scholarly journals Propofol inhibits inflammatory response by regulating the miR-494/ Nrdp1 pathway in ICH mice model

2020 ◽  
Author(s):  
Hui Shi ◽  
Qijiang Xiong ◽  
Zhongyan Huang ◽  
zhao yang
Keyword(s):  
Inflammatory Response ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Mice Model ◽  
Immune Disease ◽  
Neuroinflammatory Response ◽  
M1 Macrophage ◽  
M2 Macrophage Polarization ◽  
Neuro Protective Effect ◽  
Proinflammatory Factors

Abstract Background: Propofol is an anesthetic agent with neuro-protective effect in neuronal injury. However, the mechanism of propofol in M1 macrophage polarization following ICH has not been well studied. Ubiquitination mediated M1/M2 macrophage polarization plays important roles in pathogenesis of immune disease. The experiment analyzed anti-inflammatory effects of propofol in macrophages following ICH. Methods: In the experiment, macrophages were administrated with erythrocyte lysates, and then miR-494, Nrdp1 and M1 related markers were analyzed. In addition, brain inflammatory response, brain edema, and neurological functions of ICH mice were also assessed. Results: We found that propofol decreased miR-494 levels while increased Nrdp1 levels in macrophages after ICH. We also demonstrated that miR-494 inhibited Nrdp1 expression by directly binding its 3′-untranslated region. MiR-494 attenuated Nrdp1 levels and downstream proinflammatory factors production. Upregulation of Nrdp1 in macrophages significantly decreased M1 macrophage polarization. Conclusion: Taken together, these results suggest that propofol can attenuate the neuroinflammatory response of macrophages after ICH through regulation of the miR-494/Nrdp1 pathway.

scholarly journals Propofol inhibits inflammatory response by regulating the miR-494/ Nrdp1 pathway in ICH mice model

2020 ◽  
Author(s):  
Shudong Liu ◽  
Wenyan Li ◽  
Hui Shi ◽  
Ge Tang ◽  
Jiangwei Zhang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Mice Model ◽  
Immune Disease ◽  
Neuroinflammatory Response ◽  
M1 Macrophage ◽  
M2 Macrophage Polarization ◽  
Neuro Protective Effect ◽  
Proinflammatory Factors

Abstract Background: Propofol is an anesthetic agent with neuro-protective effect in neuronal injury. However, the mechanism of propofol in M1 macrophage polarization following ICH has not been well studied. Ubiquitination mediated M1/M2 macrophage polarization plays important roles in pathogenesis of immune disease. The experiment analyzed anti-inflammatory effects of propofol in macrophages following ICH. Methods: In the experiment, macrophages were administrated with erythrocyte lysates, and then miR-494, Nrdp1 and M1 related markers were analyzed. In addition, brain inflammatory response, brain edema, and neurological functions of ICH mice were also assessed. Results: We found that propofol decreased miR-494 levels while increased Nrdp1 levels in macrophages after ICH. We also demonstrated that miR-494 inhibited Nrdp1 expression by directly binding its 3′-untranslated region. MiR-494 attenuated Nrdp1 levels and downstream proinflammatory factors production. Upregulation of Nrdp1 in macrophages significantly decreased M1 macrophage polarization. Conclusion: Taken together, these results suggest that propofol can attenuate the neuroinflammatory response of macrophages after ICH through regulation of the miR-494/Nrdp1 pathway.

scholarly journals Propofol inhibits inflammatory response by regulating the miR-494/ Nrdp1 pathway in ICH mice model

2020 ◽  
Author(s):  
Shudong Liu ◽  
Wenyan Li ◽  
Hui Shi ◽  
Ge Tang ◽  
Jiangwei Zhang ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Mice Model ◽  
Immune Disease ◽  
Neuroinflammatory Response ◽  
M1 Macrophage ◽  
M2 Macrophage Polarization ◽  
Neuro Protective Effect ◽  
Proinflammatory Factors

Abstract Background: Propofol is an anesthetic agent with neuro-protective effect in neuronal injury. However, the mechanism of propofol in M1 macrophage polarization following intracerebral hemorrhage (ICH) has not been well studied. Ubiquitination mediated M1/M2 macrophage polarization plays important roles in pathogenesis of immune disease. The experiment analyzed anti-inflammatory effects of propofol in macrophages following ICH. Methods: In the experiment, macrophages were administrated with erythrocyte lysates, and then miR-494, Neuregulin receptor degradation protein-1 (Nrdp1) and M1 related markers were analyzed. In addition, brain inflammatory response, brain edema, and neurological functions of ICH mice were also assessed. Results: We found that propofol decreased miR-494 levels while increased Nrdp1 levels in macrophages after ICH. We also demonstrated that miR-494 inhibited Nrdp1 expression by directly binding its 3′-untranslated region. MiR-494 attenuated Nrdp1 levels and downstream proinflammatory factors production. Upregulation of Nrdp1 in macrophages significantly decreased M1 macrophage polarization. Conclusion: Taken together, these results suggest that propofol can attenuate the neuroinflammatory response of macrophages after ICH through regulation of the miR-494/Nrdp1 pathway.

scholarly journals Effect of Platelet-Rich Plasma on M1/M2 Macrophage Polarization

2021 ◽  
Vol 22 (5) ◽  
pp. 2336
Author(s):  
Ryoka Uchiyama ◽  
Eriko Toyoda ◽  
Miki Maehara ◽  
Shiho Wasai ◽  
Haruka Omura ◽  
...  
Keyword(s):  
Culture Media ◽  
Platelet Rich Plasma ◽  
Point Of Care ◽  
Macrophage Polarization ◽  
Osteoarthritis Of The Knee ◽  
M2 Macrophage ◽  
Related Factors ◽  
Humoral Factors ◽  
M1 Macrophage ◽  
M2 Macrophage Polarization

Osteoarthritis of the knee (OAK) is a chronic degenerative disease and progresses with an imbalance of cytokines and macrophages in the joint. Studies regarding the use of platelet-rich plasma (PRP) as a point-of-care treatment for OAK have reported on its effect on tissue repair and suppression of inflammation but few have reported on its effect on macrophages and macrophage polarization. Based on our clinical experience with two types of PRP kits Cellaid Serum Collection Set P type kit (leukocyte-poor-PRP) and an Autologous Protein Solution kit (APS leukocyte-rich-PRP), we investigated the concentrations of humoral factors in PRPs prepared from the two kits and the effect of humoral factors on macrophage phenotypes. We found that the concentrations of cell components and humoral factors differed between PRPs purified using the two kits; APS had a higher concentration of M1 and M2 macrophage related factors. The addition of PRP supernatants to the culture media of monocyte-derived macrophages and M1 polarized macrophages revealed that PRPs suppressed M1 macrophage polarization and promoted M2 macrophage polarization. This research is the first to report the effect of PRPs purified using commercial kits on macrophage polarization.

scholarly journals MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout Mice

2021 ◽  
Vol 7 ◽  
Author(s):  
Jing Rui Qi ◽  
Dian Ru Zhao ◽  
Li Zhao ◽  
Fan Luo ◽  
Mei Yang
Keyword(s):  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Treatment Target ◽  
Vessel Disease ◽  
Novel Treatment ◽  
M1 Macrophage ◽  
Apolipoprotein E Knockout Mice ◽  
The World ◽  
M2 Macrophage Polarization

Atherosclerosis (AS), a kind of chronic inflammatory blood vessel disease, is a main cause of cardiovascular disease, which is a leading cause of mortality around the world. Accumulation of macrophages induced by inflammation contributes to AS development. It has been indicated that microRNAs (miRNAs) are involved in the process of AS. However, the pathway and gene miRNAs targeting are poorly understood. Here we reported that miR-520a-3p was increased in mice with AS and silencing of miR-520a-3p attenuated AS process. Furthermore, inhibition of miR-520a-3p increased the expression of α-SMA and collagen. In addition, miR-520a-3p silencing inhibited the expression of M1 macrophage polarization markers and pro-inflammatory genes and promoted the M2 macrophage polarization. What’s more, forced expression of miR-520a-3p diminished IL4/IL13 induced macrophage autophagy via targeting UVRAG. Collectively, our study reveals the role of miR-520a-3p in macrophage polarization and suggests the potential of miRNA as a novel treatment target of AS.

Modulation of the inflammatory response to chitosan through M2 macrophage polarization using pro-resolution mediators

Biomaterials ◽  
2015 ◽  
Vol 37 ◽  
pp. 116-123 ◽  
Author(s):  
Daniela P. Vasconcelos ◽  
Madalena Costa ◽  
Isabel F. Amaral ◽  
Mário A. Barbosa ◽  
Artur P. Águas ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
M2 Macrophage Polarization

scholarly journals A novel delivery nanobiotechnology: engineered miR-181b exosomes improved osteointegration by regulating macrophage polarization

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Wei Liu ◽  
Muyu Yu ◽  
Feng Chen ◽  
Longqing Wang ◽  
Cheng Ye ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Macrophage Polarization ◽  
Underlying Mechanism ◽  
M2 Macrophage ◽  
Implant Loosening ◽  
M2 Polarization ◽  
M2 Macrophage Polarization ◽  
Osteogenesis In Vitro

Abstract Background Many patients suffer from implant loosening after the implantation of titanium alloy caused by immune response to the foreign bodies and this could inhibit the following osteogenesis, which could possibly give rise to aseptic loosening and poor osteointegration while there is currently no appropriate solution in clinical practice. Exosome (Exo) carrying miRNA has been proven to be a suitable nanocarrier for solving this problem. In this study, we explored whether exosomes overexpressing miR-181b (Exo-181b) could exert beneficial effect on promoting M2 macrophage polarization, thus inhibiting inflammation as well as promoting osteogenesis and elaborated the underlying mechanism in vitro. Furthermore, we aimed to find whether Exo-181b could enhance osteointegration. Results In vitro, we firstly verified that Exo-181b significantly enhanced M2 polarization and inhibited inflammation by suppressing PRKCD and activating p-AKT. Then, in vivo, we verified that Exo-181b enhanced M2 polarization, reduced the inflammatory response and enhanced osteointegration. Also, we verified that the enhanced M2 polarization could indirectly promote the migration and osteogenic differentiation by secreting VEGF and BMP-2 in vitro. Conclusions Exo-181b could suppress inflammatory response by promoting M2 polarization via activating PRKCD/AKT signaling pathway, which further promoting osteogenesis in vitro and promote osteointegration in vivo. Graphic abstract

scholarly journals A Benzenediamine Analog FC-99 Drives M2 Macrophage Polarization and Alleviates Lipopolysaccharide- (LPS-) Induced Liver Injury

2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Wei Gong ◽  
Haiyan Zhu ◽  
Li Lu ◽  
Yayi Hou ◽  
Huan Dou
Keyword(s):  
Liver Injury ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
M1 Macrophage ◽  
M2 Macrophage Polarization ◽  
Underlying Mechanisms ◽  
Sirna Knockdown ◽  
Lower Expression ◽  
Alternatively Activated

Macrophages have variable functional phenotypes, high diversity, and plasticity and are involved in the pathogenesis of sepsis-induced liver injury. Alteration of macrophage polarization through activated (M1) macrophage to alternatively activated (M2) macrophage has emerged as a potential therapeutic strategy. This study was designed to explore the effect of a benzenediamine analog FC-99 on macrophage polarization in vitro and lipopolysaccharide- (LPS-) induced liver injury followed by the underlying mechanisms. For in vitro experiments, FC-99 inhibited M1-related macrophage factors and promoted M2-related markers induced by IL-4 in the mouse macrophage cell line RAW264.7. Moreover, FC-99-induced macrophages polarized to M2 phenotype which could be repressed by a PPAR-γ inhibitor but not STAT6 siRNA knockdown, indicating FC-99-induced M2 macrophage polarization through PPAR-γ rather than STAT6 signal. In LPS-induced septic mice, FC-99 pretreated mice displayed lower expression of M1 markers together with the increased M2 marker CD206 and improvement of liver injury. These findings illustrated that FC-99 could promote M2 macrophage polarization via PPAR-γ signaling and seemed to be a potential therapeutic candidate for inflammatory liver injury.

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