murine macrophage
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Processes ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 2062
Author(s):  
Thuy Thi Trinh ◽  
Ailyn Fadriquela ◽  
Johny Bajgai ◽  
Subham Sharma ◽  
Md. Habibur Rahman ◽  
...  

Excessive oxidative stress (OS) is a common cause of various diseases such as cancer, diabetes, and obesity; thus, an anti-oxidative solution is essential for the improvement of human health. Increasing evidence suggests that alkaline reduced water (ARW), especially between pH 9.5–10.0, has antioxidant capacity; however, relatively few studies have reported the effect of weak ARW at pH 8.5 on OS, especially in vitro. This study was conducted to evaluate the anti-oxidative efficacy of weak ARW with negative oxidation-reduction potential (ORP) and relatively high hydrogen (H2) concentration, as compared to tap water (TW) and ARW at pH 9.5. RAW 264.7 murine macrophage cells, stimulated by hydrogen peroxide (H2O2) and lipopolysaccharide (LPS) to induce OS, were used as a control (Con) and then treated with TW and ARW at pH 8.5 (ARW_8.5) and pH 9.5 (ARW_9.5) at different concentrations (0.1%, 1%, and 10% v/v). Results showed that cell viability was significantly restored after treatment with both ARW_8.5 and ARW_9.5 compared to Con/H2O2 and Con/LPS, while TW treatment did not induce significant changes. Levels of reactive oxygen species (ROS), nitric oxide (NO), Ca2+, catalase, and glutathione peroxide (GPx) showed significant differences in a concentration-dependent manner in ARW_8.5 and ARW_9.5 groups compared to Con/H2O2 and Con/LPS groups. Likewise, the expression of p-p38, p-JNK, and p-ERK was also significantly reduced in the ARW-treated groups, but not in the TW group. In conclusion, ARW_8.5 exhibited anti-oxidative effects through the regulation of the MAPK signaling pathway in RAW 264.7 murine macrophage cells, indicating the health-promoting potential of weak ARW through daily intake.


2021 ◽  
Author(s):  
Li Feng ◽  
Qing Wang ◽  
Yanjiao Li ◽  
Wanwen Cheng ◽  
Jie Liu ◽  
...  

Abstract Objectives Matrix metalloproteinase-9 (MMP9) functions as a collagenase, it promotes the infarct expansion and cardiac rupture after myocardial infarction (MI). This study sought to identify the mechanism mediating MI-induced MMP9 expression, and explore the new therapeutic target improving healing process after MI. Materials and Methods HIMF expression is manipulated by genetic ablation of HIMF in mice (Himf−/−), and adenoviral overexpression of HIMF by recombinant adenovirus encoding a green fluorescent protein (GFP)-tagged mouse HIMF in cultured neonatal rat ventricular myocytes (NRVMs), cardiac fibroblasts (CFs) and the murine macrophage RAW264.7 cells. The mouse model of left descending coronary artery ligation was established to investigate the expression of MMP9 and HIMF. Results MMP9 was predominantly expressed in macrophages of MI hearts, and positively correlated to the expression of HIMF, a marker for anti-inflammatory macrophage polarization. HIMF deficiency (Himf−/−) results in significantly decreased MMP9 expression, increased collagen deposition, reduced infarction size and improved cardiac contraction. Mechanistic analysis reveals that HIMF increases MMP9 expression by activating STAT3 signaling in murine macrophage RAW264.7. This was verified by the inhibited STAT3 phosphorylation in the MI heart of Himf−/− mouse. Conclusions This study identified a novel HIMF-STAT3-MMP9 regulation module in macrophages that influences collagen deposition in infarct heart, providing a new sight for MI treatment.


2021 ◽  
Vol 141 ◽  
pp. 83-89
Author(s):  
Irvine Niyonizigiye ◽  
Daniel Ngabire ◽  
David Nkurunziza ◽  
Maheshkumar Prakash Patil ◽  
Alka Ashok Singh ◽  
...  

2021 ◽  
Author(s):  
A. Taylor ◽  
D. Jenner ◽  
C. Rowland ◽  
T. Laws ◽  
I. Norville ◽  
...  

Melioidosis is a neglected tropical disease caused by the bacterium Burkholderia pseudomallei . The bacterium is intrinsically resistant to various antibiotics and melioidosis is therefore difficult to treat successfully without relapse in infection. B. pseudomallei is an intracellular pathogen, and therefore to eradicate the infection, antimicrobials must be able to access bacteria in an intracellular niche. This study assessed the ability of a panel of monoclonal antibodies to opsonise Burkholderia species and determine the effect that the antibody has on bacterial virulence in vitro . Murine macrophage infection assays demonstrated that monoclonal antibodies to the capsule of B. pseudomallei are opsonising. Furthermore, one of these monoclonal antibodies reduced bacterial actin tail formation in our in vitro assays, indicating antibodies could reduce the intracellular spread of B. thailandensis . The data presented in this paper demonstrates that monoclonal antibodies are opsonising and can decrease bacterial actin tail formation, thus decreasing their intracellular spread. This data has informed selection of an antibody for development of an antibody-antibiotic conjugate for melioidosis. Importance statement Melioidosis is difficult to treat successfully due to the bacterium being resistant to many classes of antibiotics, therefore available therapeutic options are limited. New and improved therapies are urgently required to treat this disease. Here we have investigated the potential of monoclonal antibodies to target this intracellular pathogen. We have demonstrated that monoclonal antibodies can target the bacterium, increase uptake into macrophages and reduce actin tail formation required by the bacterium for spread between cells. Through targeting the bacterium with antibodies we hope to disarm the pathogen, reducing the spread of infection. Ultimately we aim to use an opsonising antibody to deliver antibiotics intracellularly by developing an antibody-antibiotic conjugate therapeutic for melioidosis.


Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 777
Author(s):  
Cátia Sousa ◽  
Bruno Miguel Neves ◽  
Alcino Jorge Leitão ◽  
Alexandrina Ferreira Mendes

The signaling pathways involved in age-related inflammation are increasingly recognized as targets for the development of preventive and therapeutic strategies. Our previous study elucidated the structure–activity relationship of monoterpene compounds derived from p-menthane as potential anti-inflammatory drugs and identified (S)-(+)-carvone as the most potent among the compounds tested. This study aims at identifying the molecular mechanism underlying the anti-inflammatory properties of (S)-(+)-carvone. The murine macrophage cell line, Raw 264.7, was stimulated with bacterial lipopolysaccharide (LPS) to simulate inflammation. Western blot was used to assess protein levels and post-translational modifications. The subcellular localization of NF-κB/p65 was visualized by immunocytochemistry. An in vitro fluorometric assay was used to measure Sirtuin-1 (SIRT1) activity. (S)-(+)-carvone inhibited LPS-induced JNK1 phosphorylation, but not that of p38 and ERK1/2 and also did not affect the phosphorylation and degradation of the NF-κB inhibitor, IκB-α. Accordingly, (S)-(+)-carvone did not affect LPS-induced phosphorylation of NF-κB/p65 on Ser536 and its nuclear translocation, but it significantly decreased LPS-induced IκB-α resynthesis, a NF-κB-dependent process, and NF-κB/p65 acetylation on lysine (Lys) 310. Deacetylation of that Lys residue is dependent on the activity of SIRT1, which was found to be increased by (S)-(+)-carvone, while its protein levels were unaffected. Taken together, these results show that (S)-(+)-carvone is a new SIRT1 activator with the potential to counteract the chronic low-grade inflammation characteristic of age-related diseases.


Molecules ◽  
2021 ◽  
Vol 26 (11) ◽  
pp. 3070
Author(s):  
Mariela Gonzalez-Ramirez ◽  
Ivan Limachi ◽  
Sophie Manner ◽  
Juan C. Ticona ◽  
Efrain Salamanca ◽  
...  

In addition to the trichilianones A–D recently reported from Trichilia adolfi, a continuing investigation of the chemical constituents of the ethanol extract of the bark of this medicinal plant yielded the five new limonoids 1–5. They are characterized by having four fused rings and are new examples of prieurianin-type limonoids, having a ε-lactone which in 4 and 5 is α, β- unsaturated. The structures of the isolated metabolites were determined by high field NMR spectroscopy and HR mass spectrometry. The new metabolites were shown to have the ε-lactone fused with a tetrahydrofuran ring which is connected to an oxidized hexane ring joined with a cyclo-pentanone having a 3-furanyl substituent. As the crude extract possesses antileishmanial activity, the compounds were assayed for cytotoxic and antiparasitic activities in vitro in murine macrophage cells (raw 264.7 cells) and in Leishmania amazoniensis as well as L. braziliensis promastigotes. Metabolites 1–3 and 5 showed moderate cytotoxicity (between 30–94 µg/mL) but are not responsible for the antileishmanial effect of the extract.


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