WORLD JOURNAL OF MICROBIOLOGY & BIOTECHNOLOGY
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2025
·Vol. 41
·期 7
·1-16
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IF 4.2
Gao Qingchao,Feng Zhiruo,Wang Zuli,Zhao Fangyuan,Ju Jian
Carvacrol, a phenolic monoterpenoid and major active constituent of plant essential oils, exhibits broad-spectrum antimicrobial activity with potential applications in food preservation and agricultural biocontrol. Previous studies have shown that one of the antifungal mechanisms of carvacrol may be the induction of reactive oxygen species (ROS) burst, but its specific action mechanism is still unclear. This study investigated the apoptosis mechanism of Aspergillus niger caused by ROS burst induced by carvacrol in the molecular level. Carvacrol induced ROS burst, leading to the accumulation of intracellular hydrogen peroxide (H 2 O 2 ) concentration in A. niger which caused the cellular oxidative stress and lipid peroxidation, leading to an increase in the content of unsaturated fatty acids as well as a decrease in the content of glycerophospholipids in the cell membrane, and then disrupted the integrity of cell membranes. RT-qPCR was used to analyze the expression levels of different subunit genes of NADPH oxidase, and the result showed that NoxA , Cdc24 , NoxD and NoxR were all upregulated to varying degrees. And the inhibitory effect of carvacrol on A. niger can be alleviated by adding an additional ROS scavenger. Meanwhile, NADPH oxidase inhibitors eliminated the ROS production induced by carvacrol. In summary, carvacrol can induce ROS burst in A. niger by regulating the gene expression levels of different subunits of NADPH oxidase, leading to membrane lipid peroxidation, irreversible damage to the cell membrane, the disruption of redox dynamic balance and finally cell death.
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JOURNAL OF HAZARDOUS MATERIALS
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2025
·
IF 11.3
Ruonan Ma,Junxia Feng,Hangbo Xu,Xiaoying Zhou,Chunli Liu,Guoyu Zhou,Dongjie Cui,Yupan Zhu,Junhu Wan,Dezheng Yang,Gautam Sethi,Xudong Yang,Lifeng Li,Zhen Jiao
Deoxynivalenol (DON) widely contaminates cereals, causing severe kidney damage in human and animal. However, its underlying mechanisms and efficient detoxification strategy is still limited. Cold atmospheric plasma (CAP) containing rich reactive oxygen species is regarded as an emerging approach for mycotoxin decontamination in cereals. Here we focus on the potential mitigating role CAP in DON-induced nephrotoxicity by exploring DON degradation pathways, toxicity mitigation, and cellular recovery. The results show that CAP-derived 1 O 2 , ∙OH, ∙O 2 - , and H 2 O 2 degraded over 98 % of DON after 120-s treatment and destroyed the toxic epoxy, double bond and hydroxyl group of DON to generate 5 degradation products. The toxicity test was conducted using human renal proximal tubular epithelial cells (HKC-8) in-vitro and murine acute kidney injury model in-vivo . The mechanistic insights into oxidative stress and apoptosis pathways, including Nrf2/HO-1/NQO-1 signaling and JNK-mediated Nrf2 degradation were explored. DON caused serious nephrotoxicity in-vitro and mice by inducing mitochondrial oxidative damage and cell apoptosis via activating Nrf2 phosphorylation and sequentially inhibiting Nrf2/HO-1/NQO-1 signaling pathway, resulting in 45 % loss of HKC-8 cell viability, 85 % of elevation in serum creatinine, and 89 % of increase in blood urea nitrogen (BUN) levels compared with control. While, CAP-treated DON (Pla-DON) can reverse the mitochondrial damage and maintain intracellular redox homeostasis via blocking JNK-mediated Nrf2 degradation, rescuing 50 % of HKC-8 cell activity and reducing creatinine and BUN by 89 % and 83 % compared with DON group. Overall, this study demonstrates the considerable potential of CAP to mitigate DON-induced nephrotoxicity.
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CHEMICAL RESEARCH IN TOXICOLOGY
·
2024
·
IF 3.7
Xiuhao Yu,Shaokun Chen,Hailin Wang
Chlorobenzoquinones (CBQs) are a class of emerging water disinfection byproducts that pose significant risks to public health. In this study, we found that three CBQs (tetrachloro-1,4-benzoquinone, 2,5-dichloro-1,4-benzoquinone, and 2-chloro-1,4-benzoquinone) can significantly aggravate cell death caused by Ras-selective lethal small molecule 3 (RSL3). Further study showed that the cell death caused by CBQs, either alone or in combination with RSL3, was related to iron accumulation and GPX4 inactivation, suggesting the occurrence of ferroptosis. Furthermore, reactive oxygen species are found to play a potential key role in mediating the toxicity of CBQs in CBQs and RSL3-induced ferroptosis. These findings will be helpful in understanding the toxic mechanism of CBQs to mammalian cells.
研究领域:
毒理学
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细胞生物学
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环境科学
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公共卫生
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Advanced Healthcare Materials
·
2023
·
IF 10
Wenjing Mo,Shujie Liu,Xiaozhi Zhao,Fayun Wei,Yuhang Li,Xinan Sheng,Wenmin Cao,Meng Ding,Wenlong Zhang,Xiaoqing Chen,Longxiyu Meng,Sheng Yao,Wenli Diao,Hui Wei,Hongqian Guo
Myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs), two immunosuppressive myeloid components within the tumor microenvironment (TME), represent fundamental barriers in cancer immunotherapy, whereas current nanomedicines rarely exert dual modulatory roles on these cell types simultaneously. Reactive oxygen species (ROS) not only mediates MDSC-induced immunosuppression but also triggers differentiation and polarization of M2-TAMs. Herein, an ROS scavenging nanozyme, Zr-CeO, with enhanced superoxide dismutase- and catalase-like activities for renal tumor growth inhibition is reported. Mechanistically, intracellular ROS scavenging by Zr-CeO significantly attenuates MDSC immunosuppression via dampening the unfolded protein response, hinders M2-TAM polarization through the ERK and STAT3 pathways, but barely affects neoplastic cells and cancer-associated fibroblasts. Furthermore, Zr-CeO enhances the antitumor effect of PD-1 inhibition in murine renal and breast tumor models, accompanied with substantially decreased MDSC recruitment and reprogrammed phenotype of TAMs in the tumor mass. Upon cell isolation, reversed immunosuppressive phenotypes of MDSCs and TAMs are identified. In addition, Zr-CeO alone or combination therapy enhances T lymphocyte infiltration and IFN- γ production within the TME. Collectively, a promising strategy to impair the quantity and function of immunosuppressive myeloid cells and sensitize immunotherapy in both renal and breast cancers is provided.
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Pharmaceutics
·
2023
·Vol. 15
·期 8
·2161
·
IF 5.4
Fen Zheng,Wei Du,Minggang Yang,Kaige Liu,Shanming Zhang,Long Xu,Yong Wen
Bacterial infections, especially antibiotic-resistant bacterial infections, pose a significant threat to human health. Supramolecular gel with innate antibacterial properties is an advanced material for the treatment of bacterial infections, which have attracted great attention. Herein, a reactive oxygen species (ROS)-responsive innate antibacterial supramolecular gel is developed by a bottom-up approach based on phenylalanine and hydrazide with innate antibacterial properties. The structure of gelators and intermediate products was characterized by proton nuclear magnetic resonance (1H NMR) and a high-resolution mass spectrum (HRMS). The results of1H NMR and the Fourier transform infrared spectrum (FT–IR) experiment disclosed that hydrogen bonding and the π–π stacking force are the important self-assembly driving forces of gelators. The microstructure and mechanical properties of gel were studied by Scanning electron microscope (SEM) and Rheometer, respectively. An in vitro degradation experiment proved that the gelator has ROS-responsive degradation properties. The in vitro drug release experiment further manifested that antibiotic-loaded gel has ROS-responsive drug-release performances. An in vitro cytotoxicity experiment showed that the supramolecular gel has good biocompatibility and could promote cell proliferation. The in vitro antibacterial experiment proved that the supramolecular gel has excellent inherent antibacterial properties, and the antibacterial rate againstStaphylococcus aureus(S. aureus) andEscherichia coli(E. coli) was 98.6% and 99.1%, respectively. The ROS-responsive supramolecular gel as a novel antibacterial agent has great application prospects in treating antibiotic-resistant bacterial-infected wounds and preventing the development of bacterial resistance.Keywords:antibacterial gel;supramolecular gel;ROS-responsive;low molecular weight gelator;biocompatibility
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Frontiers in Microbiology
·
2024
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IF 4
Shuo Xie,Junze Ma,Zheng Lu
This study probes into the unique metabolic responses of Bacteroides thetaiotaomicron (B. thetaiotaomicron), a key player in the gut microbiota, when it metabolizes rhamnose rather than typical carbohydrates. Known for its predominant role in the Bacteroidetes phylum, B. thetaiotaomicron efficiently breaks down poly- and mono-saccharides into beneficial short-chain fatty acids (SCFAs), crucial for both host health and microbial ecology balance. Our research focused on how this bacterium’s SCFA production differ when utilizing various monosaccharides, with an emphasis on the oxidative stress responses triggered by rhamnose consumption. Notably, rhamnose use results in unique metabolic byproducts, including substantial quantities of 1,2-propanediol, which differs significantly from those produced during glucose metabolism. Our research reveals that rhamnose consumption is associated with a reduction in reactive oxygen species (ROS), signifying improved resistance to oxidative stress compared to other sugars. This effect is attributed to specific gene expressions within the rhamnose metabolic pathway. Notably, overexpression of the rhamnose metabolism regulator RhaR in B. thetaiotaomicron enhances its survival in oxygen-rich conditions by reducing hydrogen peroxide production. This reduction is linked to decreased expression of pyruvate:ferredoxin oxidoreductase (PFOR). In contrast, experiments with a rhaR-deficient strain demonstrated that the absence of RhaR causes B. thetaiotaomicron cells growing on rhamnose to produce ROS at rates comparable to cells grown on glucose, therefore, losing their advantage in oxidative resistance. Concurrently, the expression of PFOR is no longer suppressed. These results indicate that when B. thetaiotaomicron is cultured in a rhamnose-based medium, RhaR can restrain the expression of PFOR. Although PFOR is not a primary contributor to intracellular ROS production, its sufficient inhibition does reduce ROS levels to certain extent, consequently improving the bacterium’s resistance to oxidative stress. It highlights the metabolic flexibility and robustness of microbes in handling diverse metabolic challenges and oxidative stress in gut niches through the consumption of alternative carbohydrates.
研究领域:
微生物学
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代谢组学
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肠道健康
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Cell Death & Disease
·
2024
·Vol. 15
·期 11
·1-10
·
IF 8.1
Luo Yusong,Liu Ruolan,Zhang He,Wang Hongyu,Yin Hang,Tian Guopeng,Wang Bo,Yan Yunji,Ding Zilin,Dai Junqiang,Niu Liang,Yuan Guoqiang,Pan Yawen
Glioma is a common primary nervous system malignant tumor with poor overall cure rate and low survival rate, yet successful treatment still remains a challenge. Here, we demonstrated that amantadine (AMT) exhibits the powerful anti-glioma effect by promoting apoptosis and autophagy in vivo and in vitro. Mechanistically, amantadine induces a large amount of reactive oxygen species (ROS) accumulation in glioma cells, and then triggers apoptosis by destroying mitochondria. In addition, amantadine induces the initiation of autophagy and inhibits the fusion of autophagosome and lysosome, consequently performing an anti-glioma role. Taken together, our findings suggest that amantadine could be a promising anti-glioma drug that inhibits glioma cells by inducing apoptosis and autophagy, which may provide a novel potential treatment option for patients.
研究领域:
肿瘤学
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神经科学
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药理学
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JOURNAL OF POLYMER SCIENCE
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2024
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IF 3.9
Xing Wang,Haohao Cui,Qingyun Ning,Huayang Feng,Xue Sun,Boyuan An,Zhanrong Li,Jianliang Shen,Jingguo Li
The excessive accumulation of reactive oxygen species (ROS) on wound surfaces poses considerable challenges to the wound healing process, as it exacerbates inflammation and heightens the risk of skin infections. Consequently, the development of multifunctional dressings that possess both ROS-scavenging and antimicrobial properties is of clinical significance for enhancing wound healing. To address these challenges, we synthesized a dual-scavenging hydrogel utilizing dual-dynamic crosslinking techniques. This hydrogel is composed of poly-lysine-grafted D-glucono-1,5-lactone, dithiodipropionic acid/lipoic acid, and dopamine (PLGDTD), in conjunction with borax. The multifunctional attributes of the hydrogel can be attributed to the incorporation of borate esters, dopamine, and disulfide bonds. Experimental results demonstrate that this hydrogel exhibits a robust antioxidant capacity and a pronounced inhibitory effect against Staphylococcus aureus and Escherichia coli . The results of cellular studies indicate that the hydrogel is capable of effectively scavenging ROS and mitigating oxidative stress, attributable to its dual-scavenging mechanism involving borate and disulfide bonds. This multifunctional hydrogel demonstrates significant potential as a candidate for enhancing wound healing associated with ROS. Graphical
研究领域:
生物材料学
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医学工程
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药剂学
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Materials Today Bio
·
2025
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IF 10.2
Yuling Zhang,Silue Zeng,Chuanyu Tang,Shuangqin He,Yingying Pan,Shuchang Li,Yaguang Ren,Mifang Li,Jianwei Tan,Min Zhang,Jingqin Chen,Chengbo Liu,Lingyan Zhang
Chemodynamic therapy (CDT) provides an alternative strategy for tumor therapy. However, the insufficient generation of intratumoral reactive oxygen species (ROS) has been a key challenge encountered in the application and translation of CDT. Herein, we develop a sustainable ROS cycle generator (SRCG) capable of continuously producing ROS for high-efficiency tumor CDT. SRCG uses a porous metal‒organic framework material (Cu-ZIF8) as a carrier for concurrent delivery of glucose oxidase (GOX) and hyaluronidase (HAase). This approach results in a highly efficient nanoreactor, Cu-ZIF8@GOX@HAase (CZGH), capable of releasing GOX and HAase under acidic conditions to hydrolyze glucose and hyaluronic acid. The resulting products can react with the Cu ions in CZ to produce high concentrations of ROS, promoting tumor cell death. Furthermore, CZGH can degrade the extracellular matrix (ECM) and enhance tumor permeability, which facilitates its delivery and relieves hypoxia. This allows for the infiltration of glucose into the tumor, ensuring a sufficient glucose supply from the bloodstream to the SRCG system, and hence resulting in a sustainable ROS production. The effectiveness of SRCG in CDT has been demonstrated both in vitro and in vivo studies in a breast tumor mouse model, highlighting its potential as a groundbreaking approach for extensive tumor treatment.
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BIOMATERIALS
·
2025
·
IF 12.9
Wen Zhang,Yang Liu,Yu Wu,Zhicun Wang,Xiyu Liu,Qinsheng Hu,Li Yang,Cheng Hu,Yunbing Wang
Millions of individuals worldwide suffer from ischemic stroke (IS). The focal hypo-perfused brain brings about hostile pathological environment, which further restricts endogenous neurogenesis post-stroke. In this work, we report an ROS-triggered hyaluronic acid (HA) and platelet lysates (pls) composite biomimetic hydrogel soft scaffold (pls gel) encapsulating matrix metalloproteinase (MMPs)-responsive triglycerol monostearate nanoparticles loaded with docosahexaenoic acid (TGMS@DHA, TD). Pls gel was chosen to be the hydrogel matrix to mimic brain extracellular matrix (ECM) to provide physical support for cell infiltration and accelerate angiogenesis as a growth factors (GFs) box. The borate ester bonded hydrogel could respond to reactive oxygen species and relieve oxidative stress. The loaded TD nanoparticles could be enzymatically cleaved by overexpressed MMPs in cerebral infarcted site, which could improve the adverse effects triggered by overexpressed MMPs. DHA with rich unsaturated bonds was proven that not only inhibit neuroinflammatory and oxidative stress, but also take part in promote neurogenesis. In brief, the ROS-triggered hydrogel scaffold pls gel@TD created an optimized microenvironment to manipulate the survival and differentiation of neural stem cells and promote endogenous regenerative repair processes. The in vitro results exhibited the biomimetic soft scaffold eliminated oxygen-glucose deprivation-derived free radical, saved mitochondrial dysfunction, reduced neuronal apoptosis, and promoted neovascularization. In the mice focal IS model, the biomimetic hydrogel scaffold regulated pathological environment in the ischemic site and induced migration and differentiation of endogenous neural stem cells, consequently relieved neuron ischemia injury. During the long-term observation, the hydrogel improved mice neurobehavioral functions. In conclusion, the hydrogel soft scaffold pls gel@TD was demonstrated to have promising therapeutic effects on remodeling pathological environment by transforming the hostile state into a pro-regenerative one in the infarct site, consequently promoting endogenous regenerative repair processes.
研究领域:
生物材料学
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神经科学
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再生医学
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Advanced Science
·
2026
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IF 14.1
Menghao Qiao,Liqun Zhou,Minhua Zhou,Yu Fang,Haiying Mai,Lingbo Cao,Kun Xu,Yuan Sang,Minyi Chen,Jiewei Huang,Peiyi Huang,Zhipeng Yan,Chao Wang,Zhangshuai Dai,Dichun Huang,Ronghan He,Lijuan Pang,Yunmiao Guo,Ting Gang Chew,Junqi Huang
Ferroptosis is an iron-dependent form of programmed cell death governed by redox homeostasis. Although Ezrin, Radixin, and Moesin (ERM) proteins are established membrane-actin cytoskeleton linkers, their role in ferroptosis remains unexplored. Here, ERM proteins are identified as modulators of erastin-induced ferroptosis. In human fibrosarcoma HT-1080 cells, pharmacological inhibition of ERM phosphorylation, knockdown of individual ERM members, or overexpression of a phospho-deficient Ezrin mutant (T567A) consistently attenuated ferroptosis, whereas wild-type ERM overexpression enhances ferroptosis susceptibility. Mechanistically, ERM inhibition leads to F-actin depolymerization accompanied by a modest rise in reactive oxygen species (ROS). F-actin stabilization prevents this ROS surge and restores ferroptotic sensitivity, whereas its depolymerization mimics the protective effect of ERM inhibition. ROS elevation triggers KEAP1 degradation, stabilizing NRF2 and promoting its nuclear translocation. Activated nuclear NRF2 induces antioxidant genes, particularly HMOX1 , a key effector of heme catabolism that enhances redox buffering and limits lipid peroxidation, ultimately conferring resistance to ferroptosis. The protective effects of ERM inhibition are further validated in ferroptosis-relevant ex vivo and in vivo models. Notably, other pro-oxidants similarly attenuate ferroptosis at appropriate concentrations. Together, these results establish ERM proteins as regulators of ferroptosis and reveal an underappreciated group of ferroptosis inhibitors that engage ROS-NRF2-mediated redox-adaptation.
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CHEMICAL ENGINEERING JOURNAL
·
2026
·
IF 12.5
Yang-Qing He,Peng Guo,Qiu-Lian Hao,Zhenyong Wu,Hai-Hao Han
Epilepsy, a global therapeutic challenge, is often drug-resistant due to poor blood–brain barrier (BBB) permeability of conventional antiepileptics, which also suffer from non-specific release and long-term safety issues. Here, a glucose-functionalized, reactive oxygen species (ROS)-responsive nanodisc system (GLND-TP) is presented, designed to overcome these via enhanced BBB traversal and epilepsy-specific drug release. It integrates GLUT1-targeting ligand (DSPE-PEG 2000 -Glucose) and glycaemic control (fasting-induced hypoglycemia plus glucose replenishment) to enhance GLUT1 expression/recycling. Incorporating ROS-cleavable phenytoin (PHT) prodrug (DSPE-PEG 2000 -TK-PHT), the 10–20 nm GLND-TP enables prolonged circulation, efficient BBB penetration, and ROS-triggered PHT release with ROS scavenging, alleviating oxidative stress and gliosis. In vivo, GLND-TP (0.1 mg/kg) achieves superior seizure suppression and reduced neural damage vs free PHT (10 mg/kg), with a 100-fold increase in potency. Mechanistically, it boosts local PHT bioavailability to inhibit pathological hyperexcitability and remodels epileptic microenvironment via ROS clearance. By bridging physiological targeting and pathological modulation, GLND-TP pioneers precision nanotherapy for neurological disorders, offering a translatable epilepsy-targeted strategy.
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