JOURNAL OF COLLOID AND INTERFACE SCIENCE
·
2022
·
IF 9.965
Rui Zhang,Changlin Liu,Ruoxi Zhao,Yaqian Du,Dan Yang,He Ding,Guixin Yang,Shili Gai,Fei He,Piaoping Yang
There is an urgent need to develop photosensitive nanoenzymes with better phototherapeutic efficiency through simple processes. By exploiting semiconductor catalysis and defect chemistry principles, herein, a MnMoO x composite semiconductor nanoenzyme was developed to achieve a fully integrated theranostic nanoenzyme for highly efficient photo/chemo-enzyme-dynamic eradication of deep tumors. Relative to iron oxides, manganese oxides offer ideal catalytic performance under near-neutral conditions, which helps to broaden the suitable pH range of the MnMoO x nanoenzyme for antitumor therapy. Furthermore, with the assistance of glutathione depletion, Mn 4+ /Mo 6+ was successfully converted to Mn 2+ /Mo 5+ , inhibiting the scavenging of reactive oxygen species (ROS) and promoting cycling. Therefore, MnMoO x has favorable catalase (CAT)-like activity and oxidase (OXD)-like activity in the tumor microenvironment (TME) for promoting the “H 2 O 2 O 2 O 2 − ” and “H 2 O 2 OH” cascade reactions. The abundant oxygen vacancy defects also promote the surface plasmon resonance (SPR) effect in the second near-infrared (NIR-II) window of MnMoO x , which significantly enhanced its photothermal therapy (PTT) effect and catalytic activity. In detail, ROS production was significantly enhanced due to the adsorption of water and oxygen molecules by the rich oxygen vacancies of MnMoO x . MnMoO x also exhibited excellent multi-modal imaging activity (including computed tomography (CT), magnetic resonance imaging (MRI), and photoacoustic (PA)), which can be exploited to better guide the administration of medication.
研究领域:
生物医学工程
·
纳米医学
·
肿瘤治疗
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Materials Chemistry Frontiers
·
2022
·Vol. 6
·期 10
·1269-1281
·
IF 8.683
Xiaohui Wang,Xiaoyue Feng,Mengjie Sun,Mingzhu Wang,Wei Wang,Zhi Yuan
Poor perfusion and low accumulation of drugs caused by abnormal tumor blood vessels significantly reduce the chemotherapy efficacy. Nowadays, the synergistic therapy of vascular normalization and chemotherapy has become an ideal choice to increase the tumor inhibition rate. Delivering an appropriate amount of NO around tumor vessels proved to be an effective vascular normalization strategy. In order to meet the demand for continuous and stable production of NO at the tumor site, herein, we developed a strategy to normalize tumor blood vessels by catalyzing NO generation from endogenous NO donors (RSNO). Concretely, the surface of copper-doped mesoporous silica was modified with PAA by electrostatic interactions to form CuMSN-PAA nanoparticles. The system was simple in structure and could catalyze NO production by exposing the CuMSN surface in response to a slightly acidic environment. In vivo, the NO level in the tumor increased 5.8-fold after CuMSN-PAA treatment, and blood perfusion increased by 70%, which in turn induced vascular normalization. Consequently, DOX accumulation of the CuMSN-PAA group increased 2.4-fold compared with the control group. More importantly, after the synergistic treatment of vascular normalization and chemotherapy, the anti-tumor efficacy was increased by 37.2% compared with the DOX-treated group with no overt toxicity observed.
研究领域:
癌症治疗
·
纳米技术
·
药学
·
生物医学工程
✓ 已验证
产品关联
DOI
高影响因子
MOLECULAR AND CELLULAR ENDOCRINOLOGY
·
2022
·
IF 4.369
Dandan Wang,Yixin Zhang,Liangyi Cui,Qing Yang,Jiao Wang
Endometriosis , defined as the abnormal growth of functional endometrium outside the uterus , is characterized by the abnormal phenotype of endometrial cells. This study aimed to investigate the role of latent transforming growth factor beta binding protein 2 (LTBP2), an extracellular matrix protein , in the occurrence and development of endometriosis. Elevated LTBP2 expression levels were observed in endometrial tissues and serum of endometriosis patients and their area under the ROC curve (AUC) values for distinguishing endometriosis were 0.9044 and 0.9534, respectively. Overexpressing-LTBP2 could promote proliferation, migration, and invasion, whereas suppressing apoptosis of endometrial stromal cells (ESCs). Moreover, LTBP2 downregulation induced the opposite effect. The supernatant from ESCs overexpressing LTBP2 promoted the tube formation of human umbilical vein endothelial cells (HUVECs), thus indicating an angiogenic effect. Furthermore, overexpression of LTBP2 facilitated the inflammation and might promote endometriosis progression through the NF- k B signaling pathway . Conclusively, LTBP2 might be a potential target in the diagnosis and treatment of endometriosis.
研究领域:
妇科学
·
分子生物学
·
细胞生物学
·
病理学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
DNA AND CELL BIOLOGY
·
2022
·Vol. 41
·期 4
·424-436
·
IF 3.55
Feng Chi,Fang Qiu,Xiaoming Jin,Long Chen,Guijin He,Sijia Han
Breast cancer (BC) is one of the most frequently occurring malignant tumors in female adults. The long intergenic nonprotein coding RNA 00982 (LINC00982) has been regarded as a cancer suppressor in several human cancers. However, the function and the underlying mechanisms of LINC00982 have not been studied in BC. The present study found that LINC00982 was significantly downregulated in BC tumor tissues, and the low LINC00982 level predicts a poor prognosis of BC. Through the overexpression and suppression of LINC00982 in two BC cell lines, we found that LINC00982 could inhibit cell proliferation, migration, and invasion by suppressing the activity of the signal transducer and activator of transcription 3 (STAT3)/nuclear factor kappa B (NF-κB) signal pathway. Furthermore, luciferase reporter assay has been used to verify that LINC00982 functions as a molecular sponge for miR-765, which could target DPF3. The relative expression of miR-765 decreased with LINC00982 overexpressing, and DPF3 increased at the same time.In addition, the suppression of cell malignant phenotype caused by overexpression of LINC00982 can be reversed by inhibition of DPF3. To verify the function of LINC00982 in vivo, the BC cells were implanted in nude mice and the results suggested the tumor growth and malignant phenotype were suppressed by LINC00982. In this study, we prove that LINC00982 regulates the growth and development of BC through STAT3/NF-κB signal pathway, mediated by the miR-765/DPF3 axis. LINC00982 may function as a target molecule to take part in the prognosis and therapy of BC.
研究领域:
肿瘤学
·
分子生物学
·
癌症研究
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ACTA BIOCHIMICA POLONICA
·
2022
·Vol. 69
·期 2
·363-370
·
IF 2.349
Jian-li Qiu,Yu-na Chai,Feng-yang Duan,Hui-juan Zhang,Xiao-yan Han,Ling-yan Chen,Fei Duan
Liver fibrosis is a global health problem caused by a number of diseases related to liver damage. 6-Shogaol is a biologically active substance derived from the rhizome of Zingiber officinale Roscoe with anti-tumor, anti-inflammatory, and antioxidant properties. To explore the effects of 6-Shogaol on liver fibrosis, we used a mouse model of the condition in which mice were injected intraperitoneally with carbon tetrachloride (CCl4) at a dose of 2 mL/kg three times per week for a period of 4 weeks. 6-Shogaol was administered orally at two different doses (5 mg/kg, 20 mg/kg) 30 min before CCl4 injection. CCl4 induced severe liver injury and fibrosis, as indicated by significant inflammatory cell infiltration, disordered liver structure, increased activities of aspartate aminotransferase and alanine aminotransferase (liver damage markers) in serum, elevated collagen deposition, and overexpressed alpha-smooth muscle actin (α-SMA, marker of hepatic stellate cells activation) in liver tissues, whereas 6-Shogaol administration rescued those alterations dose-dependently. We found that 6-Shogaol suppressed CCl4-induced inflammatory response by inhibiting macrophage recruitment, release of pro-inflammatory factors, and activation of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in liver tissues. Additionally, we demonstrated that 6-Shogaol blocked CCl4-induced activation of the nuclear factor-kappa B (NF-κB) pathway, which is a vital transcriptional regulator of the inflammatory response. Altogether, this study demonstrates that 6-Shogaol can prevent CCl4-induced liver fibrosis by suppressing inflammatory response through the NF-κB pathway and suggests that 6-Shogaol can be used for liver fibrosis prevention.
研究领域:
药理学
·
肝病学
·
免疫学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
ACS Applied Polymer Materials
·
2022
·
IF 4.855
Xi Chen,Hao Zhang,Chenyao Tian,Jingzhi Jia,Hui Xie
Tremendous progress in applying small-scale magnetic robots for targeted drug delivery has sparked a growing interest among researchers. However, significant effort is needed to design and fabricate robots to meet the needs of clinical treatments, such as biocompatibility, biodegradation, and synergistic therapy. Here, we propose a multiscale magnetic hydrogel robot (MMHR) with a core–shell structure in which superparamagnetic nanoparticles and curcumin-loaded chitosan microparticles (CCMs) are encapsulated inside the core, while doxorubicin-loaded chitosan microparticles (DCMs) are embedded inside the shell. The core and shell of the MMHR are composed of pH-sensitive calcium alginate hydrogels that can alleviate the sudden release of drugs from CCMs and DCMs in gastric fluid. MMHRs can be precisely actuated to the target region through magnetic driving systems for further drug delivery. The experimental results demonstrate that the MMHR possesses superior obstacle-crossing ability and can successfully locomote on the surface of the intestine. Additionally, the co-delivery of doxorubicin and curcumin is realized through the different fabrication methods of CCMs and DCMs and shows excellent synergistic therapeutic effects against colon cancer cells. The powerful propulsion, good biocompatibility, and remarkable synergistic efficacy of the MMHR offer a promising route for active drug delivery through the gastrointestinal tract.
研究领域:
生物医学工程
·
药物递送系统
·
磁性材料
·
癌症治疗
✓ 已验证
产品关联
DOI
高影响因子
COLLOIDS AND SURFACES B-BIOINTERFACES
·
2022
·
IF 5.999
Jinxin Liu,Zixi Zheng,Jialu Luo,Pan Wang,Gaohui Lu,Jianming Pan
Development of wound dressings that not only have multiple advantages including good biocompatibility, barrier properties, adhesive properties , but also exhibit anti-bacterial, anti-infection, and promote cell adhesion , accelerated wound healing process, remains challenging in the skin tissue engineering. In this work, a noninvasive adhesive biofoam with interconnectivity structure and antibacterial property was first-time designed through solid surfactant stabilized high internal phase emulsion (HIPE) template , where bacteriostatic Zn-CuO@GO nanosheets dynamic assemble with 4-vinylphenylboronic acid at the oil/water interface as cooperative emulsifier . Taking advantage of the cooperative assembly of the PBA/Zn-CuO@GO, the biofoams display microfibrousity and interconnectivity to facilitate material-cellular interaction as well nutrient exchange, and can effectively inhibit the growth of E. coli and S. aureus. Meanwhile, phenylboronic acid functional groups not only endow biofoam reversible adhesive property though dynamic phenylboronic acid/cis-diol interaction, but also facilitate the rearrangement of Zn-CuO@GO nanosheets in more uniform way at emulsion interface. Taken together, the biofoams can strongly adhere to the wound bed reducing the risk of infection and accelerate earlier tissue regeneration , which exhibit great potential in bioengineering application.
研究领域:
组织工程学
·
生物材料学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
Genes & Genomics
·
2022
·Vol. 45
·期 1
·1-11
·
IF 2.164
Cao Qingfei,Ma Jiaji,Li Weitao,Hong Peng,Shen Tong,Tong Ming
Background Guanine nucleotide-binding protein 2 (GNBP2) is a GTPase that has critical roles in host immunity and some types of cancer, but its function in clear cell renal cell carcinoma (ccRCC) is not fully understood. Objective This work explored the role of GNBP2 in ccRCC progression and the underlying molecular mechanism. Methods Two public human cancer databases TNMplot and TISIDB were employed to analyze the expression pattern of GNBP2 during ccRCC progression and the correlation between GNBP2 expression and clinical features of ccRCC patients. GNBP2 functions in ccRCC cells were determined by EdU staining, flow cytometry, scratch wound assay, transwell assay, and xenograft model. Gene expression was evaluated using qPCR, Western blot, immunofluorescence staining, and immunohistochemical staining. Results GNBP2 expression was significantly elevated in ccRCC tissues and increased gradually with the increasing tumor grades. Patients with higher GNBP2 expression had shorter overall survival times. Knockdown of GNBP2 suppressed tumor cell proliferation and cell cycle progression and reduced the capability of migration and invasion, while GNBP2 overexpression exhibited protumor effects. GNBP2 silencing by RNA interference significantly inhibited the tumor growth of tumor-bearing nude mice and decreased the proliferation marker Ki67. Mechanistically, GNBP2 downregulation suppressed the STAT3 signaling transduction, as it reduced the phosphorylation of STAT3 and modulated the expression of the target genes, including c-Myc, MMP2, N-cadherin, and E-cadherin. Conclusion These findings reveal that GNBP2 promotes ccRCC progression by regulating STAT3 signaling transduction, indicating that GNBP2 might be a promising molecular target for ccRCC therapy.
研究领域:
肿瘤学
·
分子生物学
·
细胞生物学
·
癌症生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
EUROPEAN JOURNAL OF NEUROSCIENCE
·
2022
·Vol. 57
·期 1
·64-77
·
IF 3.698
Weimin Ni,Jie Zhang,Bing Wang,Feng Liang,Long Bao,Pengfei Li,Yan Fang
Obesity is a major health crisis in the modern society. Studies have shown that the consumption of a high-fat diet (HFD) induces hypothalamic inflammation and leptin resistance, which consequently favours body mass gain. Actin related protein 2/3 complex subunit 1 (ARPC1B), an actin-binding protein, is highly expressed in immune cells. Recent studies have shown that ARPC1B has a certain anti-inflammatory effect. While ARPC1B expression is decreased in the hypothalamus of mice fed a HFD, the role of ARPC1B in HFD-induced obesity remains unclear. Thus, we investigated whether ARPC1B up-regulation in the hypothalamic arcuate nucleus (ARC) could inhibit the development of obesity. Herein, ARPC1B overexpression lentiviral particles were stereotaxically injected into the ARC of male C57BL/6J mice (7 weeks old) fed with HFD. Overexpression of ARPC1B in the hypothalamic ARC attenuated HFD-induced ARC inflammation, reduced body-weight gain and feed efficiency. Furthermore, up-regulation of ARC ARPC1B improved the glucose tolerance and reduced subcutaneous/epididymal fat mass accumulation, which decreased the serum total cholesterol, serum triglyceride and leptin levels. In addition, upon ARPC1B overexpression in the hypothalamic ARC, intraperitoneal injection of leptin increased the phosphorylation level of signal transducer and activator of transcription 3 (STAT3), an important transcription factor for leptin's action, in the ARC of obese mice. Accordingly, we suggest that up-regulation of ARPC1B in the hypothalamic ARC may improve the HFD-induced hypothalamic inflammation and leptin resistance. Our findings demonstrate that ARPC1B is a promising target for the treatment of diet-induced obesity.
研究领域:
神经科学
·
代谢学
·
内分泌学
·
免疫学
·
分子生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CARBOHYDRATE POLYMERS
·
2022
·
IF 10.723
Ruhe Zhang,Xinru You,Moucheng Luo,Xinyu Zhang,Yifen Fang,Hai Huang,Yang Kang,Jun Wu
The use of cisplatin is restricted by systemic toxicity and drug resistance. Supramolecular nano-drug delivery systems involving drugs as building blocks circumvent these limitations promisingly. Herein, we describe a novel supramolecular system [Pt(IV)-SSNPs] based on poly(β-cyclodextrin), which was synthesized for efficient loading of adamantly-functionalized platinum(IV) prodrug [Pt(IV)-ADA 2 ] via the host-guest interaction between β-cyclodextrin and adamantyl. Pt(IV)-ADA 2 can be converted to active cisplatin in reducing environment in cancer cells, which further reduces systemic toxicity. The introduction of the adamantane group-tethered mPEG 2k endowed the Pt(IV)-SSNPs with a longer blood circulation time. In vitro assays exhibited that the Pt(IV)-SSNPs could be uptaken by CT26 cells, resulting in cell cycle arrest in the G2/M and S phases, together with apoptosis. Furthermore, the Pt(IV)-SSNPs showed effective tumor accumulation, better antitumor effect , and negligible cytotoxicity to major organs. These results indicate that supramolecular nanoparticles are a promising platform for efficient cisplatin delivery and cancer treatment.
研究领域:
药学
·
癌症治疗
·
纳米技术
·
药物递送系统
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CARBON
·
2022
·
IF 11.307
Keke Kang,Limin Wang,Yajie Ma,Kai Yu,Jingwei Liu,Fengyu Qu,Huiming Lin
Here, Co 9 S 8 / [email protected] ( [email protected] ) nanocomposites are synthesized by a two-step hydrothermal process. Firstly, sulfur-doped carbon dots (S-CDs) are prepared by using 3-mercaptopropionic acid as a precursor. A region with denser –SH group is regarded as nucleation site on S-CDs for the growth of Co 9 S 8 to induce heterostructure. As-synthesized [email protected] possess great harvest in NIR region and hyperthermia (51.5%, 1064 nm) for photothermal (PTT). Besides, hyperthermia can elevate the thermal energy of nanocomposite to assist low-energy NIR-II irradiation (1064 nm, 1.16 eV), realizing the excitation of Co 9 S 8 (1.46 eV) and reactive oxygen species (ROS) generation for photodynamic therapy (PDT). What's more, [email protected] exhibits GOx-like activity that could consume glucose to elevate H 2 O 2 level and inhibit intracellular energy supply. In addition, they also show mimic peroxidase (POD) and catalase (CAT) characterization, and the tandem multi-nanozye activities endue the enhanced chemotherapy (CDT) and PDT. [email protected] reveals the greater ROS generation and nanozyme activity compared with pure Co 9 S 8 @PEG, attributing to the efficient charge separation in heterostructure. The novel biodegradation of [email protected] makes the elimination via feces and urine within 2 weeks. That is associated with PTT/PDT/CDT/starvation therapy to activate immune response for anticancer.
研究领域:
材料科学
·
纳米技术
·
生物医学工程
·
癌症治疗
✓ 已验证
产品关联
DOI
高影响因子
JOURNAL OF INTERFERON AND CYTOKINE RESEARCH
·
2022
·Vol. 42
·期 6
·267-278
·
IF 3.657
Jing Hu,Yan Cheng,Ping Chen,Zhaoqi Huang,Liqi Yang
Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction without overt central nervous system infection. Caffeine citrate has therapeutic effect on different brain diseases, while its role in SAE remains unclear. The expression levels of interleukin (IL)-18 and IL-1β were upregulated in the cerebrospinal fluid of the subjects. In this study, a rat model of SAE was established by cecal ligation and puncture. Caffeine citrate inhibited SAE-induced neuronal apoptosis and astrocytic activation, decreased reactive oxygen species (ROS) generation, and elevated mitochondrial membrane potential (MMP) level in the cerebral cortex. In vitro, primary astrocytes were isolated from rat cerebral cortex and incubated with lipopolysaccharide (LPS) and interferon-γ (IFN-γ). Caffeine citrate reduced ROS and MMP levels and mitochondrial complex enzyme activities in LPS plus IFN-γ-induced astrocytes. Moreover, caffeine citrate inhibited the activation of nucleotide-binding and oligomerization domain (NOD)-like receptor (NLRP3) inflammasome and decreased the production of IL-1β and IL-18 in vivo and in vitro. Notably, caffeine citrate promoted UCP2 expression in astrocytes. The neuroprotective role of UCP2 has been reported in several experimental brain diseases. These results suggest that caffeine citrate inhibits neuronal apoptosis, astrocytic activation, mitochondrial dysfunction in rat cerebral cortex, thereby alleviating SAE. The protection of caffeine citrate against SAE may be achieved by the UCP2-mediated NLRP3 pathway inhibition in astrocytes.
研究领域:
神经科学
·
免疫学
·
药理学
·
细胞生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）