Systemic administration of fractions from Nyctanthes arbor-tristis attenuates chronic inflammatory response in Freund′s-complete-adjuvant-induced arthritis in rats

2014 ◽  
Vol 8 (3) ◽  
pp. 147
Author(s):  
Swapnil Goyal ◽  
NavinR Sheth ◽  
DN Srivastava
Neurosurgery ◽  
1990 ◽  
Vol 26 (4) ◽  
pp. 649-654 ◽  
Author(s):  
Charles E. Nussbaum ◽  
Joseph V. McDonald ◽  
Raymond B. Baggs

Abstract A variety of substances have been used at laminectomy sites to prevent postoperative epidural scarring. Free grafts of autologous subcutaneous fat are commonly used both clinically and experimentally. The free fat grafts usually survive, but decrease in size by about 50%. Postoperatively, subcutaneous seroma has been observed with the use of fat grafts, as well as recurrent symptoms of neural compression by the graft that required additional operations. When compared to the use of free fat grafts after laminectomy in dogs, Vicryl mesh produced slightly more scarring, but consistently less than that observed in control animals. The Vicryl mesh was resorbed by a minimal chronic inflammatory response over about 45 days. Seven of 11 fat-grafted zones showed signs of necrosis, at times with a greater collection of inflammatory cells than that associated with the Vicryl mesh. Of the 4 fat-grafted zones that showed good survival. 2 had gross evidence of neural compression. No surgical zone treated with Vicryl mesh exhibited evidence of neural compression. In view of these results, the use of Vicryl mesh at laminectomy sites may be a safer method of limiting postoperative epidural scar formation.


PLoS ONE ◽  
2013 ◽  
Vol 8 (5) ◽  
pp. e62926 ◽  
Author(s):  
Yen-You Lin ◽  
Yen-Hsuan Jean ◽  
Hsin-Pai Lee ◽  
Wu-Fu Chen ◽  
Yu-Min Sun ◽  
...  

2010 ◽  
Vol 125 (Supplement) ◽  
pp. 14
Author(s):  
T Avraham ◽  
SV Daluvoy ◽  
JC Zampell ◽  
A Yan ◽  
E Kueberuwa

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2797
Author(s):  
Evangeline Deer ◽  
Lorena M. Amaral ◽  
Nathan Campbell ◽  
Sarah Fitzgerald ◽  
Owen Herrock ◽  
...  

IL-2 is a cytokine released from CD4+T cells with dual actions and can either potentiate the inflammatory response or quell a chronic inflammatory response depending on its circulating concentration. IL-2 is elevated in many chronic inflammatory conditions and is increased during preeclampsia (PE). PE is characterized by new-onset hypertension during pregnancy and organ dysfunction and increasing evidence indicates that proinflammatory cytokines cause hypertension and mitochondrial (mt) dysfunction during pregnancy. The reduced uterine perfusion pressure (RUPP) model of placental ischemia is a rat model of PE that we commonly use in our laboratory and we have previously shown that low doses of recombinant IL-2 can decrease blood pressure in RUPP rats. The objective of this study was to determine the effects of a low dose of recombinant IL-2 on multi-organ mt dysfunction in the RUPP rat model of PE. We tested our hypothesis by infusing recombinant IL-2 (0.05 ng/mL) into RUPP rats on GD14 and examined mean arterial pressure (MAP), renal, placental and endothelial cell mt function compared to control RUPP. MAP was elevated in RUPP rats (n = 6) compared to controls (n = 5) (122 ± 5 vs. 102 ± 3 mmHg, p < 0.05), but was reduced by administration of LD recombinant IL-2 (107 ± 1 vs. 122 ± 5 mmHg, n = 9, p < 0.05). Renal, placental and endothelial mt ROS were significantly increased in RUPP rats compared to RUPP+ IL-2 and controls. Placental and renal respiration rates were reduced in RUPP rats compared to control rats but were normalized with IL-2 administration to RUPPs. These data indicate that low-dose IL-2 normalized multi-organ mt function and hypertension in response to placental ischemia.


2019 ◽  
Vol 41 (6) ◽  
pp. 757-766 ◽  
Author(s):  
Miguel Carracedo ◽  
Gonzalo Artiach ◽  
Hildur Arnardottir ◽  
Magnus Bäck

Abstract Omega-3 fatty acids serve as the substrate for the formation of a group of lipid mediators that mediate the resolution of inflammation. The cardiovascular inflammatory response in atherosclerosis and vascular injury is characterized by a failure in the resolution of inflammation, resulting in a chronic inflammatory response. The proresolving lipid mediator resolvin E1 (RvE1) is formed by enzymatic conversion of the omega-3 fatty acid eicosapentaenoic acid (EPA), and signals resolution of inflammation through its receptor ChemR23. Importantly, the resolution of cardiovascular inflammation is an active, multifactorial process that involves modulation of the immune response, direct actions on the vascular wall, as well as close interactions between macrophages and vascular smooth muscle cells. Promoting anti-atherogenic signalling through the stimulation of endogenous resolution of inflammation pathways may provide a novel therapeutic strategy in cardiovascular prevention.


Inflammation ◽  
2020 ◽  
Author(s):  
Karina Scheuermann ◽  
Laura Alejandra Ariza Orellano ◽  
Celso Tarso Rodrigues Viana ◽  
Clara Tolentino Machado ◽  
Marcela Guimarães Takahashi Lazari ◽  
...  

2019 ◽  
Vol 103 ◽  
pp. 109742 ◽  
Author(s):  
P.T. Ramos ◽  
N.S. Pedra ◽  
M.S.P. Soares ◽  
E.F. da Silveira ◽  
P.S. Oliveira ◽  
...  

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