the improvement of antioxidant enzyme activities, ascorbate-glutathione cycle and phenylpropanoid metabolism. This work demonstrates that the novel CMC-based water barrier coating is promising to control the water loss of pakchoi and further maintain the whole quality by regulating ROS metabolism.
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Nanomaterials
·
2021
·Vol. 11
·期 11
·2875
·
IF 5.076
Yi-Mei Zhang,Meng Xia,Rui Ao,Li-Xia Gao,Yan Tang,Jiu-Hong Huang,Ya-Fei Luo,Zhong-Zhu Chen,Bo-Chu Wang,Zheng Huang
Mitochondria, as the powerhouse of most cells, are not only responsible for the generation of adenosine triphosphate (ATP) but also play a decisive role in the regulation of apoptotic cell death, especially of cancer cells. Safe potential delivery systems which can achieve organelle-targeted therapy are urgently required. In this study, for effective pancreatic cancer therapy, a novel mitochondria-targeted and ROS-triggered drug delivery nanoplatform was developed from the TPP-TK-CPI-613 (TTCI) prodrug, in which the ROS-cleave thioketal functions as a linker connecting mitochondrial targeting ligand TPP and anti-mitochondrial metabolism agent CPI-613. DSPE-PEG2000 was added as an assistant component to increase accumulation in the tumor via the EPR effect. This new nanoplatform showed effective mitochondrial targeting, ROS-cleaving capability, and robust therapeutic performances. With active mitochondrial targeting, the formulated nanoparticles (TTCINPs) demonstrate much higher accumulation in mitochondria, facilitating the targeted delivery of CPI-613 to its acting site. The results of in vitro antitumor activity and cell apoptosis revealed that the IC50values ofTTCINPs in three types of pancreatic cancer cells were around 20~30 µM, which was far lower than those of CPI-613 (200 µM); 50 µMTTCINPs showed an increase in apoptosis of up to 97.3% in BxPC3 cells. Therefore, this mitochondria-targeted prodrug nanoparticle platform provides a potential strategy for developing safe, targeting and efficient drug delivery systems for pancreatic cancer therapy.Keywords:mitochondria-targeting;ROS-responsive;drug delivery;nanoparticles;pancreatic cancer therapy;CPI-613
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FOOD CONTROL
·
2023
·
IF 6
Yuge Guan,Xinghua Lu,Jiyu Cheng,Sainan Lu,Liqing Yin,Junfeng Cheng,Mingyi Yang,Yunjie Chen,Jian Sun,Guoquan Lu,Linjiang Pang
The quality deterioration of sweetpotatoes easily during postharvest storage owing to their high respiration rate and accumulation of reactive oxygen species (ROS). In this study, an edible coating (MCW) assembled using montmorillonite, chitosan, and whey protein isolate was fabricated to improve the postharvest quality of sweetpotatoes, and the regulatory mechanism of the edible coating treatment on sweetpotato quality has investigated. The results confirmed that edible coating treatment had a positive effect on maintaining the appearance, firmness, colour, and sensory quality of sweetpotatoes, especially in maintaining free water, starch and soluble protein content, inhibiting respiration rate and delaying weight loss of sweetpotatoes stored at 25 °C for 30 d. Meanwhile, this study illuminated the MCW coating regulates ROS metabolism by upregulating superoxide dismutase, ascorbate peroxidase, and glutathione reductase gene expression, resulting in lower O 2 −. content in postharvest sweetpotato. Furthermore, the relative expression of the genes encoding lipoxygenase, phospholipase C, and phospholipase D was downregulated by the edible coating treatment and contributed to lower enzyme activity, electrolyte leakage and malondialdehyde content, which further reduced the degree of membrane lipid peroxidation and effectively maintained the structure of plasma membrane and then protected the cell integrity of sweetpotato. Collectively, this study provides useful information at the transcriptional level that MCW coating can enhance the post-harvest quality of sweetpotatoes by regulating ROS and membrane lipid metabolism.
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