scholarly journals Autophagy deficiency exacerbates acute lung injury induced by copper oxide nanoparticles

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Junting Xiao ◽  
Baijie Tu ◽  
Xin Zhou ◽  
Xuejun Jiang ◽  
Ge Xu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Copper Oxide ◽  
Copper Ions ◽  
Intratracheal Instillation ◽  
Copper Oxide Nanoparticles ◽  
Oxide Nanoparticles ◽  
Dependent Manner

AbstractCopper oxide nanoparticles (CuONPs) are one of the widely used metal nanoparticles in the industrial and commercial fields. Autophagy is an intracellular degradation system that delivers cytoplasmic constituents to the lysosome and has been linked to nanoparticles-induced toxicity. In particular, the roles of autophagy in response to CuONPs have been explored in vitro, although the conclusions are controversial. To clarify the role of autophagy in CuONPs-induced acute lung injury, microtubule-associated protein 1 light chain 3 beta (Map1lc3b or lc3b) knockout mice and their corresponding wild type mice are applied. Our results showed that single-dose intratracheal instillation of CuONPs with dosages of 1.25, 2.5 or 5 mg/kg caused acute lung injury 3 days after treatment in a dose-dependent manner, as evidenced by deteriorative lung histopathology, more infiltration of macrophage cells, increased oxidative stress and copper ions. Loss of lc3b resulted in aggravated lung injury induced by CuONPs, which was probably due to the blockade of mitophagy and consequently the accumulation of aberrant mitochondria with overloaded copper ions. Our study provides the first in vivo evidence that autophagy deficiency exacerbates CuONPs-induced acute lung injury, and highlights that targeting autophagy is a meaningful strategy against CuONPs-associated respiratory toxicity.

scholarly journals Biocompatible N-acetyl-nanoconstruct alleviates lipopolysaccharide-induced acute lung injury in vivo

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Seongchan Kim ◽  
Shin Young Kim ◽  
Seung Joon Rho ◽  
Seung Hoon Kim ◽  
So Hyang Song ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Responses ◽  
Therapeutic Potential ◽  
Intratracheal Instillation ◽  
Sprague Dawley ◽  
In Vivo Experiments ◽  
Anti Inflammatory

AbstractOxidative stress plays important roles in inflammatory responses during acute lung injury (ALI). Recently, nanoconstruct (Nano)-based drug-delivery systems have shown promise in many models of inflammation. In this study, we evaluated the anti-inflammatory effects of N-acetylcysteine (NAC) loaded in a biocompatible Nano using a rat model of ALI. We synthesized a Nano with a good NAC-releasing capacity using porous silica Nano, which was used to produce Nano/NAC complexes. For in vivo experiments, Sprague–Dawley rats were intraperitoneally administered NAC or Nano/NAC 30 min after intratracheal instillation of lipopolysaccharide. After 6 h, bronchoalveolar lavage fluids and lung tissues were collected. The anti-oxidative effect of the Nano/NAC complex was confirmed by demonstrating reduced levels of reactive oxygen species after treatment with the Nano/NAC in vitro. In vivo experiments also showed that the Nano/NAC treatment may protect against LPS‐induced ALI thorough anti‐oxidative and anti‐inflammatory effects, which may be attributed to the inactivation of the NF‐κB and MAPK pathways. In addition, the effects of Nano/NAC treatment were shown to be superior to those of NAC alone. We suggest the therapeutic potential of Nano/NAC treatment as an anti‐inflammatory agent against ALI. Furthermore, our study can provide basic data for developing nanotechnology-based pharmacotherapeutics for ALI.

Characterization and Anticancer Activities of Green Synthesized CuO Nanoparticles, A Review

2020 ◽  
Vol 20 ◽  
Author(s):  
Seyedeh R. Alizadeh ◽  
Mohammad A. Ebrahimzadeh
Keyword(s):  
Drug Delivery ◽  
Cancer Therapy ◽  
Copper Oxide ◽  
Medical Science ◽  
Copper Oxide Nanoparticles ◽  
Cuo Nanoparticles ◽  
Oxide Nanoparticles ◽  
Anticancer Activities

Background: Cancer is defined as an abnormal/uncontrolled cell growth that shows rapid cell division. This disease is annually recognized in more than ten million people. Nanomaterials can be used as new strategies for cancer therapy. Nanostructured devices have developed for drug delivery and controlled release and created novel anticancer chemotherapies. Nanomaterials were taken into consideration because of their new properties, containing a large specific surface area and high reactivity. Copper oxide nanoparticles (CuONPs) have potential applications in many fields like heterogeneous catalysis, antibacterial, anticancer, antioxidant, antifungal, antiviral, imaging agents, and drug delivery agents in biomedicine. CuONPs display different physical properties, such as hightemperature superconductivity, electron correlation effects, and spin dynamics. NPs can be synthesized using different methods like physical, chemical, and biological methods. Methods: Copper oxide nanoparticles (CuONPs) have been suggested for its broad usage in biomedical applications. In this review, we tried to exhibit the results of significant anticancer activity of green synthesized CuONPs and their characterization by different analytical techniques such as UV-Vis, FT-IR, XRD, EDAX, DLS, SEM, and TEM. Results: The green method for the synthesis of CuO nanoparticles as eco-friendly, cost-effective, and facile method is the more effective method. Synthesized CuONPs from this method have an appropriate size and shape. The Green synthesized CuONPs exhibited high potential against several breast cancer (AMJ-13, MCF-7, and HBL-100 cell lines), cervical cancer (HeLa), colon cancer (HCT-116), gastric cancer (human adenocarcinoma AGS cell line), lung cancer (A549), leukemia cancer, and other cancers with the main toxicity approach of increasing ROS production. Conclusion: The present review confirms the importance of green synthesized CuO nanoparticles in medical science especially cancer therapy that exhibited high activity against different cancer in both in vitro and in vivo. The main toxicity approach of CuONPs is increasing the production of reactive oxygen species (ROS). It needs to perform more studies about in vivo cancer therapy and following clinical trial testing in the future. We believe that green synthesized CuO nanoparticles can be used for the improvement of different diseases.

Folic acid modified copper oxide nanoparticles for targeted delivery in in vitro and in vivo systems

RSC Advances ◽  
2015 ◽  
Vol 5 (83) ◽  
pp. 68169-68178 ◽  
Author(s):  
Dipranjan Laha ◽  
Arindam Pramanik ◽  
Sourav Chattopadhyay ◽  
Sandip kumar Dash ◽  
Somenath Roy ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Folic Acid ◽  
Cancer Therapy ◽  
Copper Oxide ◽  
Targeted Delivery ◽  
Copper Oxide Nanoparticles ◽  
Oxide Nanoparticles ◽  
Breast Cancer Therapy

Targeted delivery of copper oxide nanoparticles for breast cancer therapy.

scholarly journals Copper Oxide Nanoparticles Stimulate Cytotoxicity and Apoptosis in Glial Cancer Cell Line

2018 ◽  
Vol 17 (1) ◽  
pp. 105-111 ◽  
Author(s):  
Nasim Rahmani Kukia ◽  
Ardeshir Abbasi ◽  
Seyyed Maysam Abtahi Froushani
Keyword(s):  
Copper Oxide ◽  
Cancer Cells ◽  
Cell Line ◽  
Cytotoxic Effect ◽  
Cancer Cell Line ◽  
Copper Oxide Nanoparticles ◽  
Oxide Nanoparticles ◽  
Cuo Nps

Due to cytotoxic potential, Copper Oxide Nanoparticles (CuO NPs) have recently been studied in various in vivo and in culture cell line. Also, CuO has received much attention in cancer therapy. We aimed to evaluate the cytotoxicity of CuO NPs on glial cancer (B92) cell line. B92 cancer cells were cultured with CuO NPs at different concentrations (5, 10, and 20 μg/ml) with 30 and 60 nm particle size. Then, cancer cells were incubated for 24 hrs. The apoptosis and cytotoxicity of cells were estimated by acridine orange/propidium iodide staining and MTT assay, respectively. Both sizes of CuO NPs had cytotoxic effect. Even with the lowest concentration, the cytotoxic impact accommodated 32% of cell apoptosis with 30 nm size. When the concentration of CuO NPs increased, viability decreased and apoptosis increased. However, these amounts have no significant changes in the concentration of 10 to 20 μg/ml between two particle sizes (30 and 60 nm). The IC50 was decreased as the size of particles increased, but there was no significant change. This finding suggests that exposure to CuO NPs had significant cytotoxic effect with the sizes tested when compared to unexposed control in a way that the smaller size and higher concentration exerted the maximum cytotoxic effects. It seems that augmentation may not have any impact on their in vitro cytotoxicity.Dhaka Univ. J. Pharm. Sci. 17(1): 105-111, 2018 (June)

Lipid A fraction of LPS induces a discrete MAPK activation in acute lung injury

2007 ◽  
Vol 293 (2) ◽  
pp. L336-L344 ◽  
Author(s):  
Wen-Feng Fang ◽  
Jae Hwa Cho ◽  
Qianbin He ◽  
Meng-Chih Lin ◽  
Chao-Chien Wu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Lipid A ◽  
Intratracheal Instillation ◽  
Toll Like Receptor 4 ◽  
Mapk Activation ◽  
Erk Activation ◽  
The Relationship

Lipopolysaccharide (LPS) induces acute lung injury (ALI) via Toll-like receptor 4 (TLR4)-mediated MAPK activation. The lipid A fraction of LPS is considered to be the active moiety, but whether the lipid A-TLR4 interaction accounts completely for ALI-associated MAPK activation in vivo has not been determined. The lipid A fraction of LPS induces a discrete MAPK activation pattern in murine ALI. Mice (C57BL/6J, C3H/HeJ) were treated with intratracheal instillations of purified lipid A or LPS (10, 30, and 100 μg per mouse) or vehicle. ALI was assessed by histology. Chromogenic myeloperoxidase (MPO) activity was measured in lung homogenates. MAPK expression was quantified by immunoblotting. In vitro ERK inhibitor studies using thioglycollate-elicited macrophages were also performed. MPO increased in a dose- and time-responsive fashion. Notably, MPO was 2.4-fold greater after lipid A compared with LPS and vehicle at 6 h after instillation (lipid A, 0.88 ± 0.25 vs. LPS, 0.37 ± 0.21 optical density units·min−1·mg−1; P < 0.05). However, ALI scores were comparable at 6 and 24 h between LPS and lipid A. MPO was also comparable in vehicle-treated or C3H/HeJ mice treated with LPS or lipid A at 6 and 24 h. Phospho-ERK activation was pronounced at 6 and 24 h after lipid A but not LPS treatment. In vitro studies confirmed the relationship between phospho-ERK activation and cytokine expression in macrophage stimulated with either LPS or lipid A. Compared with whole LPS, the lipid A fraction is associated with amplified whole lung MPO and ERK activation 6 h after intratracheal instillation in mice.

Biodistribution and toxickinetic variances of chemical and green Copper oxide nanoparticles in vitro and in vivo

2019 ◽  
Vol 55 ◽  
pp. 154-169 ◽  
Author(s):  
Aditi Dey ◽  
Subhankar Manna ◽  
Jaydeep Adhikary ◽  
Sourav Chattopadhyay ◽  
Sriparna De ◽  
...  
Keyword(s):  
Copper Oxide ◽  
Copper Oxide Nanoparticles ◽  
Oxide Nanoparticles

scholarly journals Statistical Optimization of Copper Oxide Nanoparticles Using Response Surface Methodology and Box–Behnken Design Towards In Vitro and In Vivo Toxicity Assessment

2020 ◽  
Vol 11 (3) ◽  
pp. 10027-10039
Keyword(s):  
Response Surface Methodology ◽  
Copper Oxide ◽  
Response Surface ◽  
Copper Oxide Nanoparticles ◽  
Toxicity Assessment ◽  
P Value ◽  
Oxide Nanoparticles ◽  
Box Behnken Design

The current study focusses on the optimization of Copper oxide nanoparticles (CuO NPs) biosynthesis with Alternanthera sessilis (L.) extract using response surface methodology (RSM). The effect of time, pH, and extract to metal concentration ratio on the yield of synthesized nanoparticles (NPs) were estimated using Box–Behnken design. The influence of each of the parameters, as mentioned earlier, was determined by synthesizing nanoparticles under different conditions. A total of 29 experimental runs were carried out to estimate the crucial parameters. Extract to the metal ratio was found to be the vital parameter for yield optimization based on the p-values (p-value < 0.05). The physicochemical property of NPs, like size, was estimated to be in the range of 10-20 nm. In zebrafish, 48 hpf and 72 hpf were measured at 90 µM to reduce dysfunction and mortality during organ development. These results can have a valuable impact on eco-toxicological effects.

scholarly journals In vitro and in vivo assessment of the protective effect of sufentanil in acute lung injury

2021 ◽  
Vol 49 (2) ◽  
pp. 030006052098635
Author(s):  
Qi Gao ◽  
Ningqing Chang ◽  
Donglian Liu
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Protective Effect ◽  
High Mobility ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Hmgb1 Protein

Objectives To investigate the mechanisms underlying the protective effect of sufentanil against acute lung injury (ALI). Material and Methods Rats were administered lipopolysaccharide (LPS) by endotracheal instillation to establish a model of ALI. LPS was used to stimulate BEAS-2B cells. The targets and promoter activities of IκB were assessed using a luciferase reporter assay. Apoptosis of BEAS-2B cells was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling. Results Sufentanil treatment markedly reduced pathological changes in lung tissue, pulmonary edema and secretion of inflammatory factors associated with ALI in vivo and in vitro. In addition, sufentanil suppressed apoptosis induced by LPS and activated NF-κB both in vivo and in vitro. Furthermore, upregulation of high mobility group box protein 1 (HMGB1) protein levels and downregulation of miR-129-5p levels were observed in vivo and in vitro following sufentanil treatment. miR-129-5p targeted the 3ʹ untranslated region and its inhibition decreased promoter activities of IκB-α. miR-129-5p inhibition significantly weakened the protective effect of sufentanil on LPS-treated BEAS-2B cells. Conclusion Sufentanil regulated the miR-129-5p/HMGB1 axis to enhance IκB-α expression, suggesting that sufentanil represents a candidate drug for ALI protection and providing avenues for clinical treatment.

scholarly journals Group V Phospholipase A2 Mediates Endothelial Dysfunction and Acute Lung Injury Caused by Methicillin-Resistant Staphylococcus aureus

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1731
Author(s):  
Yu Maw Htwe ◽  
Huashan Wang ◽  
Patrick Belvitch ◽  
Lucille Meliton ◽  
Mounica Bandela ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Acute Lung Injury ◽  
Endothelial Dysfunction ◽  
Lung Injury ◽  
Phospholipase A2 ◽  
Methicillin Resistant Staphylococcus Aureus ◽  
Group V ◽  
Methicillin Resistant

Lung endothelial dysfunction is a key feature of acute lung injury (ALI) and clinical acute respiratory distress syndrome (ARDS). Previous studies have identified the lipid-generating enzyme, group V phospholipase A2 (gVPLA2), as a mediator of lung endothelial barrier disruption and inflammation. The current study aimed to determine the role of gVPLA2 in mediating lung endothelial responses to methicillin-resistant Staphylococcus aureus (MRSA, USA300 strain), a major cause of ALI/ARDS. In vitro studies assessed the effects of gVPLA2 inhibition on lung endothelial cell (EC) permeability after exposure to heat-killed (HK) MRSA. In vivo studies assessed the effects of intratracheal live or HK-MRSA on multiple indices of ALI in wild-type (WT) and gVPLA2-deficient (KO) mice. In vitro, HK-MRSA increased gVPLA2 expression and permeability in human lung EC. Inhibition of gVPLA2 with either the PLA2 inhibitor, LY311727, or with a specific monoclonal antibody, attenuated the barrier disruption caused by HK-MRSA. LY311727 also reduced HK-MRSA-induced permeability in mouse lung EC isolated from WT but not gVPLA2-KO mice. In vivo, live MRSA caused significantly less ALI in gVPLA2 KO mice compared to WT, findings confirmed by intravital microscopy assessment in HK-MRSA-treated mice. After targeted delivery of gVPLA2 plasmid to lung endothelium using ACE antibody-conjugated liposomes, MRSA-induced ALI was significantly increased in gVPLA2-KO mice, indicating that lung endothelial expression of gVPLA2 is critical in vivo. In summary, these results demonstrate an important role for gVPLA2 in mediating MRSA-induced lung EC permeability and ALI. Thus, gVPLA2 may represent a novel therapeutic target in ALI/ARDS caused by bacterial infection.

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