PLANTA
·
2022
·Vol. 256
·期 5
·1-11
·
IF 4.54
Yang Daoyong,Peng Qiding,Cheng Yongchao,Xi Dehui
Main conclusion G6PDH negatively regulates viral accumulation in Nicotiana benthamiana through RBOHB-associated ROS signaling. Anti-oxidative metabolism and phytohormone-mediated immunity responses play important roles in virus infection. Abstract Glucose-6-phosphate dehydrogenase (G6PDH) is an enzyme in the pentose phosphate pathway, which plays an important role in maintaining intracellular redox homeostasis and has functions in plant growth, development and stress tolerance. However, the role of G6PDH in plants response to virus infection is poorly understood. In this study, NbG6PDH was found to be down-regulated after Chilli veinal mottle virus (ChiVMV-GFP) infection in Nicotiana benthamiana . Subcellular localization of NbG6PDH showed that it was punctate distributed in the protoplasm. Silencing of NbG6PDH reduced the sensitivity of N. benthamiana plants to ChiVMV-GFP. By contrast, transient overexpression of NbG6PDH promoted the accumulation of the virus. The results of physiological indexes showed that glutathione (GSH), catalase (CAT) and proline played an important role in maintaining plants physiological homeostasis. The results of gene expression detection showed that jasmonic acid/ethylene (JA/ET) signaling pathway was significantly correlated with the response of N. benthamiana to ChiVMV-GFP infection, and the changes of N. benthamiana respiratory burst oxidase homologues B (NbRBOHB) indicated that the NbG6PDH-dependent ROS may be regulated by NbRBOHB. Pretreatment of the inducer of reactive oxygen species (ROS) promoted virus infection, whereas inhibitor of ROS alleviated virus infection. Thus, our results indicate that the promoting effect of NbG6PDH on ChiVMV-GFP infection may be related to the NbRBOHB-regulated ROS production.
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Journal of Materials Chemistry B
·
2021
·Vol. 9
·期 39
·8253-8262
·
IF 6.331
Yali Chen,Yujun Cai,Xingsu Yu,Hong Xiao,Haozhe He,Zecong Xiao,Yong Wang,Xintao Shuai
Reactive oxygen species (ROS) mediated tumor therapy strategies have exhibited great prospects and attracted increasing attention, among which photodynamic therapy (PDT) has been well-established. However, the anticancer effects of PDT are greatly limited by the hypoxic tumor microenvironment (TME). Hence, exploring a therapeutic strategy that can relieve tumor hypoxia is regarded as the key to overcoming this problem. Herein, we develop a novel nano-enzyme (MnO2@TPP-PEG) that can accurately conduct tumor-specific catalysis of H2O2 to produce oxygen through a Fenton-like reaction, leading to an enhanced PDT under the irradiation of light. More importantly, the process of catalyzing H2O2 decomposition at the tumor location can also generate a cytotoxic hydroxyl radical (˙OH), achieving an excellent chemodynamic therapy (CDT) to enhance the ROS mediated anti-cancer effect. Notably, the nano-enzyme exerts a high loading content of the photosensitizer, which minimizes the side effects probably caused by the vector.
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Biomaterials Science
·
2018
·Vol. 6
·期 7
·1986-1993
·
IF 5.831
Wenxin Zhang,Yang Zhou,Xudong Li,Xin Xu,Yongbing Chen,Rongying Zhu,Lichen Yin
As one of the intractable challenges in the clinic, the treatment of acute liver failure (ALF) is limited due to high mortality and resource cost. RNA interference (RNAi) provides a new modality for the anti-inflammatory therapy of ALF, while its therapeutic efficacy is greatly hampered by the lack of effective carriers to cooperatively overcome the various systemic barriers. Herein, we developed macrophage-targeting and reactive oxygen species (ROS)-responsive polyplexes to enable efficient systemic delivery of TNF-α siRNA (siTNF-α) to attenuate hepatic inflammation in mice bearing ALF. Se-PEI, obtained from the cross-linking of 600 Da polyethylenimine (PEI) via the ROS-responsive diselenide bond, was developed to condense siTNF-α, and the obtained polyplexes were further coated with carboxylated mannan (Man-COOH). Man-COOH coating allowed active targeting of polyplexes to macrophages with over-expressed mannose receptors (MRs), and it shielded the surface positive charges to enhance the serum stability of polyplexes. Se-PEI could be degraded by ROS in inflammatory macrophages to promote intracellular siRNA release to potentiate the gene knockdown efficiency, and in the meantime reduce the material cytotoxicity associated with high molecular weight. As such, i.v. injected Man-COOH/Se-PEI/siTNF-α polyplexes afforded notable TNF-α silencing by ∼80% in inflamed liver tissues at 500 μg siRNA per kg, and notably reduced serum TNF-α levels to achieve potent anti-inflammatory performance against ALF.
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JOURNAL OF ORTHOPAEDIC RESEARCH
·
2012
·Vol. 31
·期 3
·364-369
·
IF 2.811
Liping Jiang,Longjie Li,Chengyan Geng,Dezheng Gong,Lijie Jiang,Nobuyuki Ishikawa,Koji Kajima,Laifu Zhong
Monosodium iodoacetate (MIA) is an inhibitor of glyceraldehyde-3-phosphate dehydrogenase activity, and causes dose-dependent cartilage degradation resembling the pathological changes of human osteoarthritis (OA). In this study, we assessed the apoptosis induced by MIA and clarified the underlying mechanisms using the primary rat chondrocytes. The apoptosis of primary rat chondrocytes was analyzed by flow cytometry. The levels of mitochondrial membrane potential (ΔΨm) were evaluated using fluorescence spectrophotometer. The production of reactive oxygen species (ROS) was determined by fluorescence spectrophotometer. Apoptosis-related protein cytochrome c and procaspase-3 expressions were examined by Western blotting. We found that MIA treatment induces apoptosis in chondrocytes, as confirmed by increases in the percent of apoptotic cells, up-regulation of cytochrome c and caspase-3 protein levels. Treatment with MIA increases ROS production and decreases the levels of ΔΨm. The antioxidant, N -acetylcysteine (NAC), significantly prevented the production of ROS, the reduction of ΔΨm, the release of cytochrome c and the activation of caspase-3. Further, NAC completely protected the cells from MIA-induced apoptosis. Together these observations suggest that the mechanisms of MIA-induced apoptosis are primarily via ROS production and mitochondria-mediated caspase-3 activation in primary rat chondrocytes. © 2012 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 31: 364–369, 2013
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NEW JOURNAL OF CHEMISTRY
·
2017
·Vol. 41
·期 9
·3273-3279
·
IF 3.269
Chen-Tao Xu,Guang Chen,Xuan Nie,Long-Hai Wang,Sheng-Gang Ding,Ye-Zi You
Poly(amidoamine)s (PAMAMs) of high-generations (G > 5) exhibit high efficacy in gene transfection, but their high cost and severe cytotoxicity limit their use in biomedicine. In contrast, PAMAMs of low-generations (G < 3) are less toxic and easy to synthesize, but exhibit low transfection efficacy. In this report, we design a novel amphiphilic dendrimer by conjugating reactive oxygen species (ROS)-responsive poly(propylenesulfide) (PPS) to a low generation PAMAM dendrimer (G = 2, Mw = 3500 Da) via disulfide bonds. This amphiphilic conjugate can self-assemble into stable nanomicelles. The results show that the obtained nanomicelles have a high zeta potential, which can condense DNA tightly. Moreover, the DNA/nanomicelle polyplexes can be fully dissociated by intracellular ROS and easily release the entrapped DNA. As gene vectors, the nanomicelles exhibited high transfection efficacy and fairly low cytotoxicity in vitro.
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CARBOHYDRATE POLYMERS
·
2025
·
IF 12.5
Tong Lin,Ziyi He,Tianhao Zhao,Qiaochu Fan,Ruibo Hu,Junhui Jiang,Junbo Dang,Mei Zhang,Dahui Sun
Iron overload in the bone microenvironment elevates reactive oxygen species (ROS) and triggers osteoblast ferroptosis, exacerbating osteoporosis. We developed a genipin-crosslinked hydrogel composed of 3-aminophenylboronic acid-grafted hyaluronic acid and hydrocaffeic acid (DHCA)-grafted chitosan (CS-DHCA/HA-3-APBA) and loaded with chromium picolinate (CrPic). In the environment of osteoporosis, Fe 3+ coordination compacted the network and increased compressive modulus by approximately twofold, while elevated ROS accelerated network degradation, supporting ROS-responsive CrPic release, whereas under physiological buffer conditions the release remained slow and stable. In vitro, in iron-overloaded rat bone marrow mesenchymal stem cells (rBMSCs), the CS-DHCA/HA-3-APBA/CrPic hydrogel lowered ROS, preserved mitochondrial membrane potential, blocked ferroptosis, and restored migration and osteogenic differentiation. Treated cells showed alkaline phosphatase activity and mineral deposition near control levels despite iron overload. In vivo, in rabbits with iron overload-induced osteoporosis, defects treated with the Fe 3+ -chelating, CrPic-loaded hydrogel (F-Gel@CrPic) formed robust new bone. At 4 weeks, BV/TV in this group was about 30 %, roughly threefold higher than in untreated defects, and it nearly doubled again by 8 weeks, approaching healthy levels. New bone showed higher mineral density and markedly reduced iron deposition. This work highlights the unique ability of engineered hyaluronic acid/chitosan hydrogels to actively correct a pathological microenvironment and achieve functional tissue repair, showcasing the promise of natural polysaccharide-based engineering for advanced therapy.
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JOURNAL OF FISH DISEASES
·
2025
·
IF 2.2
Bo Li,Penghui Yu,Lei Su,Jianguo Su,Yu Gao,Gailing Yuan
Aeromonas hydrophila- induced bacterial sepsis is a major threat to aquaculture, characterised by excessive inflammation, ferroptosis (an iron-dependent lipid peroxidation-driven cell death) and oxidative damage, which collectively lead to high mortality. Taurine (TAU) and glutathione (GSH) have been demonstrated to have potential therapeutic efficacy against ferroptosis-associated pathologies through redox modulation. However, their combined effects and underlying mechanisms in alleviating A. hydrophila infection remain unclear. In this study, we investigated the protective roles of TAU, GSH and their combination in vitro using yellow catfish ( Pelteobagrus fulvidraco ) macrophages and grass carp ( Ctenopharyngodon idella ) kidney (CIK) cells and in vivo using yellow catfish challenged with A. hydrophila . The results showed that TAU and GSH, either alone or in combination, alleviated oxidative stress by significantly reducing reactive oxygen species (ROS) accumulation and inhibited nuclear factor-κB (NF-κB) pathway activation. This led to downregulated expression of pro-inflammatory cytokines ( IL- 1β and TNF -α) and upregulated anti-inflammatory cytokines ( IL- 10 and TGF -β), accompanied by alleviated ferroptosis. In vivo, dietary supplementation with TAU (10 g/kg) or GSH (350 mg/kg) alone improved survival rates (51.7% and 38.3%, respectively), reduced tissue bacterial loads and protected intestinal and hepatic tissues by preserving mucosal barrier function. However, the TAU + GSH combination unexpectedly decreased survival (28.3%) due to excessive immunosuppression (overproduction of IL- 10 and TGF -β) and impaired mucosal barrier, which exacerbated pathogen colonisation. Together, our findings demonstrate that TAU and GSH alleviate A. hydrophila -induced oxidative stress by reducing mitochondrial ROS overproduction and disrupting the ROS/NF-κB signalling pathway, thereby attenuating inflammatory cytokine storms and ferroptosis. These results provide novel insights into the pathological mechanisms of bacterial sepsis in fish and develop sustainable strategies to improve disease resistance in aquaculture.
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Pharmaceutics
·
2025
·Vol. 17
·期 11
·1478
·
IF 5.5
Hao Li,Xiaowei Xie,Yu Zhang,Xiaopeng Han,Ting Shi,Jiayin Li,Wanyu Chen,Qin Wei,Hong Pan,Shuxian Xu,Qiuyu Chen,Lifang Yin,Chao Qin
Background/Objectives:Cerebral ischemia–reperfusion injury (CIRI) remains a major challenge in the treatment of ischemic stroke, characterized by intertwined oxidative stress and neuroinflammation. Existing monotherapies often fail to address this dual pathology effectively. We developed PLSCZ, a biomimetic nanoplatform integrating a catalytic core of imidazolate framework-8 (ZIF-8)-encapsulated superoxide dismutase (SOD) and catalase (CAT) enzymes with a hybrid platelet membrane shell. This design strategically employs metal–organic frameworks (MOFs) to effectively overcome the critical limitations of enzyme instability and provide a cascade catalytic environment, while the biomimetic surface modification enhances targeting capability, thereby enabling dual-pathway intervention against CIRI.Methods:PLSCZ was engineered by co-encapsulating SOD and CAT within a ZIF-8 core to form a cascade antioxidant system (SCZ). The core was further coated with a hybrid membrane composed of rapamycin-loaded phospholipids and natural platelet membranes. The nanoparticle was characterized by size, structure, enzyme activity, and targeting capability. In vitro and in vivo efficacy was evaluated using oxygen–glucose deprivation/reoxygenation (OGD/R) models and a transient middle cerebral artery occlusion/reperfusion (tMCAO/r) rat model.Results:In vitro, PLSCZ exhibited enhanced enzymatic stability and cascade catalytic efficiency, significantly scavenging reactive oxygen species (ROS) and restoring mitochondrial function. The platelet membrane conferred active targeting to ischemic brain regions and promoted immune evasion. PLSCZ effectively polarized microglia toward the anti-inflammatory M2 phenotype, reduced pro-inflammatory cytokine levels, restored autophagic flux, and preserved blood–brain barrier integrity. In vivo, in tMCAO/r rats, PLSCZ markedly targeted the ischemic hemisphere, reduced infarct volume, improved neurological function, and attenuated neuroinflammation.Conclusions:By synergistic ROS scavenging and anti-inflammatory action, the PLSCZ nanozyme overcomes the limitations of conventional monotherapies for CIRI. This biomimetic, multi-functional platform effectively reduces oxidative stress, modulates the phenotype of microglia, decreases infarct volume, and promotes neurological recovery, offering a promising multi-mechanistic nanotherapeutic for CIRI and a rational design model for MOF-based platforms.
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Food Bioscience
·
2025
·
IF 5.9
Yun-Lu Song,Jia-Lin Xing,Charles Ampomah-Dwamena,Shuai-Hui Ma,Mao-Song Pei,Han-Li Liu,Rui-Ping Feng,Yong-Ke Wu,Tong-Lu Wei,Hai-Nan Liu,Da-Long Guo
Grape seed extract (GSE) is a natural polyphenolic compound with potent antioxidant activity. We developed a composite preservation coating material by combining GSE with nano-zinc oxide (Nano-ZnO) and chitosan (CHI), two widely used agents in postharvest preservation. The CHI-GSE-Nano-ZnO coating effectively inhibited postharvest decay and berry abscission while delaying quality deterioration in grapes. Treatment with the composite coating enhanced the activities of antioxidant enzymes (SOD, POD, CAT, and APX) while reducing oxidative stress markers (O 2 - , H 2 O 2 , and malondialdehyde), thereby mitigating ROS accumulation to preserve postharvest grape quality. To elucidate the underlying mechanism, transcriptome sequencing was conducted on ‘Kyoho’ grape samples collected 3, 6, and 9 days post-treatment with CHI, CHI-GSE, and CHI-GSE-Nano-ZnO. Transcriptomic profiling revealed upregulation of VvSTS484 , a pivotal stilbene synthase (STS)-encoding gene, in the CHI-GSE-Nano-ZnO group. Promoter analysis identified multiple MYB-binding cis-elements in VvSTS484 . Yeast one-hybrid and transient dual-luciferase assays demonstrated that the transcription factor VvMYB714 directly binds to four specific MBS motifs in the VvSTS484 promoter (MBS1, -410 to -416 bp; MBS2, -1201 to -1207 bp; MBS3, -1554 to-1560 bp; and MBS4, -1906 to -1912 bp). This molecular interaction activated VvSTS484 expression, leading to enhanced resveratrol biosynthesis that peaked at day 9 post-treatment. The elevated resveratrol level in the CHI-GSE-Nano-ZnO group aligned with reduced oxidative stress and delayed quality deterioration, consistent with its established role in enhancing plant stress tolerance. In conclusion, the CH-GSE-Nano-ZnO composite coating inhibits postharvest decay via the MYB- pSTS module, providing a theoretical basis for developing natural product-based preservation technologies for fruit and vegetables.
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FOOD CHEMISTRY
·
2024
·
IF 8.5
Quan Ma,Dong Li,Yicheng Ren,Yanpei Chen,Jing Huang,Bin Wu,Qingqing Wang,Zisheng Luo
Autophagy (AU) and programmed cell death (PCD) are dynamically regulated during tomato fruit defense against Botrytis cinerea , which are also manipulated by pathogenic effectors to promote colonization. Present study demonstrated that the enhanced defense induced by transient inhibition on AU by hydroxychloroquine (HCQ) facilitated the restriction of B. cinerea lesion on postharvest tomato. Pre-treatment of 2 mM (16.08 ± 3.42 cm at 7 d) and 6 mM (7.80 ± 2.39 cm at 7 d) HCQ inhibited the lesion development of B. cinerea compared with Mock treatment (50.02 ± 7.69 cm at 7 d). Transient inhibition of AU induced expression of fungal defense and transcriptional regulation related genes, but attenuated reactive oxygen species (ROS) burst gene expression. The ROS-induced PCD was compromised by HCQ with promoted ROS scavenging. The transient pre-treatment of HCQ slightly inhibited AU which triggered the feedback loop that enhanced the autophagic activity defensing against B. cinerea infection.
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JOURNAL OF ENVIRONMENTAL MANAGEMENT
·
2024
·
IF 8
Meichen Liu,Meichen Gao,Xu Shi,Yilin Yin,Huanyi Liu,Ruirui Xie,Chenxi Huang,Wenwen Zhang,Shiwen Xu
With the increasing development of the society, silicon dioxide (SiO 2 ) has been used in various fields, such as agriculture, food industry, etc., and its residues can pose a potential health threat to organisms. Quercetin (Que) is a potent free radical scavenger commonly found in plants. C57BL/6 mice were chosen to established a mouse model of SiO 2 exposure and Que antagonism to investigate the mechanism of action of Que in rescuing the toxic damage of SiO 2 on mouse cerebellum tissue. The results showed that cytoplasmic vacuolization, and inflammatory cell infiltration caused by SiO 2 were alleviated by the addition of Que, and reduced oxidative stress in mouse cerebellum, alleviated the activation of TLR4 pathway induced by SiO 2 , and substantially reduced the occurrence of ZBP-1-mediated PANoptosis induced by SiO 2 exposure in mouse cerebellum. In NS20Y cells, the oxidative stress activator (Elesclomol) and inhibitor N-acetyl cysteine (NAC), and the NF-κB activator 2 (NA2) were added. Elesclomol and NAC confirm the involvement of ROS in regulating the TLR4/NF-κB pathway, the TLR4/NF-κB pathway regulated ZBP-1-mediated PANoptosis in cerebellum and NS20Y cells induced by SiO 2 exposure. In conclusion, the present experimental data suggest that Que mitigates the onset of ZBP-1-mediated PANoptosis in neuronal cells induced by SiO 2 through the ROS/TLR4/NF-κB pathway. The present experimental findings help to understand the detoxification effect of Que in more tissues and provide an important reference for the rescue of organisms in long-term SiO 2 environment.
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FASEB JOURNAL
·
2025
·Vol. 39
·期 11
·e70681
·
IF 4.2
Yao Chen,Heqi Dai,Fei Mao,Yangbai Li,Ruizhi Feng,Yun Qian
Polycystic ovary syndrome (PCOS) is one of the most prevalent endocrine disorders in women of reproductive age. However, the underlying molecular mechanism remains unclear. In this study, we employed RNA sequencing analysis to identify differentially expressed protein‐coding genes and long noncoding RNA (lncRNA) expression profiles in granulosa cells from women with and without PCOS. It was established that the level of NONHSAT233728.1 was diminished in women with PCOS. The present study demonstrated the role of NONHSAT233728.1 in granulosa cells from patients with PCOS and further investigated the potential mechanism of NONHSAT233728.1 in the KGN cell line. Additionally, the knockdown of NONHSAT233728.1 has been observed to promote cell apoptosis, inhibit cell proliferation, promote mitochondrial dysfunction, and inflammation. Western blot analyses confirmed that phospho‐extracellular regulated protein kinases (ERK)1/2 were decreased following lnc‐NONHSAT233728.1 knockdown. Consequently, we propose that ROS accumulation activates the endogenous mitochondrial apoptosis pathway, leading to granulosa cell apoptosis via the MEK/ERK1/2 pathway, which contributes to follicular atresia. We observed a negative correlation between NONHSAT233728.1 and both LH levels and the LH/FSH ratio. These findings indicate that lncRNA NONHSAT233728.1 is linked to the pathogenesis of PCOS and offer new insights into its underlying mechanisms. Through isolation and transcriptomic profiling of granulosa cells, we identified the functional significance of lncRNA NONHSAT233728.1 in polycystic ovary syndrome (PCOS) pathogenesis. Knockdown of lncRNA NONHSAT233728.1 in granulosa cells elevated ROS levels, reduced the Bcl2/Bax ratio, downregulated phospho‐ERK1/2, and increased IL‐8 secretion. These results demonstrate ROS‐mediated mitochondrial apoptosis via MEK/ERK1/2 suppression, alongside inhibited proliferation and enhanced inflammation, consistent with follicular atresia in PCOS. Negative correlations between NONHSAT233728.1 and LH/FSH ratios further support its pathogenic role.
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