JOURNAL OF ETHNOPHARMACOLOGY
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2025
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IF 5.4
Lei Yan,Qin Zeng,Wenru Wang,Ying Liang,Rui Lang,Jingyi Zhan,Jiayi Yang,Renhuan Yu,Xinhui Wang
Ethnopharmacological relevance Jianpi Qushi Heluo formula (JQHF) is an evidence-based herbal formula based on "Fangji Huangqi Decoction" in the classic of traditional Chinese medicine (TCM) synopsis of the Golden Chamber. Its effectiveness in reducing idiopathic membranous nephropathy (IMN) proteinuria, edema and other clinical symptoms and improving kidney injury has been confirmed by clinical trials and animal experiments. These results demonstrate the critical significance of reducing podocyte injury by regulating mitophagy through integrating ethnopharmacology. Aim of the study This study aimed to explore the protective effects of JQHF on podocyte injury in IMN, focusing on its role in promoting PINK1-dependent mitophagy to inhibit reactive oxygen species (ROS) mediated activation of the NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome. Materials and Methods The main components of JQHF were identified by ultra-performance liquid chromatography combined with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MSE). Passive Heymann nephritis (PHN) was induced in rats using anti-Fx1A antiserum, while podocyte injury in vitro was stimulated with sublytic complement C5b-9 (sC5b-9). The PHN rats were treated with JQHF, and autophagy inhibitor 3-methyladenine (3-MA) combined with JQHF was used for pathway verification, and Benazepril served as a positive control. In vitro, podocytes were exposed to palmitic acid (PA, a ROS inducer) and N-acetylcysteine (NAC, a ROS scavenger). Further, we silenced the expression of PINK1 in podocytes model and intervened with JQHF-containing serum. Renal function was assessed through biochemical analyses and histopathology. Mitochondrial function was measured by detecting mitochondrial membrane potential (MMP), ROS levels as well as mitochondrial ultrastructure. The expression of podocyte structural proteins (desmin, nephrin, podocin) and inflammasome-related markers (NLRP3, caspase-1, IL-1β, IL-6) was analyzed to assess podocyte injury and inflammasome activation. Results (1) In vitro, in contrast to the control group, PA intervention caused increased ROS accumulation, reduced MMP, upregulated NLRP3 and caspase-1 expression, as well as elevated expression of inflammatory factors IL-1β and IL-6. The expression of nephrin and podocin was notably reduced. By contrast, NAC reversed these effects. (2) In vivo, JQHF effectively ameliorated mitochondrial damage, reduced NLRP3 expression and mitigated podocyte injury in PHN rats. The protective effects of JQHF were diminished by 3-MA, confirming the involvement of autophagy. (3) In vitro, JQHF-containing serum attenuated C5b-9-induced podocyte injury, improved mitochondrial dysfunction, and inhibited ROS-mediated activation of NLRP3 inflammasome. Silencing PINK1 significantly reversed these protective effects. Conclusion JQHF can alleviate podocyte damage, that through inhibiting ROS-mediated NLRP3 inflammasome activation by improving PINK1-mediated mitophagy.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2025
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IF 8.5
Xing Wang,Fang Zhang,Na Li,Lingling Yuan,Xiaolan Zhang,Lihui Zhang,Yu Liu
Background Diabetic hyperlipidemia, which is characterized by oxidative stress and chronic inflammation, plays a significant role in atherosclerosis (AC), a key cause of cardiovascular disease. To reduce the progression of AC, effective treatment options that target the underlying causes of diabetic hyperlipidemia are required. Methodology This study used macrophage-membrane-loaded β-CD functionalized thiolated ROS-responsive NPs (MM@R-β-tCh NPs) as a targeted therapy for diabetic hyperlipidemia-induced AC. The NPs targeted MM and used the β-CD core's ROS sensitivity to deliver drugs to specific locations. Transmission electron microscopy (TEM) was employed to evaluate the structural characteristics. In vitro investigations with HUVEC and MOVAS cell lines evaluated the effect on inflammatory markers IL-6 and TNF-α. In vivo investigations utilizing an animal model evaluated the effects of nanoparticles on blood glucose, lipid concentrations, and arterial plaque levels. Results The TEM analysis of MM@R-β-tCh NPs displayed the emergence of spherical nanoparticles with a diameter of 170 ± 8 nm. MM@R-β-tCh NPs exhibited high drug loading efficiency and ROS-triggered release, achieving 85 % release under enhanced ROS conditions. Accordingly, FRET index (1.8 ± 0.05) confirms the NP's ROS sensitivity. In vitro tests revealed substantial reductions in IL-6 and TNF-α levels. In vivo , findings decreased blood glucose (300 mg/dL to 90 mg/dL), total plasma cholesterol (37 % to 36 %), and serum triglycerides (40 %). H&E staining demonstrated that MM@R-β-tCh-NP-treated mice decreased macrophage infiltration and lipid accumulation in arterial plaques. Conclusion MM@R-β-tCh NPs successfully reduce oxidative stress and dyslipidemia, providing a targeted treatment approach for diabetic hyperlipidemia-induced AC. These findings suggest that MM@R-β-tCh NPs can reduce AC development and improve cardiovascular health in diabetics.
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CHEMICAL ENGINEERING JOURNAL
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2025
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IF 13.2
Yang Chen,Wenting Cheng,Hailong Tian,Yilin Wang,Weifeng He,Canhua Huang
Burns catastrophically compromise the skin barrier, driving impaired healing, infection susceptibility, and regenerative failure, primarily through dysregulated inflammation, immune dysfunction, and overwhelming oxidative stress. While reactive oxygen species (ROS) mediate essential host defense, their pathological excess necessitates targeted modulation for burn repair. We engineered a ROS-responsive nanoassembly (PTC@Cu NPs) for co-delivering chlorogenic acid (CGA) and copper ions (Cu 2+ ). Synthesizing the amphiphilic polymer mPEG-TK-CGA (PTC) via a ROS-cleavable thioketal linker enabled self-assembly with Cu 2+ into NPs. This system achieves triggered release specifically within high-ROS burn sites. CGA and Cu 2+ act synergistically to potently scavenge ROS, polarize macrophages to a pro-regenerative M2 phenotype, and thereby ameliorate oxidative damage, infection, and healing deficits in deep partial-thickness burns. In vitro and in vivo studies demonstrate PTC@Cu NPs significantly suppress apoptosis, enhance cell migration, exert potent antibacterial effects, and markedly accelerate healing. These comprehensive therapeutic benefits are mechanistically underpinned by dual ROS reduction and macrophage M2 polarization. Collectively, this platform presents a promising strategy for infected deep burn wounds by simultaneously targeting oxidative damage, microbial infection, and impaired tissue repair.
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Biomaterials Advances
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2025
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IF 6
Shuting Peng,Lantao Wang,Zhengfeng Lu,Xinyi Yang,Yanxin Lu,Zhengxiao Wang,Qingxin Wu,Xiaofei Qin
The hypoxic, hyperglycemic, ischemic and inflammatory at the chronic diabetic wound microenvironment often leads to persistent oxidative stress and dysfunctional immune responses, as evidenced by hindrance of angiogenesis, neuropathy and impaired macrophage M2-type transition. In addition, bacterial infections lead to further exacerbation of chronic inflammatory responses, which severely impedes wound healing. In this study, hydroxypropyl chitosan (HCS) and 2,3,4-trihydroxybenzaldehyde (TBA) hydrogel was prepared via a one-step method, while Fe 3+ was used to initiate the in-situ oxidative polymerization of pyrrole (Py) in the hydrogel network, that conferred the HCS-TBA@Py hydrogel with excellent electrical conductivity. The outstanding physicochemical properties of the hydrogel, including swelling ability, injectability and electrosensitivity, confirmed its potential for applications in rapid filling of irregular wounds and strain sensors. Meanwhile, HCS-TBA@Py hydrogel can effectively scavenge reactive oxygen species and inhibit bacterial growth. More importantly, the combination of HCS-TBA@Py with electrical stimulation (ES) can effectively enhance the proliferation and migration of endothelial cells, promote axonal growth of nerve cells, rapid angiogenesis and accomplish the phagocytosis of M1 macrophages while realizing the M2 polarization of macrophages, comprehensively and systematically ameliorating the healing of diabetic wounds. This advanced study opens a meaningful way for chronic diabetic wound repair.
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Scientific Reports
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2024
·Vol. 14
·期 1
·1-12
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IF 3.8
Liu Li,Li Siyu,Zhu Wei,Bao Qifu,Liang Yan,Zhao Tiangui,Li Xiaolong,Zhou Jianer
In this study, pure V 6 O 13 and nickel ion-doped V 6 O 13 powders were synthesized by a simple hydrothermal-calcination method, and their broad-spectrum antimicrobial properties and mechanisms were investigated. The crystal structure, morphology, and chemical state of the powders were thoroughly analyzed by XRD, SEM, TEM, XPS, and UV–Vis. Their antimicrobial properties and mechanisms were evaluated by the ring of inhibition, bio-SEM, live-dead cell staining, ROS detection, and protein leakage experiments. The results showed that nickel ion doping modulated the oxygen defects of V 6 O 13 , generating more reactive oxygen species and leading to more severe oxidative stress, resulting in a broad-spectrum and highly efficient antimicrobial effect. This study also revealed the antimicrobial mechanism based on oxygen defect -induced ROS production, which caused cellular oxidative stress damage, leading to leakage of intracellular substances and cell death. This study not only demonstrates the potential of V 6 O 13 as an efficient antimicrobial agent but also provides a strong experimental basis and theoretical support for the engineering design and optimization of novel antimicrobial materials by modulating material defects through ion doping.
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Small
·
2024
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IF 13
Yapeng Wang,Jing Yang,Yunhong Ma,Jun Liu,Peng Wang,Junhao Luo,Yongjun Rui,Yongwei Wu
The accumulation of excessive reactive oxygen species (ROS) and recurrent infections with drug-resistant bacteria pose significant challenges in diabetic wound infections, often leading to impediments in wound healing. Addressing this, there is a critical demand for novel strategies dedicated to treating and preventing diabetic wounds infected with drug-resistant bacteria. Herein, 2D tantalum carbide nanosheets (Ta 4 C 3 NSs) have been synthesized through an efficient and straightforward approach, leading to the development of a new, effective nanoplatform endowed with notable photothermal properties, biosafety, and diverse ROS scavenging capabilities, alongside immunogenic attributes for diabetic wound treatment and prevention of recurrent drug-resistant bacterial infections. The Ta 4 C 3 NSs exhibit remarkable photothermal performance, effectively eliminating methicillin-resistant Staphylococcus aureus ( MRSA ) and excessive ROS, thus promoting diabetic wound healing. Furthermore, Ta 4 C 3 NSs enhance dendritic cell activation, further triggering T helper 1 (T H 1)/T H 2 immune responses, leading to pathogen-specific immune memory against recurrent MRSA infections. This nanoplatform, with its significant photothermal and immunomodulatory effects, holds vast potential in the treatment and prevention of drug-resistant bacterial infections in diabetic wounds.
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CARBOHYDRATE RESEARCH
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2025
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IF 2.5
Yuting Sun,Junnan He,Yongyan Sun,Lidong Wang,Haidu Li,Yaqi Miao,Ping Shi,Jin Zhang,Kaixuan Luo,Yan Zhao
The development of reactive oxygen species (ROS)-responsive nanodrug delivery systems faces critical challenges. Excessive cross-linking degree prevents complete degradation of nanocarriers under tumor microenvironment ROS levels, significantly compromising drug release efficiency. Conversely, insufficient cross-linking degree impairs the structural stability of nanoparticles, resulting in premature drug leakage during systemic administration. Herein, we present an innovative strategy for constructing dual cross-linked chitooligosaccharide nanoparticles (NPs) co-loaded with curcumin and glucose oxidase (GOx) to enhance structural stability. These engineered NPs can amplify intracellular ROS concentration through GOx-mediated catalytic conversion of glucose to H 2 O 2 , thereby establishing a ROS-triggered self-accelerating drug release nanosystem for enhanced tumor chemotherapy. In vitro studies have shown that the curcumin release behavior of CTCG NPs depends on the GOx encapsulated inside the nanoparticles. Compared with nanoparticles without GOx, CTCG NPs can effectively prevent the premature release of curcumin in a simulated normal physiological environment. The nanoparticles also showed significant anti-tumor effect and could effectively inhibit the proliferation of tumor cells in vivo . These results proved that CTCG NPs achieve controllable release of drugs through in situ production of ROS in the tumor microenvironment. This nanodrug delivery system shows promising potential for breast cancer therapy.
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2024
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IF 7.7
Ya-li Xiang,De-yu Tang,Ling-ling Yan,Luo-lin Deng,Xing-han Wang,Xin-yang Liu,Qing-han Zhou
The challenge of drug resistance in bacteria caused by the over use of biotics is increasing during the therapy process, which has attracted great attentions of the clinicians and scientists around the world. Recently, photodynamic therapy (PDT) triggered by photosensitizer (PS) has become a promising treatment method because of its high efficacy, easy operation, and low side effect. Herein, the poly- l -lysine (PLL) modified metal-organic framework (MOF) nanoparticles, ZIF/PLL-CIP/CUR, were synthesized to allow both reactive oxygen species (ROS) responsive drug release and photodynamic effect for synergistic therapy against drug resistant bacterial infections. The PLL was modified on the shell of the zeolite imidazole framework (ZIF) by the ROS-responsive thioketal linker for controllable CIP release. CUR were encapsulated in ZIF as the photosensitizer for blue light mediated photodynamic effect to produce singlet oxygen ( 1 O 2 ) and superoxide anion radical ( O 2 − ) for efficient inhibition towards methicillin-resistant Staphylococcus aureus ( MRSA ). The charge conversion from negative charge (−4.6 mV) to positive charge (2.6 mV) was observed at pH 7.4 and pH 5.5, and 70.9 % CIP was found released at pH 5.5 in the presence of H 2 O 2 , which suggests the good biosafety at physiological pH and ROS-responsive drug release of the as-prepared nanoparticle in the bacterial microenvironment. The as-prepared nanoparticles could effectively kill MRSA and disrupt bacterial biofilm by combination of chemo- and photodynamic therapy. In mice model, the as-prepared nanoparticles exhibited excellent biosafety and synergistic effect with 98.81 % healing rate in treatment of MRSA infection, which is considered as a promising candidate in combating drug resistant bacterial infection.
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Science Advances
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2020
·Vol. 6
·期 41
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IF 13.117
Di Liu,Gaofeng Shu,Feiyang Jin,Jing Qi,Xiaoling Xu,Yan Du,Hui Yu,Jun Wang,Mingchen Sun,Yuchan You,Minxia Zhu,Meixuan Chen,Luwen Zhu,Qiying Shen,Xiaoying Ying,Xuefang Lou,Saiping Jiang,Yongzhong Du
The development of drugs with rapid distribution in the kidney and long-term retention in the renal tubule is a breakthrough for enhanced treatment of acute kidney injury (AKI). Here, l-serine–modified chitosan (SC) was synthesized as a potential AKI kidney–targeting agent due to the native cationic property of chitosan and specific interaction between kidney injury molecule–1 (Kim-1) and serine. Results indicated that SC was rapidly accumulated and long-term retained in ischemia-reperfusion–induced AKI kidneys, especially in renal tubules, which was possibly due to the specific interactions between SC and Kim-1. SC-TK-SS31 was then prepared by conjugating SS31, a mitochondria-targeted antioxidant, to SC via reactive oxygen species (ROS)–sensitive thioketal linker. Because of the effective renal distribution combined with ROS-responsive drug release behavior, the administration of SC-TK-SS31 led to an enhanced therapeutic effect of SS31 by protecting mitochondria from damage and reducing the oxidative stress, inflammation, and cell apoptosis.
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Materials Science & Engineering C-Materials for Biological Applications
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2021
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IF 7.328
Yilin Yu,Xiaolei Li,Jiarun Li,Dongying Li,Qinmei Wang,Wei Teng
Environments with high reactive oxygen species (ROS) levels, which are common in patients with diseases such as diabetes, periodontitis, and osteoporosis, impair the osseointegration of implants. To address this issue, by using a one-pot dopamine-assisted co-deposition method, we constructed a three-dimensional coating of hydroxyapatite-functionalised nanoparticles of polydopamine (HA/nPDAs) on implant surfaces, where polydopamine is designed to protect cells via scavenging excessive ROS and HA facilitates osteogenesis. First, nanoparticles of polydopamine (nPDAs) were prepared by self-polymerization and assembly of dopamine under alkaline conditions, and HA/nPDAs were obtained by incubating nPDAs in simulated body fluid (SBF) due to metal chelation and ionic interactions triggered by the catechol moieties of PDA. Thereafter, HA/nPDAs with thickness of ~4 μm were constructed on titanium surfaces by immersing titanium discs in a weak alkaline solution of HA/nPDAs and dopamine through interface interactions driven by catechol chemistry. The properties of coatings (e.g., thickness, composition, hydrophilia and morphology) can be controlled by preparation conditions such as mineralization time and reactant concentration. The coatings display efficient ROS-scavenging ability, promote cell proliferation, and upregulate the activity of alkaline phosphatase and the expression of osteogenesis-related genes in environments with high or normal ROS levels, demonstrating the great promise of such coatings for osseointegration promotion, especially in the state of high ROS in diseases. This study provides a facile, efficient, mild, and universal strategy in engineering functional surfaces on any substrates for diversified applications by simple variation of co-deposited components, through taking advantages of versatile catechol chemistry and nanoparticles with stereo structure and great specific surface area.
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MEDICINAL CHEMISTRY RESEARCH
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2023
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IF 2.6
Long Xing,Yang Peilin,Chen Lin,Zhong Wen,Chen Shaofeng,Li Yanping,Lin Shijie,Tian Wei
Oral cancer severely affects the quality of life of patients, and the primary treatment is surgery, due to a lack of specific drugs. Aloe emodin, a natural product of anthraquinone, is considered a potential antitumor drug. However, it has poor water solubility and low biological activity. In this study, we designed and synthesized a novel aloe emodin–hydroxyethyl piperazine hybrid dihydrochloride ( AE-NPC ), which improved the water solubility and antitumor activity of aloe emodin in vitro. According to the results, the IC 50 value of AE-NPC on CAL-27 cancer cells was 14.4 ± 2.9 μM. The flow cytometry results showed that AE-NPC induced the production of reactive oxygen species (ROS) and apoptosis in CAL-27 cells. The spectroscopy and molecular docking results showed that AE-NPC can be well intercalated into DNA grooves. Further molecular mechanism studies revealed that AE-NPC not only regulates the expression levels of key proteins (Bax/Bcl-2, cytochrome C, cleaved caspase-9 and cleaved caspase-3) of the mitochondrial apoptotic pathway but also activates the expression levels of a key protein ( γ -H 2 AX) of the DNA damage pathway. Therefore, AE-NPC induces CAL-27 cell apoptosis via DNA damage and mitochondrial pathways. This study provides new insights into the further development of anthraquinone compounds as potential chemotherapeutic agents for oral cancer treatment.
The novel aloe emodin derivative AE-NPC induces oral cancer CAL-27 cells apoptosis through ROS production, DNA damage and mitochondrial pathways. The anthraquinone compound AE-NPC may be a potential agent for the treatment of oral cancer.
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JOURNAL OF PHOTOCHEMISTRY AND PHOTOBIOLOGY B-BIOLOGY
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2024
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IF 3.9
Xian Xiao,Qiang Gao,Lan-Ying Wang,Yun-Fei Zhang,Yan-Ping Luo
An aromatic ring-containing compound with a wide range of biological activities, 9-methylacridine (AD-9-Me) is a precursor for the synthesis of various drugs. However, its photoactivation properties and mechanism of damage as a photo activator against Aedes aegypti are unknown. The toxic effects of AD-9-Me on Aedes aegypti mosquitoes were determined under light and non-light conditions. The results showed that the toxicity of AD-9-Me to mosquito larvae was significantly higher than that of the dark treatment after 24 h of light exposure; AD-9-Me was mainly distributed in the midgut of larvae, after 24 h of treatment, it can cause an increase in calcium ion concentration, reactive oxygen species (ROS) eruption and ROS accumulation by blocking the ROS elimination pathway in midgut cells. This in turn caused an increase in protein carbonyl and malondialdehyde (MDA) content, a decrease in mitochondrial membrane potential (MMP), a disruption of the barrier function of midgut tissues, a significant decrease in midgut weight and chitin content, which induced the up-regulation of AeDronc , AeCaspase8 and AeCaspase7 genes, leading to apoptotic cell death. In this study, we confirmed that AD-9-Me has photoactivation activity and mainly acts on the midgut of mosquito larvae, which can generate a large amount of ROS in the cells of the midgut and induce apoptosis to occur, resulting in the disruption of the function of the tissues of mosquito larvae, accelerating the death and delaying the development of the mosquito larvae.
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