scholarly journals Anti-inflammatory agents other than corticosteroid in SARs-CoV-2 pneumonia

2021 ◽  
Author(s):  
Pongdhep Theerawit
Keyword(s):  
Treatment Option ◽  
Interleukin 6 ◽  
Essential Role ◽  
Kinase Inhibitor ◽  
Severe Complication ◽  
Organ Injury ◽  
Inadequate Response ◽  
Anti Inflammatory

The SARs-CoV-2 results in hyperinflammation among infected patients. This condition leads to serious organ injury, especially in the lungs. Therefore, the main treatment option, in addition to anti-viral agents, is the administration of corticosteroids. However, in many cases, inadequate response to corticosteroids has been observed—other anti-inflammatory agents, such as interleukin-6 inhibitor, kinase inhibitor, etc., play an essential role in reducing this severe complication.

A brief review on the use of cannabis as a treatment option for local inflammation in peripheral tissue01

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Secondary Metabolites ◽  
Treatment Option ◽  
Cell Injury ◽  
Local Inflammation ◽  
Topical Formulations ◽  
Central Effects ◽  
Complex Process ◽  
Anti Inflammatory

Inflammation is a complex process which, ideally, comes about as a “mop up’ response to cell injury. Ithowever occasionally results in undesired effects that should otherwise be prevented or resolvedspeedily. There are available numerous medicines with varied modes of administration commerciallyavailable for the management of inflammation. With the growing evidence of cannabis’ therapeuticeffects, its anti-inflammatory properties being one of them, debates among proponents and opponents ofcannabis use are ever growing. These debates are centered on the undesired central effects of some of theplants secondary metabolites an argument that can be moderated by using the plant in a manner thatsteers clear of these effects. Effective topical formulations could very well be one avenue through whichnature can be allowed to heal with minimal negative repercussions.

scholarly journals BAM15, a Mitochondrial Uncoupling Agent, Attenuates Inflammation in the LPS Injection Mouse Model: An Adjunctive Anti-Inflammation on Macrophages and Hepatocytes

2021 ◽  
pp. 1-17
Author(s):  
Cong Phi Dang ◽  
Jiraphorn Issara-Amphorn ◽  
Awirut Charoensappakit ◽  
Kanyarat Udompornpitak ◽  
Thansita Bhunyakarnjanarat ◽  
...  
Keyword(s):  
Atp Depletion ◽  
Organ Injury ◽  
Flux Analysis ◽  
Energy Status ◽  
Mitochondrial Uncoupling ◽  
Inflammatory Monocytes ◽  
Tnf Α ◽  
Cell Energy ◽  
Anti Inflammatory ◽  
Anti Inflammation

Controlof immune responses through the immunometabolism interference is interesting for sepsis treatment. Then, expression of immunometabolism-associated genes and BAM15, a mitochondrial uncoupling agent, was explored in a proinflammatory model using lipopolysaccharide (LPS) injection. Accordingly, the decreased expression of mitochondrial uncoupling proteins was demonstrated by transcriptomic analysis on metabolism-associated genes in macrophages (RAW246.7) and by polymerase chain reaction in LPS-stimulated RAW246.7 and hepatocytes (Hepa 1–6). Pretreatment with BAM15 at 24 h prior to LPS in macrophages attenuated supernatant inflammatory cytokines (IL-6, TNF-α, and IL-10), downregulated genes of proinflammatory M1 polarization (iNOS and IL-1β), upregulated anti-inflammatory M2 polarization (Arg1 and FIZZ), and decreased cell energy status (extracellular flux analysis and ATP production). Likewise, BAM15 decreased expression of proinflammatory genes (IL-6, TNF-α, IL-10, and iNOS) and reduced cell energy in hepatocytes. In LPS-administered mice, BAM15 attenuated serum cytokines, organ injury (liver enzymes and serum creatinine), and tissue cytokines (livers and kidneys), in part, through the enhanced phosphorylated αAMPK, a sensor of ATP depletion with anti-inflammatory property, in the liver, and reduced inflammatory monocytes/macrophages (Ly6C +ve, CD11b +ve) in the liver as detected by Western blot and flow cytometry, respectively. In conclusion, a proof of concept for inflammation attenuation of BAM15 through metabolic interference-induced anti-inflammation on macrophages and hepatocytes was demonstrated as a new strategy of anti-inflammation in sepsis.

Analgesic and anti-inflammatory effects of A-286501, a novel orally active adenosine kinase inhibitor

Pain ◽  
2002 ◽  
Vol 96 (1) ◽  
pp. 107-118 ◽  
Author(s):  
Michael F. Jarvis ◽  
Haixia Yu ◽  
Steve McGaraughty ◽  
Carol T. Wismer ◽  
Joe Mikusa ◽  
...  
Keyword(s):  
Kinase Inhibitor ◽  
Adenosine Kinase ◽  
Anti Inflammatory ◽  
Orally Active

scholarly journals Focal intra-colon cooling reduces organ injury and systemic inflammation after REBOA management of lethal hemorrhage in rats

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Awadhesh K. Arya ◽  
Kurt Hu ◽  
Lalita Subedi ◽  
Tieluo Li ◽  
Bingren Hu
Keyword(s):  
Inflammatory Response ◽  
Inflammatory Cytokines ◽  
Troponin I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Balloon Catheter ◽  
Organ Injury ◽  
Upper Body ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

AbstractResuscitative endovascular balloon occlusion of the aorta (REBOA) is a lifesaving maneuver for the management of lethal torso hemorrhage. However, its prolonged use leads to distal organ ischemia–reperfusion injury (IRI) and systemic inflammatory response syndrome (SIRS). The objective of this study is to investigate the blood-based biomarkers of IRI and SIRS and the efficacy of direct intestinal cooling in the prevention of IRI and SIRS. A rat lethal hemorrhage model was produced by bleeding 50% of the total blood volume. A balloon catheter was inserted into the aorta for the implementation of REBOA. A novel TransRectal Intra-Colon (TRIC) device was placed in the descending colon and activated from 10 min after the bleeding to maintain the intra-colon temperature at 37 °C (TRIC37°C group) or 12 °C (TRIC12°C group) for 270 min. The upper body temperature was maintained at as close to 37 °C as possible in both groups. Blood samples were collected before hemorrhage and after REBOA. The organ injury biomarkers and inflammatory cytokines were evaluated by ELISA method. Blood based organ injury biomarkers (endotoxin, creatinine, AST, FABP1/L-FABP, cardiac troponin I, and FABP2/I-FABP) were all drastically increased in TRIC37°C group after REBOA. TRIC12°C significantly downregulated these increased organ injury biomarkers. Plasma levels of pro-inflammatory cytokines TNF-α, IL-1b, and IL-17F were also drastically increased in TRIC37°C group after REBOA. TRIC12°C significantly downregulated the pro-inflammatory cytokines. In contrast, TRIC12°C significantly upregulated the levels of anti-inflammatory cytokines IL-4 and IL-10 after REBOA. Amazingly, the mortality rate was 100% in TRIC37°C group whereas 0% in TRIC12°C group after REBOA. Directly cooling the intestine offered exceptional protection of the abdominal organs from IRI and SIRS, switched from a harmful pro-inflammatory to a reparative anti-inflammatory response, and mitigated mortality in the rat model of REBOA management of lethal hemorrhage.

Abstract 1727: Apolipoprotein E (ApoE) Induces an Anti-inflammatory Phenotype in Macrophages

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Daniel Baitsch ◽  
Ralph Telgmann ◽  
Georg Varga ◽  
Carsten Muller-Tidow ◽  
Martine Bot ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Apolipoprotein E ◽  
Kinase Inhibitor ◽  
Plasma Cholesterol ◽  
Macrophage Phenotype ◽  
Anti Inflammatory ◽  
M2 Phenotype ◽  
Functional Phenotype ◽  
Expression And Activity ◽  
Phenotype Expression

Apolipoprotein E (apoE) exerts anti-atherogenic effects by promoting cholesterol efflux and hepatic lipoprotein clearance. However, apoE retains protective effects even under experimental settings, in which its influence on plasma cholesterol is negligible suggesting that this lipoprotein inhibits atherosclerosis independently from cholesterol transport. To gain further insight into mechanisms underlying apoE-mediated atheroprotection, we investigated its effect on the functional phenotype of RAW 264.7 macrophages overexpressing either of two apoE receptors: ApoER2/LRP8 or VLDL-R. Incubation of ApoER2/LRP8- or VLDL-R-expressing macrophages with apoE downregulated markers of pro-inflammatory M1 functional phenotype (expression and activity of iNOS, production of IL-12), whereas markers of anti-inflammatory M2 phenotype (expression and activity of arginase-I, production of IL-1RA) were upregulated. In addition, macrophage responses typical for M1 phenotype (migration, generation of reactive oxygen species, antibody-dependent cell cytotoxicity) were suppressed in ApoER2/LRP8- or VLDL-R-expressing cells in the presence of apoE. Finally, apoE prevented LPS- and IFN-γ-induced activation of ApoER2/LRP8- or VLDL-R-expressing macrophages as documented by reduced production of IL-12, TNF-α and MCP-1, reduced expression and activity of iNOS and COX2, and reduced activation and/or phosphorylation of NF-κB, IκB and STAT1. The modulatory effects of apoE on macrophage phenotype were inhibited by SB220025, a p38MAP kinase inhibitor, and PP1A, a tyrosine kinase inhibitor. Accordingly, apoE induced tyrosine kinase-dependent activation of p38MAP kinase in ApoER2/LRP8- or VLDL-R-expressing macrophages. Under in vivo conditions, apoE −/− mice transplanted with apoE-producing wild-type bone marrow presented with increased plasma IL-1RA levels. In addition, peritoneal macrophages from transplanted animals demonstrated enhanced M2 phenotype (increased IL-1RA production and CD206 expression). We conclude that apoE signalling over ApoER2/LRP8 or VLDL-R promotes macrophage conversion from pro-inflammatory M1 to anti-inflammatory M2 phenotype. This effect may represent a novel anti-atherogenic activity of apoE.

scholarly journals Interleukin-6 plays an essential role in hypoxia-inducible factor 2α-induced experimental osteoarthritic cartilage destruction in mice

2011 ◽  
Vol 63 (9) ◽  
pp. 2732-2743 ◽  
Author(s):  
Je-Hwang Ryu ◽  
Siyoung Yang ◽  
Youngnim Shin ◽  
Jinseol Rhee ◽  
Churl-Hong Chun ◽  
...  
Keyword(s):  
Interleukin 6 ◽  
Essential Role ◽  
Hypoxia Inducible Factor ◽  
Cartilage Destruction ◽  
Osteoarthritic Cartilage

scholarly journals Repurposing Anti-Malaria Phytomedicine Artemisinin as a COVID-19 Drug

2021 ◽  
Vol 12 ◽  
Author(s):  
Fatih M. Uckun ◽  
Saran Saund ◽  
Hitesh Windlass ◽  
Vuong Trieu
Keyword(s):  
High Risk ◽  
Health Condition ◽  
Infection Process ◽  
Spike Protein ◽  
Organ Injury ◽  
Cytokine Storm ◽  
Infection Cycle ◽  
Chinese Scientist ◽  
Anti Inflammatory ◽  
Post Entry

Artemisinin is an anti-inflammatory phytomedicine with broad-spectrum antiviral activity. Artemisinin and its antimalarial properties were discovered by the Chinese scientist Tu Youyu, who became one of the laureates of the 2015 Nobel Prize in Physiology or Medicine for this breakthrough in tropical medicine. It is a commonly used anti-malaria drug. Artemisinin has recently been repurposed as a potential COVID-19 drug. Its documented anti-SARS-CoV-2 activity has been attributed to its ability to inhibit spike-protein mediated and TGF-β-dependent early steps in the infection process as well as its ability to disrupt the post-entry intracellular events of the SARS-CoV-2 infection cycle required for viral replication. In addition, Artemisinin has anti-inflammatory activity and reduces the systemic levels of inflammatory cytokines that contribute to cytokine storm and inflammatory organ injury in high-risk COVID-19 patients. We postulate that Artemisinin may prevent the worsening of the health condition of patients with mild-moderate COVID-19 when administered early in the course of their disease.

Requirements of src family kinase activity associated with CD45 for myeloma cell proliferation by interleukin-6

Blood ◽  
2002 ◽  
Vol 99 (6) ◽  
pp. 2172-2178 ◽  
Author(s):  
Hideaki Ishikawa ◽  
Naohiro Tsuyama ◽  
Saeid Abroun ◽  
Shangqin Liu ◽  
Fu-Jun Li ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Interleukin 6 ◽  
Kinase Inhibitor ◽  
Myeloma Cell ◽  
Src Family Kinases ◽  
Src Family Kinase ◽  
Receptor Complexes ◽  
Intracellular Signals ◽  
Cellular Context

Abstract Specific intracellular signals mediated by interleukin-6 (IL-6) receptor complexes, such as signal transducer and activator of transcription 3 (STAT 3) and extracellular signal–regulated kinase (ERK) 1/2, are considered to be responsible for inducing a variety of cellular responses. In multiple myeloma, IL-6 only enhanced the proliferation of CD45+ tumor cells that harbored the IL-6–independent activation of src family kinases even though STAT3 and ERK1/2 could be activated in response to IL-6 in both CD45+ and CD45− cells. Furthermore, the IL-6–induced proliferation of CD45+ U266 myeloma cells was significantly suppressed by Lyn-specific antisense oligodeoxynucleotides or a selective src kinase inhibitor. These results indicate that the activation of both STAT3 and ERK1/2 is not enough for IL-6–induced proliferation of myeloma cell lines that require src family kinase activation independent of IL-6 stimulation. Thus, the activation of the src family kinases associated with CD45 expression is a prerequisite for the proliferation of myeloma cell lines by IL-6. We propose a mechanism for IL-6–induced cell proliferation that is strictly dependent upon the cellular context in myelomas.

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