Background: Neonatal pneumonia (NP) has a high fatality rate in neonatal illness. This research investigated the functions of emodin on lipopolysaccharide (LPS)-evoked inflammatory injury in WI-38 cells. Methods: Cell counting kit-8 (CCK-8) assay and flow cytometry were utilized for examining the impacts of LPS and emodin on viability and apoptosis, respectively. Taurine up-regulated gene 1 (TUG1) level was altered through cell transfection and investigated by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Moreover, RT-qPCR, western blot and enzyme-linked immunosorbent assay (ELISA) were utilized for investigating expressions of monocyte chemoattractant protein-1 (MCP-1) and interleukin (IL)-6. Western blot was carried out for investigating the levels of Bcl-2, Bax, pro-Caspase-3, cleaved-Caspase-3 and NF-κB and p38MAPK pathway-related proteins. Results: LPS treatment restrained cell viability, enhanced apoptosis, and expressions of inflammation-related IL-6 and MCP-1. Emodin alleviated LPSevoked inflammatory injury and restrained the NF-κB and p38MAPK pathways. Furthermore, emodin positively regulated TUG1 expression and TUG1 silencing could reverse the efficacy of emodin on IL-6 and MCP-1 expressions. Finally, TUG1 regulates the expression of inflammatory factors through NF-κB and p38MAPK pathways. Conclusion: Emodin alleviated LPS-evoked inflammatory injury by raising TUG1 expression via NF-κB and p38MAPK pathways in WI-38 cells. K E Y W O R D S emodin, inflammatory damage, NF-κB and p38MAPK pathways, neonatal pneumonia, TUG1 1 | INTRODUCTION Neonatal pneumonia (NP) is the most familiar respiratory diseases in the neonatal stage. Most NP is caused by lung infections which are caused by inhalation of
Objective: To analyze the efficacy and safety of decitabine combined with CAG ((cytarabine + aclacinomycin + granulocyte colony stimulating factor)) regimen and CAG regimen alone in the treatment of elderly acute myeloid leukemia. Methods: 96 elderly patients with acute myeloid leukemia who were admitted to our hospital from July 2015 to July 2017 were randomly divided into an observation group and a control group, 48 cases in each group. The patients in the control group were treated with CAG regimen, while the patients in the observation group were treated with decitabine on the basis of the control group. The clinical curative effect, changes of immune indicators, occurrence of adverse reactions and survival rate at different time after treatment were compared between the two groups. Results: The total effective rate of the observation group was significantly higher than that of the control group (P<0.05). After treatment, the indicators of cellular immunity in the two groups were significantly lower than those before treatment, and the indicators of cellular immunity in the observation group were significantly lower than those in the control group (P<0.05). There was no significant difference in the incidence of adverse reactions between the two groups (P>0.05). The 9-month survival rate and 1-year survival rate in the observation group were significantly higher than those in the control group (P<0.05). Conclusion: The combination of decitabine and CAG regimen is effective in the treatment of elderly patients with acute myeloid leukemia. The therapy can fully inhibit cellular immune function and improve long-term survival rate, and its safety has a small difference with that of CAG regimen alone. It is worth clinical promotion. doi: https://doi.org/10.12669/pjms.36.2.850 How to cite this:Zhao H, Wang C, Yu F, Guo Q. Decitabine combined with CAG regimen in the treatment of elderly patients with acute myeloid leukemia. Pak J Med Sci. 2020;36(2):---------. doi: https://doi.org/10.12669/pjms.36.2.850 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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