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A549 cells were analyzed for miR-16-5p and CXCR3 expression, as well as its mechanism. Methods LPS-induced lung cancer cell injury and apoptosis; MiR-16-5p is a precursor and apoptosis; its mechanism. The expression of CXCR3, IL-6, and TNF- in A549 cells was significantly reduced in the LPS group, and flow cytometry results of CXCR3 were also elevated in comparison to the control group; apoptosis of A549 cells was found in A549 cells; results were also observed by flow cytometry. MiR-16-5p has improved the protective effect of LPS-induced A549 cell injury, and it may have a new target for lung cancer targeted therapy.
Source link: https://doi.org/10.1080/21691401.2019.1593998
It was discovered that particle size around 50 nm, which is an impressive nano dimension, was achieved by plant-mediated synthesis in the AuNPs synthesized by M. tenacissima extracts, which is an admirable nano dimension. According to a dose-dependent A549 cells growth inhibition, AuNPs cause toxicity, according to a MTT assay. In A549 cells, the anti-apoptotic protein expression is stimulated by caspase expression and down-regulates the anti-apoptotic protein expression. The AuNPs from M. tenacissima extract were found to be apposite stabilizing agents, and they acted as an effective anticancer agent against lung cancer cell lines, according to our study.
Source link: https://doi.org/10.1080/21691401.2019.1575844
For the testing of their operation, Human lung adenocarcinoma cell line A549 and Lewis tumor-bearing C57BL/6 mice were used. To determine proliferation inhibition in A549 cells, a MTT assay was used. Enzyme-linked immunosorbent assay was performed to determine the presence of inflammatory mediators interleukin-6 and tumor necrosis factor- in serum. In A549 cells, the IC50 values of 14. 4 g/mL and 9. 3 g/mL were shown, respectively. Compared to alkaloids or triterpenes alone, the alkaloids and triterpenes combination could significantly reduce tumor formation in tumor-bearing C57BL/6 mice. In addition, Annexin-V/PI double staining and flow cytometry revealed that the combination of alkaloids and triterpenes could cause apoptosis and result in cell cycle arrest in A549 cells. Their combination drastically down-regulated Bcl-2 expression and pro-casp8 levels in A549 cells, according to a Western blot report, although it did notably raise the level of cleaved caspase-8, triggering apoptosis in A549 cells.
Source link: https://doi.org/10.3390/molecules181113920
On the A549 lung cancer cell line, the present study reports for the first time the HPLC analysis and in vitro antioxidant testing of mango peel phenols and their cytotoxic effects on the A549 lung cancer cell line. 833. 2 mg· 91 mg·kg−1 dry mango peel;1 dry mango peel; mainly vanillic aldehyde, caffeic acid, gallic acid, procyanidin B2 and oleanolic acid These findings showed that mango peel had the highest phenolic content of 723. 2 &plus million; 0. 93 mg·; 1. 93 mg· mango peel extract had an IC50 value of 15 mg/middote;mL−1;M2−1 and MPPs had a larger inhibitory effect on the A549 cell line, according to in vitro cytotoxic tests; MFPs had a higher inhibitory effect on the A549 cell line.
Source link: https://doi.org/10.3390/molecules23061395
Cells in 2D are not exposed to the same conditions as cells in 3D tissues in the body and are therefore a poor representation of the in vivo microenvironment, although these simplified culture techniques are useful in understanding the fundamentals of host-pathogen interactions. In this work, we intend to create the first 3D culture model for RSV infection using A549 cells to determine its suitability for RSV pathogenesis. Trypan blue exclusion assay and flow cytometry revealed abundant live cells in the spheroids, indicating high viability over seven days of incubation. Conclusions: A549 spheroids are susceptible and permissive for RSV because they show RSV infection characteristics such as syncytia formation and mucin overexpression, suggesting that A549 spheroids can be used as a promising model for studying RSV in vitro.
Source link: https://doi.org/10.1016/j.jiph.2020.03.011
Antitumor effects on A549 cells were found during a systematic review of the anticancer effects of Scutellaria barbata, one of the main alkaloids in S. barbata. The anti-tumor effects of SBT-A were examined in vivo, using transplanted tumor nude mice, and the findings revealed that SBT-A has a major antitumor presence on A549 cancer by mitochondria-mediated apoptosis. SBT-A demonstrated significant antitumor activity on A549 cells in vivo and in vitro by up-regulating expressions of caspase-3 and 9, as well as down-regulating Bcl-2.
Source link: https://doi.org/10.3390/molecules19078740
However, the role of SIRT1 in the regulation of LPS-induced human epithelial A549 cells apoptosis is unknown. Methods: Cell viability, apoptosis, and reactive oxygen species production in A549 cells treated with LPS were first investigated. Cell viability was reduced by exposure to LPS in a dose- and time-dependent manner. While reducing the expression of SIRT1 in A549 cells, LPS promoted cell proliferation and ROS production. Conclusion: SIRT1 is a key player in regulating the human alveolar epithelial A549 cell apoptosis process induced by LPS.
Source link: https://doi.org/10.1159/000343352
Beijing, China's Republic of ChinaTel 13161281016Email lyhhlx@126. comMotori China's Republic of ChinaTotal Hospital No. 28 Fuxing Road, Haidian District, Beijing 100853;s People's Republic of ChinaTel +86 10 1316180101616 Email: People's Republic of ChinaNo. 28 Fuxing Road, Haidian District, Beijing 100853, People's Republic of ChinaTetetelHa10Email 1316128 FxX11136810Email 1316128Fetelx@6 131611610Email 1316128 Fuxing Road, Beijing 10085311Email: People's Republic of ChinaTel101616112151016128 Fuxing Road, ChinaTelx, People's Republic of ChinaTel03101610161Email 131681016101312121266111340161016313213010162Email 13161121310 paraphrasedoutput:Methods: We discovered that SIRT1 promotes P53 deacetylation, promotes cell survival, and promotes cell survival by inhibiting P53-induced P53 arrest and apoptosis in A549 cells, but that YAP-mediated P53 deacetylation has not been well investigated. P53, YAP, SIRT1, crosstalk: P53, YAP, SIRT1, crosstalk: Our results show that SIRT1 is responsible for YAP and P53 deacetylation, and decreases A549 cell survival by increasing YAP acetylation, P53 deacetylation and cell death, as well as in vivo and apoptosis, which may be involved in lung tumor formation.
Abstract Background: Exposure to air pollution particles has been shown to be associated with excess production of oxidative damage to DNA in experimental model systems and humans. This research was conducted to determine the DNA oxidizing effects of real street particles on SRM1650 and SRM2975. Authentic street particles and SRMs differ in their ability to oxidize DNA in a cell-free environment, according to cell culture experiments, the particle preparations resulted in the same degradation of DNA damage and little differences in cytotoxicity. This research reveals that SRM1650 and SRM2975 are good surrogate samples for the investigation of real street particles on the cellular level, although it cannot be ruled out that SRMs and genuine street particles can cause different outcomes in animal experiment models.
Source link: https://doi.org/10.1186/1743-8977-5-6
In vivo, we treated A549 cell xenograft-bearing nude mice with EGCG. αSMA;SMA;SMA;SMA;SMA) and collagen IV were tagged and measured using quantum-dot double-labeled immunofluorescence to determine microvessel density, microvessel permeation index, and collagen IV expression. Using graphite-furnace atomic absorption spectrophotometry, Cisplatin concentrations in tumor tissue was determined in tumor tissue. The vascular normalization window was divided into five groups: treated with saline, cisplatin, EGCG, cisplatin, EGCG, cisplatin, EGCG, cisplatin, EGCG, cisplatin, eGCG, cisplatin, EGCG, Pretreatment with EGCG helped raise cisplatin concentration in tumor tissue during vascular normalization, relative to treatment with cisplatin only. Tumor-growth delay after treatment in the five groups during the vascular normalization window was 6. 3&plus millionn;1. 79, 12. 1±1. 35, and 15. 4 million days;1. 99 days, indicating synergistic EGCG–cisplatin reactions, particularly during the vascular normalization window. Conclusion: EGCG-induced vascular normalization in human lung adenocarcinoma may be a novel strategy for raising chemotherapy effectiveness.
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