Silica nanoparticle

二氧化硅纳米颗粒
  • 文章类型: Journal Article
    设计并验证了制备具有自修复性能的高疏水复合材料的概念。这种新材料是基于结晶的疏水性氟蜡的复合材料,由褐煤蜡和全氟乙烯醇合成,与配备有疏水壳的球形二氧化硅纳米颗粒结合。使用疏水性结晶蜡和二氧化硅纳米颗粒的这种组合制备高度排斥层。我们概念的新颖方面是制备疏水壳的梯状结构,允许包含一定份额的蜡分子。在混合过程中被捕获在疏水结构中的蜡分子被阻止结晶;因此,与结晶分子相比,这些分子保持更高的迁移率。当复合材料的薄层受到机械损伤时,流动的蜡分子可以在一定程度上迁移和修复缺陷。描述了复合材料的一般制备方法,XRD分析表明,复合材料中一定比例的蜡分子被阻碍结晶。此外,我们表明,得到的材料可以恢复其排斥性能后的表面损伤。
    A concept to prepare a highly hydrophobic composite with self-healing properties has been designed and verified. The new material is based on a composite of a crystalline hydrophobic fluoro wax, synthesized from montan waxes and perfluoroethylene alcohols, combined with spherical silica nanoparticles equipped with a hydrophobic shell. Highly repellent layers were prepared using this combination of a hydrophobic crystalline wax and silica nanoparticles. The novel aspect of our concept was to prepare a ladder-like structure of the hydrophobic shell allowing the inclusion of a certain share of wax molecules. Wax molecules trapped in the hydrophobic structure during mixing are hindered from crystallizing; therefore, these molecules maintain a higher mobility compared to crystallized molecules. When a thin layer of the composite material is mechanically damaged, the mobile wax molecules can migrate and heal the defects to a certain extent. The general preparation of the composite is described and XRD analysis demonstrated that a certain share of wax molecules in the composite are hindered to crystallize. Furthermore, we show that the resulting material can recovery its repellent properties after surface damage.
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  • 文章类型: Journal Article
    合成了分子印迹二氧化硅纳米颗粒(SP-MIP),用于实时光学检测低分子量化合物。偶氮引发剂改性的二氧化硅珠通过可逆加成-断裂链转移(RAFT)聚合进行官能化,这导致对接枝层的有效控制。甲基丙烯酸(MAA)和乙二醇二甲基丙烯酸酯(EDMA)在偶氮引发剂包覆的二氧化硅颗粒(≈100nm)上的共聚使用链转移剂(2-苯基丙-2-基二硫代苯甲酸酯)在目标分析物分子(1-Boc-苯丙氨酸苯胺,l-BFA)。通过扫描电子显微镜对SP-MIP的化学和形态特性进行了表征,X射线光电子能谱,Brunauer-Emmett-Teller表面分析,和热重分析。最后,SP-MIP位于金表面上,用作表面等离子体共振光谱仪(SPR)上的生物识别层。敏感性,响应时间,和SP-MIP的选择性通过三个相似的类似分子(l-Boc-色氨酸,l-Boc-酪氨酸,和l-Boc-苯丙氨酸),并且印迹颗粒表面对l-Boc-苯丙氨酸(l-BFA)显示出优异的相对选择性(k=61),而灵敏度记录为检测限=1.72×10-4m。
    Molecularly imprinted silica nanoparticles (SP-MIP) are synthesized for the real-time optical detection of low-molecular-weight compounds. Azo-initiator-modified silica beads are functionalized through reversible addition-fragmentation chain transfer (RAFT) polymerization, which leads to efficient control of the grafted layer. The copolymerization of methacrylic acid (MAA) and ethylene glycol dimethacrylate (EDMA) on azo initiator-coated silica particles (≈100 nm) using chain transfer agent (2-phenylprop-2-yl-dithiobenzoate) is carried out in the presence of a target analyte molecule (l-Boc-phenylalanine anilide, l-BFA). The chemical and morphological properties of SP-MIP are characterized by scanning electron microscopy, X-ray photoelectron spectroscopy, Brunauer-Emmett-Teller surface analysis, and thermogravimetric analysis. Finally, SP-MIP is located on the gold surface to be used as a biorecognition layer on the surface plasmon resonance spectrometer (SPR). The sensitivity, response time, and selectivity of SP-MIP are investigated by three similar analogous molecules (l-Boc-Tryptophan, l-Boc-Tyrosine, and l-Boc-Phenylalanine) and the imprinted particle surface showed excellent relative selectivity toward l-Boc-Phenylalanine (l-BFA) (k = 61), while the sensitivity is recorded as limit of detection = 1.72 × 10-4 m.
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  • 文章类型: Journal Article
    纳米粒子具有有用的功能,因为它们的比表面积增加赋予它们的特性,它们已经在各种工业领域的产品中实际使用。尽管孕妇在日常生活中接触纳米粒子是不可避免的,缺乏评估纳米颗粒对孕妇毒性的研究。为了纠正这个问题,我们专注于胎盘,并且先前发现纳米颗粒可以显示胎盘毒性。然而,关于纳米颗粒在胎盘细胞内的行为仍然知之甚少,这将使我们了解他们的行动方式。这里,我们试图阐明二氧化硅纳米颗粒在胎盘细胞内的定位,以及这如何影响胎盘毒性。我们分析了直径为10nm(nSP10)的二氧化硅纳米颗粒在JEG-3细胞中的摄取,人类绒毛膜癌细胞系。流式细胞术分析显示,用红色荧光标记的nSP10被JEG-3细胞吸收,内吞抑制剂细胞松弛素D的预处理抑制了它们的摄取,表明nSP10通过内吞途径被JEG-3细胞吸收。此外,共聚焦显微镜显示nSP10明显位于溶酶体中。用LysoTracker染色显示nSP10处理增加了JEG-3细胞的酸性区室,提示溶酶体积聚和肿胀.这些结果表明,进入胎盘细胞的nSP10被转移到溶酶体中,并可能导致溶酶体功能障碍。
    Nanoparticles have useful functions due to the characteristics conferred on them by an increase in their specific surface area, and they have already been put into practical use in products in various industrial fields. Although exposure to nanoparticles in daily life is unavoidable for pregnant women, studies that evaluate the toxicity of nanoparticles in pregnant women are lacking. To redress this, we have focused on the placenta and have previously revealed that nanoparticles can show placental toxicity. However, there is still little knowledge regarding the behavior of nanoparticles within placental cells, which would enable us to understand their mode of action. Here, we tried to clarify the intracellular localization of silica nanoparticles in placental cells and how this affects placental toxicity. We analyzed the uptake of silica nanoparticles with a diameter of 10 nm (nSP10) into JEG-3 cells, a human choriocarcinoma cell line. Flow cytometry analysis showed that nSP10 labelled with red fluorescence were taken up into JEG-3 cells, and that pre-treatment with the endocytosis inhibitor cytochalasin D inhibited their uptake, suggesting that nSP10 are taken up into JEG-3 cells by the endocytic pathway. Moreover, confocal microscopy revealed that nSP10 are prominently localized in lysosomes. Staining with LysoTracker showed that nSP10 treatment increased the acidic compartment of JEG-3 cells, suggesting lysosome accumulation and swelling. These results indicate that nSP10 taken into placental cells are transferred to lysosomes and may cause lysosomal dysfunction.
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  • 文章类型: Journal Article
    背景:二氧化硅纳米颗粒(SNPs)在生物医学研究中具有巨大的潜力,特别是在药物输送和成像应用中,由于它们的稳定性和与生物实体如组织或细胞的最小相互作用。
    结果:使用花青3.5、5.5和7(Cy3.5、Cy5.5和Cy7)合成和表征花青染料掺杂的荧光SNP(CSNP)。通过系统分析,我们辨别变化的表面电荷和荧光性质的纳米粒子取决于封装的染料-(3-氨基丙基)三乙氧基硅烷共轭,而它们的大小和形状保持不变。荧光发射光谱表现出与染料浓度增加相关的红移,这归因于级联能量转移和自猝灭效应。此外,荧光信号强度与颗粒浓度呈线性关系,特别是在较低的染料当量下,表明适用于成像应用的强大性能。体外评估显示,纳米颗粒的细胞毒性和有效的细胞摄取可忽略不计,实现长期跟踪和成像。通过小鼠体内成像进行的验证强调了CSNP的多功能性和功效,在皮下组织环境中显示单切换成像能力和线性信号增强。
    结论:这项研究为设计荧光成像和优化生物医学研究中基于纳米粒子的应用提供了有价值的见解,对靶向药物递送和组织结构和器官的体内成像具有潜在的影响。
    BACKGROUND: Silica nanoparticles (SNPs) have immense potential in biomedical research, particularly in drug delivery and imaging applications, owing to their stability and minimal interactions with biological entities such as tissues or cells.
    RESULTS: With synthesized and characterized cyanine-dye-doped fluorescent SNPs (CSNPs) using cyanine 3.5, 5.5, and 7 (Cy3.5, Cy5.5, and Cy7). Through systematic analysis, we discerned variations in the surface charge and fluorescence properties of the nanoparticles contingent on the encapsulated dye-(3-aminopropyl)triethoxysilane conjugate, while their size and shape remained constant. The fluorescence emission spectra exhibited a redshift correlated with increasing dye concentration, which was attributed to cascade energy transfer and self-quenching effects. Additionally, the fluorescence signal intensity showed a linear relationship with the particle concentration, particularly at lower dye equivalents, indicating a robust performance suitable for imaging applications. In vitro assessments revealed negligible cytotoxicity and efficient cellular uptake of the nanoparticles, enabling long-term tracking and imaging. Validation through in vivo imaging in mice underscored the versatility and efficacy of CSNPs, showing single-switching imaging capabilities and linear signal enhancement within subcutaneous tissue environment.
    CONCLUSIONS: This study provides valuable insights for designing fluorescence imaging and optimizing nanoparticle-based applications in biomedical research, with potential implications for targeted drug delivery and in vivo imaging of tissue structures and organs.
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  • 文章类型: Journal Article
    喜树碱(CPT)的治疗效果,一种有效的抗肿瘤生物碱,受到其疏水性质和不稳定性的阻碍,限制了其在治疗皮肤鳞状细胞癌(SCC)中的临床使用。这项研究介绍了一种新型的纳米药物递送系统(NDDS),利用功能化的介孔二氧化硅纳米颗粒(FMSNs)进行有效的CPT递送。用CPT加载FMSN,随后用壳聚糖(CS)包被以增强稳定性和生物粘附性。重要的是,CpG寡脱氧核苷酸(CpGODN)连接到CS包被的FMSN上,以利用CpGODN的免疫刺激特性,增强化疗的疗效。最终制剂FMSN-CPT-CS-CpG显示出241nm的平均尺寸和0.316的PdI,包封效率为95%。全面的体外和体内分析,包括B16F10细胞和DMBA/TPA诱导的SCC小鼠模型,证明了FMSN-CPT-CS-CpG制剂显着增强了对B16F10细胞的细胞毒性,并在40%的体内受试者中诱导了完全消退,超越标准CPT和FMSN-CPT治疗的疗效。这项研究强调了在NDDS中联合化疗和免疫治疗剂的潜力,有效的皮肤癌治疗。
    The therapeutic efficacy of camptothecin (CPT), a potent antitumor alkaloid, is hindered by its hydrophobic nature and instability, limiting its clinical use in treating cutaneous squamous cell carcinoma (SCC). This study introduces a novel nano drug delivery system (NDDS) utilizing functionalized mesoporous silica nanoparticles (FMSNs) for efficient CPT delivery. The FMSNs were loaded with CPT and subsequently coated with chitosan (CS) for enhanced stability and bioadhesion. Importantly, CpG oligodeoxynucleotide (CpG ODN) was attached onto the CS-coated FMSNs to leverage the immunostimulatory properties of CpG ODN, augmenting the chemotherapy\'s efficacy. The final formulation FMSN-CPT-CS-CpG displayed an average size of 241 nm and PDI of 0.316 with an encapsulation efficiency of 95 %. Comprehensive in vitro and in vivo analyses, including B16F10 cells and DMBA/TPA-induced SCC murine model, demonstrated that the FMSN-CPT-CS-CpG formulation significantly enhanced cytotoxicity against B16F10 cells and induced complete regression in 40 % of the in vivo subjects, surpassing the efficacy of standard CPT and FMSN-CPT treatments. This study highlights the potential of combining chemotherapeutic and immunotherapeutic agents in an NDDS for targeted, efficient skin cancer treatment.
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  • 文章类型: Journal Article
    无定形二氧化硅纳米颗粒(SiNPs)的利用在各种应用中越来越受欢迎,但它对人类和环境健康构成了潜在的风险。然而,SiNPs诱导的肾损伤的根本原因和机制在很大程度上仍然未知.
    本研究旨在研究SiNPs对肾脏的损伤,并进一步探讨SiNPs引起肾脏毒性的可能机制。
    将30只成年雄性大鼠分为3组。第2组和第3组的大鼠以2个剂量水平(25和100mg/kg体重)给予SiNPs,对照组大鼠28天未接受治疗。活性氧(ROS),抗氧化酶活性(谷胱甘肽过氧化物酶[GPx],超氧化物歧化酶[SOD],和过氧化氢酶[CAT]),谷胱甘肽(GSH)水平,并分析了肾脏组织中的氧化标志物(例如脂质过氧化[丙二醛(MDA)]和蛋白质氧化[蛋白质羰基(PCO)])。此外,通过组织病理学检查和纤维化生物标志物的表达水平研究了肾纤维化发生。
    这些发现揭示了用SiNP的体内治疗以剂量依赖的方式显著地触发了肾组织中的氧化应激。其特点是ROS产量增加,MDA水平升高,PCO,和一氧化氮(NO),随着SOD活性的显著下降,CAT,GPx,减少GSH。这些变化与组织病理学分析一致,这表明间质纤维化与单核炎症细胞聚集,管状变性,肾小球肾炎,和肾小球萎缩。使用Masson三色染色确认纤维化指数。此外,纤维化相关基因显著上调,包括转化生长因子-β1(TGF-β1),基质金属蛋白酶2和9(MMP-2/9),而金属蛋白酶组织抑制因子2(TIMP2)的表达下调。
    本研究为ROS和下调TGF-β信号通路在SiNPs肾毒性中的作用提供了新的研究线索。
    UNASSIGNED: The utilization of amorphous silica nanoparticles (SiNPs) is gaining popularity in various applications, but it poses a potential risk to human and environmental health. However, the underlying causes and mechanisms of SiNPs-induced kidney damage are still largely unknown.
    UNASSIGNED: This study aimed to investigate the SiNPs-induced damage in the kidney and further explore the possible mechanisms of SiNPs-induced nephrotoxicity.
    UNASSIGNED: Thirty adult male rats were divided into 3 different groups. Rats in groups 2 and 3 were administered SiNPs at 2 dosage levels (25 and 100 mg/kg of body weight), while the rats in the control group received no treatment for 28 days. Reactive oxygen species (ROS), antioxidant enzyme activities (glutathione peroxidase [GPx], superoxide dismutase [SOD], and catalase [CAT]), glutathione (GSH) levels, and oxidation markers (such as lipid peroxidation [malondialdehyde (MDA)] and protein oxidation [protein carbonyl (PCO)]) were analyzed in the kidney tissue. Additionally, renal fibrogenesis was studied through histopathological examination and the expression levels of fibrotic biomarkers.
    UNASSIGNED: The findings revealed that in vivo treatment with SiNPs significantly triggered oxidative stress in kidney tissues in a dose-dependent manner. This was characterized by increased production of ROS, elevated levels of MDA, PCO, and nitric oxide (NO), along with a significant decline in the activities of SOD, CAT, GPx, and reduced GSH. These changes were consistent with the histopathological analysis, which indicated interstitial fibrosis with mononuclear inflammatory cell aggregation, tubular degeneration, glomerulonephritis, and glomerular atrophy. The fibrosis index was confirmed using Masson\'s trichrome staining. Additionally, there was a significant upregulation of fibrosis-related genes, including transforming growth factor-beta 1 (TGF-β1), matrix metalloproteinases 2 and 9 (MMP-2/9), whereas the expression of tissue inhibitor of metalloproteinase 2 (TIMP2) was downregulated.
    UNASSIGNED: This study provided a new research clue for the role of ROS and deregulated TGF-β signaling pathway in SiNPs nephrotoxicity.
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  • 文章类型: Editorial
    当前治疗癌症方法的缺点正在推动对新型癌症的需求,创新策略,减少与化疗相关的毒性,并提高免疫治疗的有限疗效。我们认为通过合适的递送系统双重递送小干扰RNA(siRNA),有或没有相关的,额外,小分子治疗剂,将预示癌症治疗效率的新时代。
    The shortcomings of current approaches to treating cancer are driving the need for novel, innovative strategies that reduce the toxicity associated with chemotherapy and improve on the limited efficacy of immunotherapy. We believe that dual delivery of small interfering RNA (siRNA) via a suitable delivery system, with or without a relevant, additional, small-molecule therapeutic agent, will herald new era of treatment efficiency in cancer.
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  • 文章类型: Journal Article
    二氧化硅纳米颗粒(SiNP)暴露诱导严重的肺部炎症和纤维化,但其发病机制尚不清楚,目前缺乏有效的治疗方法。探讨SiNPs诱导肺纤维化的机制,我们构建了体内二氧化硅暴露动物模型和体外二氧化硅诱导的巨噬细胞焦亡和成纤维细胞转分化模型。我们发现,SiNP暴露引起与焦亡相关的肺蛋白上调,包括NLRP3,ASC,IL-1β,和GSDMD,而免疫荧光染色将NLRP3和GSDMD与巨噬细胞特异性生物标志物F4/80共定位在暴露于二氧化硅的肺组织中。然而,研究发现,NLRP3抑制剂MCC950和经典抗纤维化药物吡非尼酮(PFD)能够缓解二氧化硅诱导的肺胶原沉积.在体外研究中,我们将成纤维细胞暴露于二氧化硅诱导的变性巨噬细胞的条件培养基中,发现α-SMA的表达增强,提示成纤维细胞向肌成纤维细胞转分化增加。根据体内研究,MCC950和PFD的联合治疗被证明可以抑制α-SMA的表达并减弱成纤维细胞转分化。机械上,我们对不同处理的成纤维细胞进行高通量RNA测序,发现松弛素和破骨细胞分化通路的激活信号,其中检查了这两种途径中失调基因的表达,发现在体外和体内均发生了一致的变化。总的来说,我们的研究表明,SiNP暴露诱导巨噬细胞焦亡,随后导致成纤维细胞转分化为肌成纤维细胞,其中松弛素和破骨细胞分化信号通路起关键作用。这些发现可能为开发肺纤维化的新疗法提供有价值的参考。
    Silica nanoparticle (SiNP) exposure induces severe pulmonary inflammation and fibrosis, but the pathogenesis remains unclear, and effective therapies are currently lacking. To explore the mechanism underlying SiNPs-induced pulmonary fibrosis, we constructed in vivo silica exposure animal models and in vitro models of silica-induced macrophage pyroptosis and fibroblast transdifferentiation. We found that SiNP exposure elicits upregulation of pulmonary proteins associated with pyroptosis, including NLRP3, ASC, IL-1β, and GSDMD, while the immunofluorescence staining co-localized NLRP3 and GSDMD with macrophage-specific biomarker F4/80 in silica-exposed lung tissues. However, the NLRP3 inhibitor MCC950 and classical anti-fibrosis drug pirfenidone (PFD) were found to be able to alleviate silica-induced collagen deposition in the lungs. In in vitro studies, we exposed the fibroblast to a conditioned medium from silica-induced pyroptotic macrophages and found enhanced expression of α-SMA, suggesting increased transdifferentiation of fibroblast to myofibroblast. In line with in vivo studies, the combined treatment of MCC950 and PFD was demonstrated to inhibit the expression of α-SMA and attenuate fibroblast transdifferentiation. Mechanistically, we adopted high throughput RNA sequencing on fibroblast with different treatments and found activated signaling of relaxin and osteoclast differentiation pathways, where the expression of the dysregulated genes in these two pathways was examined and found to be consistently altered both in vitro and in vivo. Collectively, our study demonstrates that SiNP exposure induces macrophage pyroptosis, which subsequently causes fibroblast transdifferentiation to myofibroblasts, in which the relaxin and osteoclast differentiation signaling pathways play crucial roles. These findings may provide valuable references for developing new therapies for pulmonary fibrosis.
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  • 文章类型: Journal Article
    最近,二氧化硅纳米粒子(NP)作为嵌入贵金属的生物相容性和稳定的模板已经引起了相当大的关注。嵌入贵金属的二氧化硅NP利用新型金属的优异光学特性,同时克服了单个新型金属NP的局限性。此外,在二氧化硅核周围装饰有小金属NP的金属嵌入二氧化硅NP的结构导致局部表面等离子体共振和表面增强拉曼散射中的强信号增强。这篇综述总结了最近对金属嵌入二氧化硅纳米粒子的研究,专注于他们独特的设计和应用。嵌入金属的二氧化硅NP的特性取决于嵌入金属的类型和结构。基于这一进展,金属嵌入二氧化硅NP目前用于各种光谱应用,作为纳米酶,探测和成像探头,药物携带者,光热诱导器,和生物活化分子筛选标识符。由于他们多才多艺的角色,金属嵌入二氧化硅NPs有望应用于各个领域,比如生物学和医学,在未来。
    Recently, silica nanoparticles (NPs) have attracted considerable attention as biocompatible and stable templates for embedding noble metals. Noble-metal-embedded silica NPs utilize the exceptional optical properties of novel metals while overcoming the limitations of individual novel metal NPs. In addition, the structure of metal-embedded silica NPs decorated with small metal NPs around the silica core results in strong signal enhancement in localized surface plasmon resonance and surface-enhanced Raman scattering. This review summarizes recent studies on metal-embedded silica NPs, focusing on their unique designs and applications. The characteristics of the metal-embedded silica NPs depend on the type and structure of the embedded metals. Based on this progress, metal-embedded silica NPs are currently utilized in various spectroscopic applications, serving as nanozymes, detection and imaging probes, drug carriers, photothermal inducers, and bioactivation molecule screening identifiers. Owing to their versatile roles, metal-embedded silica NPs are expected to be applied in various fields, such as biology and medicine, in the future.
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  • 文章类型: Journal Article
    二氧化硅纳米颗粒(SiO2NPs)是广泛使用的工程材料,具有明显的环境暴露风险。我们先前的研究表明,不同途径的SiO2NP暴露对糖原合成酶激酶3β(GSK3β)活性的影响与富集在SiO2NPs表面的血清蛋白有关,这表明血清中的特定蛋白质改变了SiO2NPs的固有毒性行为,并抑制了SiO2NPs对GSK3β的激活。这里,我们发现SiO2NP表面富含大量载脂蛋白E(ApoE),与脂蛋白受体相关蛋白1(LRP1)结合的ApoE蛋白电晕使GSK3β失活,从而减少SiO2NP对脑的损伤。这项工作提供了第一个证据,表明特定的生物电晕在分子水平上降低了SiO2NPs的毒性,这有助于阐明特定电晕组分对纳米毒性的作用。
    Silica nanoparticles (SiO2 NPs) are widely used engineered materials that warrant their obvious environmental exposure risk. Our previous study has shown that different routes of SiO2 NP exposure on the glycogen synthase kinase 3 beta (GSK3β) activity were related to the serum proteins enriched on the surface of SiO2 NPs, which implied that a particular protein in the serum changed the inherent toxic behavior of SiO2 NPs and inhibited the activation of GSK3β by SiO2 NPs. Here, we identified that the SiO2 NP surface enriched a large amount of apolipoprotein E (ApoE), and the ApoE protein corona bound to the lipoprotein receptor-related protein 1 (LRP1) to inactivate GSK3β, thereby reducing the damage of SiO2 NPs to the brain. This work presented the first evidence that specific biocorona reduced the toxicity of SiO2 NPs at the molecular level, which helped to elucidate the role of specific corona components on nanotoxicity.
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