HUMAN GENE THERAPY
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2020
·
IF 4.51
Kaihua Zhai,Boyu Liu,Lin Gao
Long-noncoding RNA taurine upregulated gene 1 (TUG1) participates in nervous system diseases, but its function in Parkinson's disease (PD) remains unclear. This study explored the function and mechanism of TUG1 in PD. A PD model was constructed using SH-SY5Y cells induced by 1-methyl-4-phenylpyridinium (MPP+) in vitro and mice treated by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in vivo. The expressions of TUG1, miR-152-3p, phosphatase and tensin homologue (PTEN), tyrosine hydroxylase (TH), and Bcl-2, and cleaved caspase-3 expressions were determined by quantitative reverse transcription-PCR and Western blotting. The viability, apoptosis, reactive oxygen species, and release of inflammatory factors from SH-SY5Y cells and substantia nigra tissues were detected by commercial kits. The interaction between TUG1 and miR-152-3p was analyzed by dual-luciferase reporter assay. Hematoxylin/eosin and immunohistochemical staining was performed for assessing the pathological damage and proportion of TH-positive cells. In PD cell model and mice model, TUG1 expression was upregulated and that of miR-152-3p was downregulated. Further research showed that TUG1 sponged and regulated miR-152-3p expression. Silencing of TUG1 not only protected SH-SY5Y cells against cell apoptosis, oxidative stress, and neuroinflammation in vitro, pathological damage and neuroinflammation in vivo, but also suppressed the expressions of PTEN and cleaved caspase-3, and increased the expressions of TH and Bcl-2 in MPP+-treated SH-SY5Y cells. However, the protective role of siTUG1 in SH-SY5Y cells was significantly inhibited by the miR-152-3p inhibitor. Thus, knocking down TUG1 might have a protective effect on PD through the miR-152-3p/PTEN pathway.
研究领域:
神经科学
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分子生物学
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病理学
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DOI
PubMed
高影响因子
MICROCHEMICAL JOURNAL
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2026
·
IF 5.2
Fanying Deng,Jinhong Xue,Yu Wang,Yue Sun,Peng Jiang,Yumeng Luo,Zhenqiang Liu,Zhichao Hao,Mengmeng Li,Wei Guan,Qingshan Chen,Lili Zhang,Xiaochi Ma,Haixue Kuang,Yan Liu
Extraction of Paeoniae Radix Rubra polysaccharide (PRRP). • Firstly, the PRRP was extracted by Natural Deep Eutectic Solvent (NADES). • Firstly, the PRRP was extracted by ChCl-CA (1.5, 3:2) with 40% ( w / w ) water. • AGREEprep and BAGI confirmed ChCl-CA’s greenness: polysaccharide yield >9%, solvent recovery >80%. • Firstly, the neuroprotective activity of PRRP in Parkinson's disease was evaluated. Firstly, natural deep eutectic solvents (NADES) were used to extract polysaccharides from Paeoniae Radix Rubra (PRR). Using polysaccharide yield and neuroprotective cell activity as evaluation criteria, a solvent composed of 40% ( w / w ) water, choline chloride (ChCl), and citric acid (CA) was selected as the optimal solvent. It exhibited low viscosity, high surface tension, moderate polarity, and strong acidity. Fourier-transform infrared (FT-IR) spectra of the ChCl-CA confirmed the formation of hydrogen bonding. Response surface methodology (RSM) optimized conditions: molar ratio: 1.5 (3:2), extraction temperature: 60 °C, extraction duration: 64 min, solvent-solid ratio: 36 mL·g −1 , the polysaccharide yield reached 16.74%, which was 1.89 times that of the hot water extraction, and the SH-SY5Y cell activity in the methyl-4-phenylpyridinium (MPP + )-induced PD model was 86.86%. The obtained PRR polysaccharides (PRRP) were further characterized, with protein content of 5.23% and uronic acid content of 19.09%. PRRP was mainly composed of arabinose, glucose, and galacturonic acid. Its molecular weights are 73.381, 11.475, and 3.539 kDa. PRRP was characterized via Ultraviolet-Visible (UV–Vis) and FT-IR spectroscopy, confirming typical polysaccharide structures. After 6 cycles, the polysaccharide yield of recycled NADES decreased from 16.26% to 9.22% in the final extraction, a 43.30% decrease. Two classical green evaluation models quantitatively confirmed the process's environmental friendliness. In addition, in vitro experiments showed that PRRP could increase dopamine (DA) and tyrosine hydroxylase (TH) levels, reduce lactate dehydrogenase (LDH) release, and decrease α -synuclein ( α -Syn) accumulation. This study highlights the efficiency of ChCl-CA as a green extractant and reveals the neuroprotective effect of PRRP. Download: Download high-res image (162KB) Download: Download full-size image Graphical abstract created in BioRender. com
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高影响因子
Scientific Reports
·
2024
·
IF 3.8
Si-Chun Gu,Zhi-Guo Xie,Min-Jue Gu,Chang-De Wang,Li-Min Xu,Chen Gao,Xiao-Lei Yuan,You Wu,Yu-Qing Hu,Yang Cao,Qing Ye
Ferroptosis is an iron-dependent cell death form characterized by reactive oxygen species (ROS) overgeneration and lipid peroxidation. Myricetin, a flavonoid that exists in numerous plants, exhibits potent antioxidant capacity. Given that iron accumulation and ROS-provoked dopaminergic neuron death are the two main pathological hallmarks of Parkinson’s disease (PD), we aimed to investigate whether myricetin decreases neuronal death through suppressing ferroptosis. The PD models were established by intraperitoneally injecting 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) into rats and by treating SH-SY5Y cells with 1-methyl-4-phenylpyridinium (MPP + ), respectively. Ferroptosis was identified by assessing the levels of Fe 2+ , ROS, malondialdehyde (MDA), and glutathione (GSH). The results demonstrated that myricetin treatment effectively mitigated MPTP-triggered motor impairment, dopamine neuronal death, and α-synuclein (α-Syn) accumulation in PD models. Myricetin also alleviated MPTP-induced ferroptosis, as evidenced by decreased levels of Fe 2+ , ROS, and MDA and increased levels of GSH in the substantia nigra (SN) and serum in PD models. All these changes were reversed by erastin, a ferroptosis activator. In vitro, myricetin treatment restored SH-SY5Y cell viability and alleviated MPP + -induced SH-SY5Y cell ferroptosis. Mechanistically, myricetin accelerated nuclear translocation of nuclear factor E2-related factor 2 (Nrf2) and subsequent glutathione peroxidase 4 (Gpx4) expression in MPP + -treated SH-SY5Y cells, two critical inhibitors of ferroptosis. Collectively, these data demonstrate that myricetin may be a potential agent for decreasing dopaminergic neuron death by inhibiting ferroptosis in PD.
研究领域:
神经科学
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药理学
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细胞生物学
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神经退行性疾病
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PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
·
2023
·
IF 5.4
Qiang-Ming Li,Tong Xu,Xue-Qiang Zha,Xiao-Wen Feng,Feng-Yun Zhang,Jian-Ping Luo
Ethnopharmacological relevance Parkinson's disease (PD) is the second neurodegenerative disease that lacks effective treatments. Buddlejasaponin IVb (BJP-IVb) is the main bioactive component of herbs in genus Clinopodium which display antioxidative, anti-inflammatory and neuroprotective activities. However, the role of BJP-IVb in PD still remains unknown. Aim of the study This study aimed to evaluate the effect of BJP-IVb on dopaminergic neurodegeneration in PD and clarified the underlying mechanisms from the aspect of iron overload-mediated ferroptosis . Materials and methods One-methyl-4-phenylpyridinium (MPP + ) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD models were established in this study. Behavioral tests, cell cytotoxicity assay , tyrosine hydroxylase (TH) and Nissl staining were performed to evaluate the antiparkinsonian effect of BJP-IVb. Cellular ultrastructure, iron content and lipid peroxidation were detected to evaluate iron overload-mediated dopaminergic neuron ferroptosis. Iron regulatory protein 2 (IRP2) and iron transport-related proteins were detected by immunofluorescence and Western blot to evaluated iron transport. Finally, plasmid vector-mediated IRP2 overexpression were performed to further clarify the molecular mechanism. Results BJP-IVb alleviated MPP + -induced neurotoxicity in vitro and improved MPTP-induced dopaminergic neuron loss and motor dysfunctions of PD mice, confirming an effect of BJP-IVb against dopaminergic neurodegeneration of PD. Further results revealed that BJP-IVb protected against PD by suppressing iron overload-mediated dopaminergic neuron ferroptosis, as evidenced by the attenuated lipid peroxidation, decreased iron content and changes in cellular ultrastructure. Finally, the decreased iron regulatory protein (IRP2) was confirmed to be responsible for BJP-IVb-mediated ferroptosis suppression by modulating iron transport-related proteins and alleviating iron overload. Conclusion BJP-IVb suppressed iron overload-mediated dopaminergic neuron ferroptosis and improved motor dysfunctions in PD, which was achieved by inhibiting IRP2-mediated iron overload. This study provided a potential drug candidate for the treatment of PD.
研究领域:
神经科学
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药理学
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民族药理学
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神经退行性疾病
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DOI
PubMed
高影响因子
Advanced Composites and Hybrid Materials
·
2021
·Vol. 4
·期 4
·979-988
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IF 5.693
Liang Chaobo,Du Yuzhang,Wang Yiyang,Ma Aijie,Huang Shan,Ma Zhonglei
Wood is widely used in the field of construction, decoration, and electronics, but its inherent flammability has serious fire hazards. As one of the fire-retardant treatment methods of wood, fire-resistant coatings have greatly reduced and prevented the occurrence of fires in the field of combustible materials. In this work, using melamine polyphosphate (MPP) as intumescent flame retardant, graphite nanoplates (GNPs) as synergistic flame retardant/conductive filler, and acrylic resin as film forming agent, GNPs/MPP/acrylic coatings with outstanding flame retardancy, excellent heat resistance, and ideal electromagnetic interference (EMI) shielding were prepared by a simple physical blending method. The results showed that GNPs and MPP significantly improved the flame retardancy, heat resistance, and EMI shielding of acrylic coatings. By adding 20 wt% of GNPs and 20 wt% of MPP, the limiting oxygen index (LOI) value, heat resistance index ( T HRI ), and EMI shielding effectiveness (SE) of GNPs/MPP/acrylic coating at the thickness of 40 μm reach 30% and 189.1 °C and 15 dB, respectively, which are better than those of pure acrylic coating (19%, 181.0 °C, and 0.1 dB). This intumescent fire-retardant coating with excellent flame retardancy, good heat resistance, and ideal EMI shielding performances has broad application prospects in the fields of construction, decoration, and electronics. Graphical abstract Fire-retardant mechanism and combustion diagram of GNPs/MPP/acrylic resin coated wood
研究领域:
建筑材料
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消防安全
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纳米技术
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电磁屏蔽
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DOI
高影响因子
Chinese Medicine
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2024
·Vol. 19
·期 1
·1-24
·
IF 5.3
Cao Ting,Wang Xue-lian,Rao Jiang-yan,Zhu Hui-feng,Qi Hong-yi,Tian Zhen
Background Parkinson’s disease (PD) is a chronic neurodegenerative disorder that currently has no curable strategies. More and more evidence suggests that endoplasmic reticulum (ER) stress plays an essential role in PD pathogenesis. Periplaneta americana L. ( P. americana ) is a traditional Chinese medicine with diverse therapeutic properties. This study aims to investigate the neuroprotective effect and underlying mechanism of P. americana in in vitro and in vivo PD models. Methods The exposure of SH-SY5Y cells to 1-methyl-4-phenyl-pyridinium (MPP + ) was used as the in vitro PD model. MTT assay, Hoechst staining, Calcein AM-PI staining and flow cytometry were performed to measure the cell viability and apoptosis. DCFH-DA and JC-1 assay were used to measure the intracellular ROS and mitochondrial membrane potential (Δψm), respectively. Western-blot and immunostaining were conducted to detect the expression of key molecules related with ER stress. For the in vivo PD model induced by 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydro-pyridine (MPTP), the motor function of mice was assessed by behavioral tests, the level of TH was examined by western-blot and immunostaining, the expression of key molecules related with ER stress was measured by western-blot. Results Periplaneta americana ethanol extract (PAE) concentration-dependently inhibited MPP + -induced cell loss and increased cell viability. PAE also remarkably attenuated ROS accumulation, the decline of Δψm as well as the excessive ER stress. The neuroprotective effects of PAE could be blocked by ROS inducer trimethylamine N-Oxide or ER stress activator tunicaymycin, while the antioxidant N-Acetyl-L-cysteine or ER stress inhibitor sodium 4-phenylbutyrate mimicked the effects of PAE. Furthermore, we found that PAE could activate AKT/GSK3β/β-catenin pathway. The effect of PAE on ROS production, Δψm and ER stress was blocked by AKT inhibitor MK-2206. In in vivo model, PAE significantly improved motor function, prevented dopaminergic neuronal loss and attenuated ER stress in substantia nigra and striatum of MPTP-treated mice. Similarly, the effects of PAE on MPTP-treated mice were also abolished by MK-2206. Conclusions Our results suggest that P. americana exerts neuroprotective effects through inhibiting ER stress via AKT-dependent pathway. Periplaneta americana may represent a promising therapeutic agent for PD treatment and is worthy of further being exploited.
研究领域:
神经学
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药理学
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传统中药
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细胞生物学
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实验模型
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DOI
PubMed
高影响因子
JOURNAL OF DRUG DELIVERY SCIENCE AND TECHNOLOGY
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2022
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IF 5.062
Dickson Pius Wande,Yue Qiu,Shijie Chen,Lan Yao,Yanghui Xu,Jing Yao,Hui Xiong
Oxaliplatin (OXA) and rapamycin (RAPA) combination therapy have shown the advantages of synergistically inhibiting the growth of cancer cells by enhancing apoptosis in cancerous cell lines. However, drug resistance and the lack of an orally administered formulation which exhibited the best clinical dosing compliance limited the clinical application of this regimen. Here, we report a nanogel-polymersomes drug delivery system (i.e.TMOR-CDAN) based on modified chitosan, chitosan diacetate (CDA), methoxy-poly-(ethylene glycol)-b-poly (lactide) (MPP), and D-alpha-tocopheryl polyethylene glycol succinate (TPGS) with permeation-glycoprotein (P-gp) inhibition capability for enhancing the oral chemotherapy efficacy of erroneously soluble RAPA and its synergistic chemotherapy with OXA. Hydrophilic OXA and hydrophobic RAPA were co-loaded using MPP and TPGS-based polymer capsules (i.e. TMOR), which were further coated by chitosan-modified gel to form TMOR-CDAN. The TMOR-CDAN displayed higher stability in both acidic and basic pH than free OXA and RAPA and could withstand the harsh gastric environmental conditions, preventing the burst drugs release while releasing the co-loaded drugs in a sustained and controlled manner. The dual-drug-loaded TMOR-CDAN provides a bifunctional platform for synergistic tumor therapy. Compared with the single drug OXA, RAPA, or the OXA and RAPA mixtures (OR), the TMOR-CDAN showed more outstanding in vitro cytotoxicity and in vivo antitumor chemotherapeutic efficacy, endowing the TMOR-CDAN with a prodigious potential for futuristic cancer chemotherapy .
研究领域:
药学
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纳米技术
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癌症研究
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药物递送系统
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DOI
高影响因子
POLYMER TESTING
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2020
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IF 3.275
Zaihang Zheng,Chenchen Liao,Yurou Xia,Yuhang Liu,Boya Dai,Anbo Li
In this article, co-microencapsulation technology was utilized for decorating the surface of dialdehyde starch (DAS) and melamine polyphosphate (MPP) via one-step process. The aim for this design was to improve the dispersion for DAS and MPP in polypropylene (PP) and employ DAS as sustainable char-forming agent, which lied in enhancing the flame retardancy of PP. In view of chemical composition , morphology and surface wettability , the changes for DAS and MPP after modification were confirmed by energy dispersive spectrometer (EDS), scanning electron microscope (SEM) and water contact angle (WCA) tests, respectively. Most of all, the results for flame retardant tests demonstrated limiting oxygen index (LOI) value and vertical burning tests (UL-94) rating of PP/30 ph M[M&D] were 28.2% and V-1. Along with the synergistic effect, the homogeneous dispersion of DAS and MPP in PP after co-microencapsulation modification was also one of main reasons for the increased flame retardant properties. Except that, the chemical interaction between DAS and MPP in producing the char layer was also certified by TGA curves. After systematic analysis on char residue, the possible intumescent flame retardant mechanism was primarily proposed.
研究领域:
材料科学
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化学工程
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高分子科学
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消防安全工程
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DOI
高影响因子
CHEMICO-BIOLOGICAL INTERACTIONS
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2024
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IF 4.7
Changfeng Zhong,Changmei Wang,Wei Li,Wenyuan Li,Xuemei Chen,Jieqing Guo,Yifan Feng,Xia Wu
Parkinson's disease (PD) is the fastest growing neurodegenerative disease in the world at present. Neuroinflammation plays an important role in Parkinson's disease. In our study, we initially screened magnolol/honokiol derivatives synthesized by our group for their potential anti-neuroinflammatory properties. This was done using LPS-activated BV-2 microglial cell and MPP + -induced PC-12 cell models. Most of derivatives had increased anti-inflammatory activities and decreased toxicities compared to raw materials. Then, compounds were scored with inflammatory factors IL-1β, TNF-α and IL-6 by molecular docking in silico . Our studies revealed the strongest binding compound HM568 which binds with honokiol and metformin. Furthermore, HM568 showed no acute toxicity in mice through acute toxicity. And it is stable under high temperature, high humidity and strong light irradiation. Combining cell experiments and computer results, HM568 was considered for further in vivo pharmacological validations. Intraperitoneal injection administration of MPTP into C57BL/6 mice was utilized as Parkinson's animal model. Results showed that administration of HM568 for 14 days in MPTP-PD mice led to a significant alleviation in weight loss and movement disorders. Further HM568 could significantly down-regulate the expression levels of inflammatory factors IL-1β, IL-6 and TNF-α in brain tissue of the mouse model, reduce the level of caspase-3 and the ratio of Bcl-2/Bax, and up-regulate the level of transforming factor TGF-β, thus producing anti-apoptosis and anti-neuroinflammatory effects on neuronal cells. In terms of pathological features, HM568 could reduce the infiltration of neuronal cells and alleviate the development of lesions, promote the transformation of microglia from M1 negative phenotype to M2 type, and reverse the reduction of TH-positive immune cells in mouse neurons induced by MPTP. The administration of HM568 could reduce the abnormal accumulation of α-syn, and thus produce neuroprotective effect on MPTP-PD mice. Cell experiments, molecular docking and animal experiments thus depict HM568 as a promising agent to delay neuronal degeneration in PD, and its mechanism is related to anti-neuroinflammation.
研究领域:
神经科学
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药理学
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神经退行性疾病
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炎症
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药物发现
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DOI
PubMed
高影响因子
ACS Applied Materials & Interfaces
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2022
·
IF 10.383
Wei Wang,Jinyang Zheng,Hao Zhou,Qiang Liu,Li Jia,Xiuming Zhang,Dongtao Ge,Wei Shi,Yanan Sun
Overproduction of reactive oxygen species (ROS) and cumulative oxidative stress induce the degeneration of neuromelanin-containing dopaminergic neurons in the substantia nigra pars compacta (SNpc) of PD patients. Due to its redox property, melanin-like polydopamine (PDA) has been studied for its ability to remove ROS with a series of antioxidant enzyme mimetic activities including superoxide dismutase (SOD) and catalase (CAT). Glutathione peroxidase (GPx) is important for maintaining ROS metabolic homeostasis, but only a few GPx-like nanozymes have been studied for in vivo therapy. As we know, selenocysteine is essential for the antioxidant activity of GPx. Hence, we co-synthesized PDA with selenocystine (SeCys) to prepare a nanocomposite (PDASeCys) with GPx-like activity. The results showed that the PDASeCys nanocomposite has the same CAT and SOD enzymatic activities as PDA but better free radical scavenging efficiency and additional GPx enzymatic activity than PDA. In the 1-methyl-4-phenyl-pyridine ion (MPP+)-induced PD cell model, PDASeCys could increase intracellular GPx levels effectively and protect SH-SY5Y neuronal cells from oxidative stress caused by MPP+. In vivo, the PDASeCys nanocomposite effectively inhibited 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridinium (MPTP)-induced Parkinson-related symptoms of mice when it was injected into the substantia nigra (SN). This polydopamine-based nanocomposite containing selenocystine with a variety of enzymatic activities including GPx-like activity synthesized by a one-pot method provides convenience and safety in the neuromelanin-like nanozyme-based therapeutic strategy for oxidative stress-induced PD.
研究领域:
神经科学
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纳米技术
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药学
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生物化学
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DOI
PubMed
高影响因子
CELLULAR SIGNALLING
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2024
·
IF 4.4
Wentao Hu,Menghan Wang,Guifang Sun,Limin Zhang,Hong Lu
Parkinson's disease (PD) is a gradually debilitating neurodegenerative syndrome. Here, we analyzed GSE7621 chip data obtained from the Gene Expression Omnibus (GEO) database to explore the pathogenesis of PD. Early B Cell Factor 3 (EBF3), a member of the highly evolutionarily conserved EBF-transcription factor family, is involved in neuronal development. EBF3 expression is low in the substantia nigra of patients with PD. However, whether EBF3 is implicated in dopaminergic neuron death during PD has not yet been investigated. Therefore, we aimed to reveal the potential anti-apoptotic effect and molecular mechanism of EBF3 in PD. We established a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model in vivo and a 1-methyl-4-phenylpyridine (MPP + )-induced SH-SY5Y cell model in vitro . EBF3 was downregulated in the substantia nigra of PD mice and SH-SY5Y cells treated with MPP + , and the m6A methylation modification level was low. Fat mass and obesity-associated protein (FTO) siRNA upregulated m6A methylation modification of EBF3 and extended the EBF3 mRNA half-life. Functionally, as demonstrated by the results of the open-field test, pole test and gait analysis, EBF3 overexpression ameliorated MPTP-induced behavioral disorder. Further, EBF3 overexpression suppressed neuronal apoptosis in vivo , as evidenced by decreased TUNEL + cells, and the increased activation of caspase-3 and caspase-9. Similar results were obtained in vitro , as reflected by increased cell viability, decreased LDH activity and restored mitochondrial function, collectively protecting SH-SY5Y cells from MPP + -induced apoptosis. Mechanistically, the results of luciferase reporter, ch-IP and DNA pull-down assays confirmed that, as a transcription factor, EBF3 bound to the promoter of CNTNAP4 (a protein associated with neuronal differentiation) and directly regulated CNTNAP4 transcription. Strikingly, CNTNAP4 knockdown markedly abolished the effect of EBF3 on cell apoptosis, thus aggravating PD. In conclusion, the low level of m6A methylation modification may contribute to the low expression of EBF3 during PD. Additionally, EBF3 attenuates PD by activating CNTNAP4 transcription, suggesting that EBF3 may be a novel therapeutic target in PD.
研究领域:
神经科学
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分子生物学
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转化医学
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产品关联
DOI
PubMed
高影响因子
Advanced Healthcare Materials
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2024
·
IF 10
Ruxia Liu,Ting Zhou,Xinsheng Li,Quan Zou,Jiaojiao Yu,Jingjing Ye,Wenhui Wang,Yan Zhou,Shao-Kai Sun
Pulmonary hypertension (PH) is a life-threatening cardiovascular disease with a lack of effective treatment options. Nanozymes, though promising for PH therapy, pose safety risks due to their metallic nature. Here, a non-metallic nanozyme is reported for the treatment of monocrotaline (MCT)-induced PH with a therapeutic mechanism involving the ROS/TGF-β1 signaling. The synthesized melanin-polyvinylpyrrolidone-polyethylene glycol (MPP) nanoparticles showcase ultra-small size, excellent water solubility, high biocompatibility, and remarkable antioxidant capacity. The MPP nanoparticles are capable of effectively eliminating ROS in isolated pulmonary artery smooth muscle cells (PASMCs) from PH rats, and significantly reduce PASMC proliferation and migration. In vivo results from a PH model demonstrate that MPP nanoparticles significantly increase pulmonary artery acceleration time, decrease wall thickening and PCNA expression in lung tissues, as evidenced by echocardiograpy, histology and immunoblot analysis. Additionally, MPP nanoparticles treatment improve running capacity, decrease Fulton index, and attenuate right ventricular fibrosis in MCT-PH rats by using treadmill test, picrosirius red, and trichrome Masson staining. Further transcriptomic and biochemical analyses reveal that inhibiting ROS-driven activation of TGF-β1 in the PA is the mechanism by which MPP nanoparticles exert their therapeutic effect. This study provides a novel approach for treating PH with non-metallic nanozymes based on a well-understood mechanism.
研究领域:
纳米技术
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心血管疾病
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药理学
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生物医学工程
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DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）