ObjectiveTo study the effects of the new small molecular oxygen free radical scavenger Tempol on the survival and vasculogenesis of the long random pattern skin flap (LRPSF) and its mechanism.
MethodsEighty-four male Sprague Dawley rats were randomly divided into control and Tempol groups (42 rats in each group). LRPSF of 9 cm×3 cm in size were prepared on the backs of rats in two groups based on the Mcfarlane flap. Rats were administered with Tempol (100 mg/kg) in the Tempol group and with normal saline in the control group by intraperitoneal injection at 15 minutes before operation and at 1-7 day after operation. The rat and the skin flap survival conditions were observed after operation; the survival rate of skin flap was measured, and the vascular structure, vascular volume, and total length of blood vessels were analyzed with Micro-CT three-dimensional imaging after 7 days; HE staining was used to observe the structure of the skin flaps and inflammation, immumohistochemical staining to observe vascular endothelial growth factor (VEGF) expression; water-soluble tetrazolium-1 method was used to measure the content of superoxide dismutase (SOD) and malondialdehyde (MDA), and ELISA to detect the expressions of tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6) after 1, 3, and 7 days.
ResultsAll of rats survived after operation, without hemorrhage, edema, and infection. With the extension of time, necrosis occurred in the distal part of the skin flaps in 2 groups, but the necrosis degree of the Tempol group was lower than that of control group; meanwhile, the blood vessel distribution and continuity were better than those of control group. The skin flaps survival rate, vascular volume, and total length of blood vessels of Tempol group were significantly higher than those of control group after 7 days (P<0.05). The clearer skin flaps structure, lighter inflammation reaction and inflammation cell infiltration, and higher VEGF staining intensity were observed in the Tempol group than the control group after 7 days. There was no significant difference in SOD, MDA, and TNF-α, and IL-6 contents between the 2 groups at immediate after operation. SOD significantly increased, but MDA, TNF-α, and IL-6 contents significantly decreased in the Tempol group when compared with control group after 1, 3, and 7 days (P<0.05).
ConclusionTempol can significantly promote the LRPSF survival rates, its mechanism is closely related to the promotion of vasculogenesis and reduction of oxidative stress and inflammation.
ObjectiveTo summarize the advance of triggering receptor expressed on myeloid cells-1 (TREM-1). MethodsLiteratures about the recent studies on the TREM-1 were reviewed. ResultsTREM1 was a mediator of inflammation. It could amplify the inflammation and lead to overexpression of inflammation in final. ConclusionTREM-1 is very important in development of many diseases and provide a new molecule target to cure.
The hallmark lesions of age-related macular degeneration (AMD) are drusen and basal linear deposit which are lipid substances deposited in Bruch membrane or the compartment on the Bruch membrane. There is a prevailing hypothesis that lipid and its oxidized derivant deposited in retina may have important roles in the pathogenesis of AMD. Lipid oxidation products are toxic, may affect the adjacent cells, induce inflammation, and trigger neovascularization.7-ketocholestoral (7KCh), a naturally occurring oxidized form of cholesterol, had been found to be toxic to retinal cells and able to induce chronic inflammation, which may play a critical role in the development of AMD. However the precise mechanism remains to be elucidated. Thus we will make a brief review of 7KCh and its association with AMD.
Atrial fibrillation(AF)is one of the most common cardiac dysrhythmia encountered in clinical practice. Although major advances in management and prophylaxis in recent years, AF continues to be associated with increased morbidity, repeated hospitalization, reduced quality of life, and even death, causing great social and economic burden. So far, the mechanism underlying AF is not completely elucidated. There is an enormous and complicated pathogenesis involved in the occurrence and maintenance of AF. At present, a lot of studies show that inflammation is closely associated with AF. Inflammation may take part in the occurrence and maintenance of AF through the influence of cardiac electrical remodeling and structural remodeling. This review focuses on research progress of correlation evidence of inflammation and atrial fibrillation and anti-inflammatory drug therapies of AF.
Microvesicles (MVs) is small membrane vesicles released from different cell types under different conditions. Studies have shown that MVs may mediate vascular inflammation, angiogenesis, and other pathological processes. MVs may play an important role in the pathogenesis of diabetic retinopathy (DR) by mediating endothelial cell injury, thrombosis and neovascularization. The plasma MV level may be an effective parameter to monitor the development of DR. This article will summarize the research progress of the relationship between MVs and DR in recent years.
ObjectiveTo study on the relationship of serum apelin level with inflammation in patients with atrial fibrillation (AF).
MethodsWe recruited 58 patients with valvular heart disease who admitted in our hospital between October 2014 and December 2014 and planned to undergo surgery, including 29 patients with persistent AF (an AF group) and 29 patients with sinus rhythm (a SR group). There were 14 males and 15 females in the AF group at an average age of 57±8 years. There were 20 males and 9 females in the SR group at an average age of 54±10 years. The left atrial diameter (LAD) and ejection fraction (EF) were detected by echocardiography. The levels of serum apelin and interleukin-6 (IL-6) were measured by enzyme linked immuno sorbent assay, and the level of high-sensitivity C-reactive protein (hs-CRP) were determined by turbidimetric inhibition immuno assay.
ResultsCompare with the SR group, the serum apelin level (201.94±71.96 pg/ml vs. 286.72±129.33 pg/ml) and EF (54.52%±3.94% vs. 56.41%±2.85%) were significantly lower in the AF group, while the hs-CRP (5.58±12.90 mg/L vs. 1.89±3.55 mg/L), IL-6 (2.59±0.64 pg/ml vs. 2.26±0.55 pg/ml) and LAD (57.10±11.69 mm vs. 43.07±5.31 mm) were significantly higher in the AF group (P<0.05). Correlation analysis showed that the apelin level was negatively correlated with hs-CRP and LAD (r=-0.308, P=0.019; r=-0.313, P=0.017), and were positively correlated with EF (r=0.265, P=0.044).
ConclusionSerum apelin level is significantly lower in patients with AF and levels of inflammation makers are significantly higher. Apelin may be closely related to AF and inflammation, and may take part in the occurrence and maintenance of AF through the regulation of inflammatory processes.
ObjectiveTo explore the relationship of the level of inflammation and nutritional status with the occurrence and prognosis of refractory diabetic foot.MethodsA total of 70 patients with refractory diabetic foot between August 2015 and August 2017 were randomly selected as the observation group. Another 70 patients with diabetes mellitus (without foot ulcer) who visited the hospital in the same period were set as the control group. The observation group was subgrouped into the non-amputation group and the amputation group according to the follow-up endpoint events, and into the grade Ⅲ, Ⅳ, and Ⅴ groups according to Wagner classification method. The blood levels of inflammatory markers and nutritional markers between groups were compared.ResultsIn the observation group, vascular cell adhesion molecule-1 (VCAM-1), fibroblast growth factor 2 (FGF2), fibrinogen (FIB), tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-18, lipoprotein phospholipase A2 (LP-PLA2), C-reactive protein (CRP) levels were significantly higher than those in the control group, and albumin (ALB), prealbumin (PA), and transferrin (TRF) levels were significantly lower than those in the control group, with statistically significant differences (P<0.01). The blood levels of FGF2, FIB, IL-6, IL-18, LP-PLA2, and CRP in the amputation group were significantly higher than those in the non-amputation group, and the levels of TRF, ALB, and PA were significantly lower than those in the non-amputation group (P<0.01). There were statistically significant differences in the levels of FGF2, FIB, IL-6, IL-18, LP-PLA2, CRP, TRF, ALB, and PA in patients with diabetic foot with different Wagner grades (P<0.05). The result of multiple logistic regression analysis showed that IL-6 [odds ratio (OR)=1.487, 95% confidence interval (CI) (1.023, 2.120), P<0.001], IL-18 [OR=1.274, 95%CI (1.052, 1.665), P<0.001], LP-PLA2 [OR=1.478, 95%CI (1.126, 1.789), P<0.001], and CRP [OR=2.085, 95%CI (1.574, 2.782), P<0.001] were independent risk factors for the occurrence of refractory diabetic foot, and TRF [OR=0.645, 95%CI (0.002, 0.898), P<0.001], ALB [OR=0.838, 95%CI (0.429, 0.923), P<0.001], and PA [OR=0.478, 95%CI (0.201, 0.984), P<0.001] were independent protective factors for the occurrence of refractory diabetic foot.ConclusionIn the clinical treatment of diabetic foot, we should pay attention to the monitoring of the level of inflammatory factors and nutritional status, and it is necessary to timely carry out anti-inflammatory treatment and appropriate nutritional support treatment.
ObjectiveTo review the research progress of microenvironment for the treatment of peripheral nervous injuries.
MethodsThe recent literature concerning the treatment mechanism of peripheral nervous injuries was extensively consulted, and the microenvironment response involved in the treatment of peripheral nervous injuries was reviewed.
ResultsThe complex microenvironment for treatment of peripheral nervous injuries is dependent on nerve regeneration chamber, the formation of neurotrophic factors, inflammation response, regulation of hormones, signaling pathways, and related enzymes in regulation. In-depth study will help us have a clearer understanding on the distal and proximal neurons axons at the cellular and molecular levels after peripheral nervous injuries.
ConclusionIn recent years, the researches of microenvironment for the treatment of peripheral nervous injuries have achieved obvious progress. With the current nanotechnology, materials science, genetic engineering, and stem cell transplantation technology, it will provide new ideas and corresponding basis for clinical treatment.
Objective To establish a cell culture model in vitro of acute lung injury and investigate the effects of NF-κB p65 on the inflammation and oxidative stress in TNF-α-activated type Ⅱ alveolar epithelial cells. Methods A549 cells were treated with TNF-α ( 10 ng/mL, 24 h) in the absence or presence of NF-κB p65 siRNA ( 50 nmol /L) . RT-PCR and Western blot were performed to analyze the silence efficiency of RNAi targeting NF-κB p65. The contents of IL-1β, IL-4, and IL-6 in the culture supernatant were measured by ELISA. The concentration of MDA and SOD were detected by colorimetric method. The survival rate of cell was assessed by the methyl thiazolyl tetrazolium ( MTT) assay. Results P65 RNAi significantly decreased the transcription and translation of NF-κB p65 induced by TNF-α( P lt; 0. 05) . The levels of IL-1β, IL-4, and IL-6 were significantly lower in the supernatants of A549 cells pretransfected with NF-κB p65 siRNA ( P lt;0. 05) , while the concentration of MDA markedly decreased ( P lt; 0. 05) , and the activation of SOD increased dramatically ( P lt; 0. 05) . Consequently, the survival rate of A549 in the p65 siRNA group improved( P lt; 0. 05) . Conclusions NF-κB p65 plays a key role in the oxidative stress induced by TNF-α. NF-κB p65 silencing can down-regulate the inflammation and oxidative stress induced by TNF-αand enhance the proliferation of alveolar epithelial cells.
Objective To investigate the relations between the human beta defensin-2 (HBD-2) and systemic inflammatory responses in patients with lower respiratory tract infection（LRTI）. Methods Eighty-one patients with confirmed LRTI including community-acquired pneumonia，acute exacerbation of chronic obstructive pulmonary disease or concurrent lung infection，and bronchiectasis concurrent infection were enrolled，and twenty healthy volunteers were included as control. Plasma concentrations of HBD-2，IL-1β，and IL-8 were assayed with ELISA method in all patients and controls. Furthermore the patients were divided into three groups according to the onset of disease:,ie.group A （shorter than 7 days），group B （7 to 14 days），and group C （more than 14 days）. The differences between these groups were compared. Correlation between HBD-2 and IL-1β or IL-8 concentrations was analyzed. Results HBD-2，IL-1β，white blood cell （WBC） of the peripheral blood in the patients with LRTI were all significantly higher than those in the healthy controls. HBD-2 and IL-1β increased in group A and group B，and decreased in group C comparing to the control group （Plt;0.05 respectively）. There was no significant difference of IL-8 in group A，B and C. HBD-2 showed a positive linear correlation with IL-1β （r=0.313，P=0.030） and no correlation with IL-8（Pgt;0.05）. Conclusions The plasma HBD-2 concentration is increased in LRTI patients，which may be a biomarker of systemic inflammation in the early or relative early course of LRTI.
