JOURNAL OF HAZARDOUS MATERIALS
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2023
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IF 13.6
Xiaoyue Wang,Jin Wang,Shanjun Liu,Mengmeng Dou,Boru Gao
The sterilization effect of photocatalysis and biotoxicity of nanomaterial catalysts have attracted high attention. In this study, the novel visible-driven defective carbon nitride (VL/DCN) system exhibits non-photoreactivation, non-toxic superior performance compared with traditional ultraviolet radiation (UV) and UV/titanium dioxide (UV/TiO 2 ). The inactivation of antibiotic-resistant bacteria (ARB) by novel VL/DCN still reached 7 log within 4 h, and the reduction rates of aminoglycoside gene strB and tetracycline gene tetA exceeded 0.8 log and 1.2 log, respectively. Further, the sterilization mechanism and nanotoxicity were contrastively and systematically analyzed among above three systems as following. Firstly, in the VL/DCN system, reactive oxygen species (ROSs) generated from photocatalytic process leads to the destruction of cell membranes, resulting in dissolving out of potassium ion (K + ), protein and cell membrane ATP content. Thus, resistant bacteria were completely inactivated and photoreactivation disappears. In contrast, the UV only acted on bacterial DNA and existed the light resurrection. The UV/TiO 2 strictly dependent on ultraviolet light and can be used in limited scenarios. Secondly, in cell viability analysis by human lung cell line BEAS-2B experiments, the 10% inhibition of cell growth when DCN was 600 mg/L much lower than 28% inhibition of cell growth when TiO 2 was only 200 mg/L. The expression of pro-inflammatory cytokines (( Interleukin, IL) -6), IL-8, IL-1β ) under the effect of DCN was 1.5-fold, 5.7-fold and 3.7-fold lower than TiO 2 , respectively. Meanwhile, DCN induced cells to produce less ROSs, malondialdehyde (MDA), and more superoxide dismutase (SOD). Above results demonstrated that DCN has far lower cytotoxicity than TiO 2 . This study provides theoretical support for the application of photocatalytic sterilization technology and the exploration of the toxicity of nanomaterials. Environmental Implication In this study, the novel visible-driven defective carbon nitride (VL/DCN) system exhibits non-photoreactivation, non-toxic superior performance compared with traditional ultraviolet radiation (UV) and UV/titanium dioxide (UV/TiO 2 ). The VL/DCN exhibited excellent sterilization efficiency and a high rate of reduction of the E. coli resistance gene strB. The inactivation of ARB reached 7 log within 4 h without the occurrence of photoreactivation. The reduction rates of the aminoglycoside gene strB and tetracycline gene tetA exceeded 0.8 log and 1.2 log, respectively. This study provides a valuable theoretical basis for the development of a new sustainable and environmentally friendly visible light catalytic sterilization technologies.
研究领域:
环境科学
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材料科学
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生物技术
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毒理学
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DOI
PubMed
高影响因子
ACS Biomaterials Science & Engineering
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2022
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IF 5.395
Yang Zhang,Lixia Chen,Ruimeng Sun,Ruijuan Lv,Ting Du,Yuhan Li,Xinming Zhang,Rongtian Sheng,Yanfei Qi
Oxidative stress is related to many diseases, but available clinical treatment methods are currently limited. Exploitation of enzyme-mimicking nanomaterials (nanozymes) is a promising way for scavenging reactive oxygen species (ROS) and treatment of ROS-related diseases. Herein, the catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) mimicking activities are expressed by MnO2 nanoparticles (MnO2–BSA NPs) coated with BSA. Effective •OH removal activity is also expressed by MnO2–BSA NPs at neutral pH. Apoptosis inhibition and ROS scavenging capabilities of MnO2–BSA NPs are evident on the H2O2-exposed BEAS-2B cells line. Western blot analysis indicates that MnO2–BSA NPs inhibit H2O2-induced apoptosis by mediating the expression of apoptosis-related proteins.
研究领域:
纳米技术
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生物化学
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药学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
IMMUNOLOGICAL INVESTIGATIONS
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2023
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IF 2.8
Dongdong Dou,Meirong Bi,Xiuyun Li,Nan Zhang,Mi Xu,Aili Guo,Feng Li,Weiwei Zhu
Background Childhood asthma is a major global health concern. ADP-ribosylation factor 6 (ARF6) is a low-molecular-weight GTPase; however, its role in childhood asthma remains unclear.Methods Ovalbumin (OVA)-challenged neonatal mice and transforming growth factor-β1 (TGF-β1)-induced BEAS-2B cells were used as in vivo and in vitro models of childhood asthma, respectively.Results Upon OVA stimulation, ARF6 expression was upregulated in the lung tissue. Neonatal mice administered SehinH3 (an ARF6 inhibitor) exhibited improved pulmonary pathological injury, along with reduced inflammatory cell infiltration in the lungs and cytokine release in bronchial alveolar lavage fluid and serum (interleukin [IL]−3, IL−5, IL−13, IgE, and OVA-specific IgE). SehinH3 treatment restrained epithelial – mesenchymal transition (EMT) in the lungs of asthmatic mice, as evidenced by increased E-cadherin and decreased N-cadherin and α-smooth muscle actin expression. Different TGF-β1 exposures to BEAS-2B cells induced a time- and dose-dependent increase in ARF6 expression in vitro. Upon TGF-β1 stimulation, ARF6 knockdown repressed EMT and SehinH3 treatment caused similar results in BEAS-2B cells. The transcription factor E2F8 is involved in diverse biological functions and its increased expression was confirmed in vivo and in vitro. Dual-luciferase assays confirmed that E2F8 binds to the ARF6 promoter and promotes its transcriptional activity. In vitro results revealed that E2F8 silencing suppressed EMT, whereas rescue experiments showed that ARF6 overexpression partly reversed these phenomena.Conclusion Our study showed that ARF6 is associated with childhood asthma progression and may be positively regulated by E2F8. These results provide insight into the pathogenesis and treatment of childhood asthma.
研究领域:
免疫学
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呼吸病学
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分子生物学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
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2023
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IF 5.3
Fei Li,Chunyu Ye,Xiuli Wang,Xinting Li,Xiaoxia Wang
Cigarette smoking can cause damage of airway epithelial cells and contribute to chronic obstructive pulmonary disease (COPD). Honokiol is originally isolated from Magnolia obovata with multiple biological activities. Here, we investigated the protective effects of honokiol on cigarette smoke extract (CSE)-induced injury of BEAS-2B cells. BEAS-2B cells were treated with 300 mg/L CSE to construct an in vitro cell injury model, and cells were further treated with 2, 5 and 10 μM honokiol, then cell viability and LDH leakage were analysed by CCK-8 and LDH assay kits, respectively. Apoptosis was detected by flow cytometry analysis. ELISA was used to measure the levels of tumour necrosis factor (TNF)-ɑ, IL-1β, IL-6, IL-8 and MCP-1. The results showed that honokiol (0.5–20 μM) showed non-toxic effects on BEAS-2B cells. Treatment with honokiol (2, 5 and 10 μM) reduced CSE (300 mg/L)-induced decrease in cell viability and apoptosis in BEAS-2B cells. Honokiol also decreased CSE-induced inflammation through inhibiting expression and secretion of inflammatory cytokines, such as TNF-ɑ, IL-1β, IL-6, IL-8 and MCP-1. Moreover, honokiol repressed CSE-induced reactive oxygen species (ROS) production, decrease of ATP content and mitochondrial biogenesis, as well as mitochondrial membrane potential. Mechanistically, honokiol promoted the expression of SIRT3 and its downstream target genes, which are critical regulators of mitochondrial function and oxidative stress. Silencing of SIRT3 reversed the protective effects of honokiol on CSE-induced damage and mitochondrial dysfunction in BEAS-2B cells. These results indicated that honokiol attenuated CSE-induced damage of airway epithelial cells through regulating SIRT3/SOD2 signalling pathway.
研究领域:
肺病学
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药理学
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细胞生物学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Redox Biology
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2025
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IF 11.9
Dan Liu,Hui Yu,Zhicun Liu,Le Wang,Dawo Liu,Xiangyu Cao
Acrolein is a significant high priority hazardous air pollutant. This research explore the relationship of acrolein-induced ferroptosis with the pathogenesis of lung injury by combining cellular, transcriptome, and animal-level studies. The results in vivo and in vitro models indicated that a total of 18,868 differenced lncRNAs and 15,639 differenced mRNAs were obtained after acrolein exposure. After screening, 636 lncRNAs and 214 mRNAs were obviously different of the acrolein injured group with the control group. Differential genes were mainly enriched in the iron ion binding, tissue homeostasis, etc. Among them, lncRNA MIR155HG significantly responded to the toxic effects of acrolein, the knockdown of lncRNA MIR155HG could inhibit miR-155-5p expression, promote CD200R1 expression, and improve cell viability. Furthermore, it effectively inhibited acrolein-induced the activation of ferroptosis pathway in BEAS-2B cells and lung tissue, indicating that lncRNA MIR155HG might be a potential new target for the inhibition of acrolein toxicity. LncRNA-MIR155HG/miR-155-5p/CD200R1 axis played an significant role in the lung injury, and induced ferroptosis by regulating the Nrf2/SLC7A11/GPX4 pathway. This study is the first to reveal that acrolein exposure significantly affected lncRNA and mRNA expression in BEAS-2B cells, and found that lncRNA MIR155HG effectively regulated acrolein-induced ferroptosis pathway, providing novel insights for the treatment of lung injury.
研究领域:
毒理学
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分子生物学
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环境卫生
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呼吸系统疾病
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基因组学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
Biomed Research International
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2019
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IF 2.197
YiXun Li,Huan Li,Yong Duan,XueMei Cai,DingYun You,Feng Zhou,ChuanQi Yang,XiaoYu Tuo,ZiJie Liu
Background. Xuanwei City in Yunnan province has been one of the towns with highest lung cancer mortality in China. The high content of amorphous silica in the bituminous coal from Xuanwei of Yunnan is mainly present as irregular and spherical silica nanoparticles (SiNPs). It has been reported that silica nanoparticles in bituminous coal correlated with the high incidence of lung cancer in Xuanwei. To explore the role and mechanism of SiNPs in the tumorigenesis of lung cancer in Xuanwei, human mononuclear cells (THP-1) and human bronchial epithelial cells (BEAS-2B) were cocultured in a transwell chamber. Combined with Benzo[a]pyrene-7, 8-dihydrodiol-9, and 10-epoxide (BPDE), SiNPs could significantly promote the proliferation and Epithelial-Mesenchymal Transition (EMT) and inhibit apoptosis of BEAS-2B cells and induce the release of TGF-α from THP-1 cells. After neutralizing TGF-α with antibody, the proliferation and EMT were decreased and enhanced apoptosis of BEAS-2B cells. Furthermore, the results showed that TGF-α in the sera of patients with lung adenocarcinoma in Xuanwei were significantly higher than in patients with benign pulmonary lesions in Xuanwei and those with lung adenocarcinoma in outside of Xuanwei of Yunnan. Taken together, our study found that SiNPs promoted the proliferation and EMT of BEAS-2B cells by inducing the release of TGF-α from THP-1 cells.
研究领域:
癌症研究
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纳米技术
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细胞生物学
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分子生物学
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环境健康
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DOI
PubMed
高影响因子
INFLAMMATION
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2023
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IF 5.1
Feng Yong,Hu Jiapeng,Liu Fen,Shang Yunxiao
Asthma is a chronic inflammatory disease characterized by airway remodeling and lung inflammation. Collagen triple helix repeat containing 1 (CTHRC1), a glycoprotein, is involved in multiple pathological processes, including inflammation and fibrosis. However, the function of CTHRC1 in asthma remains unclear. In the present study, the mouse asthma model was successfully generated by sensitizing and challenging mice with ovalbumin (OVA). CTHRC1 expression at both RNA and protein levels was significantly upregulated in lung tissues of asthmatic mice. Asthmatic mice exhibited significant airway remodeling as evidenced by increased bronchial wall and smooth muscle cell layer thickness, goblet cell hyperplasia and collagen deposition, and epithelial-mesenchymal transition (EMT), but those characteristics were reversed by CTHRC1 silencing. The cell model with transforming growth factor-β1 (TGF-β1) induction in bronchial epithelial cells (BEAS-2B) was conducted to verify the effects of CTHRC1 on EMT, a classic mechanism that mediates airway remodeling. The results showed that TGF-β1 stimulation increased CTHRC1 expression, and CTHRC1 knockdown inhibited TGF-β1-induced EMT. OVA-treated mice also showed increased inflammatory cell infiltration and the production of OVA-specific immunoglobulin E (IgE), interleukin (IL)-4, IL-5, and IL-13, which were decreased by CTHRC1 downregulation. The effects of CTHRC1 on OVA-induced airway inflammation were further determined by treating BEAS-2B cells with IL-13, in which CTHRC1 knockdown reduced the IL-13-induced secretion of pro-inflammatory factors, including IL-4 and IL-5. In conclusion, these results indicate that CTHRC1 silencing attenuates asthmatic airway remodeling and inflammation in vivo and in vitro, suggesting that CTHRC1 may be a potential target for asthma treatment. Graphical Abstract
研究领域:
免疫学
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呼吸医学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
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