scholarly journals Evolution of the Inflammatory and Fibroproliferative Responses during Resolution and Repair after Ventilator-induced Lung Injury in the Rat

2011 ◽  
Vol 115 (5) ◽  
pp. 1022-1032 ◽  
Author(s):  
Gerard F. Curley ◽  
Maya Contreras ◽  
Brendan Higgins ◽  
Cecilia O'Kane ◽  
Daniel F. McAuley ◽  
...  
Keyword(s):  
Lung Injury ◽  
Time Course ◽  
Transforming Growth Factor ◽  
Arterial Oxygen Tension ◽  
Interleukin 10 ◽  
Transforming Growth Factor Β1 ◽  
Arterial Oxygen ◽  
Normal Lung ◽  
Factor Α ◽  
Severe Lung

Background The time course and mechanisms of resolution and repair, and the potential for fibrosis following ventilation-induced lung injury (VILI), are unclear. We sought to examine the pattern of inflammation, injury, repair, and fibrosis following VILI. Methods Sixty anesthetized rats were subject to high-stretch; low-stretch, or sham ventilation, and randomly allocated to undergo periods of recovery of 6, 24, 48, and 96 h, and 7 and 14 days. Animals were then reanesthetized, and the extent of lung injury, inflammation, and repair determined. Results No injury was seen following low-stretch or sham ventilation. VILI caused severe lung injury, maximal at 24 h, but largely resolved by 96 h. Arterial oxygen tension decreased from a mean (SD) of 144.8 (4.1) mmHg to 96.2 (10.3) mmHg 6 h after VILI, before gradually recovering to 131.2 (14.3) mmHg at 96 h. VILI induced an early neutrophilic alveolitis and a later lymphocytic alveolitis, followed by a monocyte/macrophage infiltration. Alveolar tumor necrosis factor-α, interleukin-1β, and transforming growth factor-β1 concentrations peaked at 6 h and returned to baseline within 24 h, while interleukin-10 remained increased for 48 h. VILI generated a marked but transient fibroproliferative response, which restored normal lung architecture. There was no evidence of fibrosis at 7 and 14 days. Conclusions High-stretch ventilation caused severe lung injury, activating a transient inflammatory and fibroproliferative repair response, which restored normal lung architecture without evidence of fibrosis.

Curcumin and Saikosaponin A Inhibit Chemical-Induced Liver Inflammation and Fibrosis in Rats

2010 ◽  
Vol 38 (01) ◽  
pp. 99-111 ◽  
Author(s):  
Shu-Ju Wu ◽  
Ka-Wai Tam ◽  
Ya-Hui Tsai ◽  
Chun-Chao Chang ◽  
Jane C.-J. Chao
Keyword(s):  
Transforming Growth Factor ◽  
Interleukin 10 ◽  
Transforming Growth Factor Β1 ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Histopathological Results ◽  
Necrosis Factor ◽  
Saikosaponin A

Curcumin and saikosaponin A as antioxidants improve antioxidant status. This study investigated the anti-inflammatory and antifibrotic actions of curcumin and saikosaponin A on CCl4 -induced liver damage. Sprague-Dawley rats were randomly divided into control, CCl4 , CCl4+ curcumin (0.005%; CU), CCl4 + saikosaponin A (0.004%; SS), and CCl4 + curcumin + saikosaponin A (0.005% + 0.004%; CU + SS) groups. Carbon tetrachloride (40% in olive oil) at a dose of 0.75 ml/kg was injected intraperitoneally once a week. Curcumin and saikosaponin A were supplemented alone or in combination with diet 1 week before CCl4 injection for 8 weeks. After 8-week supplementation, histopathological results showed hepatic collagen deposition was significantly reduced in the CU and SS groups, and activated nuclear factor-κ B expression induced by CCl4 in the liver was significantly inhibited by curcumin and/or saikosaponin A. Hepatic proinflammatory cytokines tumor necrosis factor-α, interleukin-1β, and interleukin-6 were significantly inhibited, and anti-inflammatory cytokine interleukin-10 was significantly increased by supplementation with curcumin and/or saikosaponin A. Additionally, curcumin and/or saikosaponin A significantly reduced the increased levels of hepatic transforming growth factor-β1 and hydroxyproline after CCl4 treatment. Therefore, supplementation with curcumin and/or saikosaponin A suppress inflammation and fibrogenesis in rats with CCl4 -induced liver injury. However, the combination has no additive effects on anti-inflammation and antifibrosis.

scholarly journals ASSOCIATION OF CD14 (C-159T) GENE POLYMORPHISM AND IRRITATED INTESTINE SYNDROME WITH OBESITY

2021 ◽  
Vol 20 (2) ◽  
Author(s):  
Yu.V. Bilooka
Keyword(s):  
Transforming Growth Factor ◽  
Interleukin 10 ◽  
Transforming Growth Factor Β1 ◽  
Polymorphic Variant ◽  
Blood Levels ◽  
Polymerase Chain ◽  
Irritable Bowel ◽  
Factor Α ◽  
Cd14 Gene ◽  
Necrosis Factor

The purpose of the study – to study the association of the polymorphic variant C-159Tof the CD14 gene in patients with irritable bowel syndrome (IBS) depending on thepredominance of diarrhea or constipation in the clinical course and the relationshipbetween genotypes of the CD14 gene (C-159T) and some blood parameters.Material and methods. The study involved 90 patients with IBS (30 men and 60women aged 22 to 56 years). The polymorphic variant of the CD 14 gene (C-159T)was analyzed by polymerase chain reaction in 90 patients with IBS without and withconcomitant obesity and 30 people in the comparison group. Blood levels of C-reactiveprotein (CRP), tumor necrosis factor α (TNFα), transforming growth factor β1(TGFβ1), interleukin-10 (IL-10), 8-isoprostane, ceruloplasmin, medium molecules andcalprotectin levels in feces were determined.Results. In patients with IBS and obesity, the frequency of TT genotype (36.7%) washigher compared to healthy subjects (TT genotype – 13.3%). Significantly higherserum levels of CRP (3.5 times and 26.7%), TNFα (1.7 times and 19.5%), TGFβ1(29.8% and 19.2%), 8-isoprostane (54.1% and 31.9%), ceruloplasmin (56.7% and33.0%), medium molecules (7, 5% and 12.9%) and calprotectin (55.7% and 37.4%) inthe feces compared to the CC and CT genotype have been determined in patients withIBS, combined with obesity, TT genotype with a predominance of diarrhea.Conclusions. The association of a polymorphic variant of the CD14 (C-159T) gene withthe risk of IBS development in obese patients has been established. The TT genotype ischaracterized by a higher content of proinflammatory cytokines (TNFα), lower levelsof anti-inflammatory cytokines (IL-10), increased CRP, more pronounced changesin the prooxidant and antioxidant blood systems (higher levels of 8-isoprostane andceruloplasmin, local inflammation (increase in calprotectin content) and severity ofendotoxicosis (higher content of medium molecules).

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