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.
ObjectiveTo investigate the expression of histone deacetylase 2 (HDAC2) in animal model of benign tracheal stenosis, and explore the mechanism of HDAC2 in development of tracheal stenosis.MethodsEighteen rabbits were randomly divided into a blank control group, a model group, and an erythromycin group, with 6 rats in each group. The model group and the erythromycin group underwent tracheostomy, the inner wall of trachea was brushed back and forth with a nylon brush for more than 20 times to induce benign tracheal stenosis. From 7 days before surgery to 9 days after surgery, the model group received gavage with saline, the erythromycin group received gavage with low-dose erythromycin in dose of 15 mg·kg–1·d–1, and the control group did not receive any treatment. On the 10th day after operation, all the rabbits were sacrificed and the trachea was cut to measure the tracheal stenosis. RNA and protein were extracted from the granulation tissue in the stenosis and the relative mRNA expressions of HDAC2, interleukin (IL)-6 and IL-8 in the granulation tissue were detected by real-time fluorescence quantitative PCR. The relative expression of HDAC2 protein was detected by Western blot.ResultsCompared with the blank control group, the tracheal stenosis in the model group was more obvious [(84.60±1.14)% vs.(27.00±6.44)%], the mRNA and protein expressions of HDAC2 were decreased (0.29±0.07 vs. 1.00±0.00, 0.20±0.02 vs. 0.49±0.04), the mRNA expressions of IL-6 and IL-8 were up-regulated (4.22±0.67 vs. 1.00±0.00, 162.72±23.23 vs.1.00±0.00). Compared with the model group, tracheal stenosis in the erythromycin group was relieved [(64.00±12.25)% vs. (84.60±1.14)%], the mRNA and protein expressions of HDAC2 were increased (0.42±0.14 vs. 0.29±0.07, 0.43±0.01 vs. 0.20±0.02), the mRNA expressions of IL-6 and IL-8 were decreased (0.72±0.24 vs. 4.22±0.67, 130.22±7.93 vs. 162.72±23.23). All the differences were statistically significant (all P<0.05). The Pearson correlation coefficient between tracheal stenosis and HDAC2 mRNA relative expression was –0.96 (P<0.05).ConclusionsThe down-regulation of HDAC2 expression in model of benign tracheal stenosis is related to the occurrence and development of tracheal stenosis. The low dose of erythromycin may be used to treat benign tracheal stenosis by up-regulating expression of HDAC2 and thus inhibiting the inflammatory disorder during tracheal injury repair.
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 establish a cell inflammation model induced by tumor necrosis factor-α (TNF-α) in human bronchus epithelial cells, and investigate the effects of glutathione S-transferase mu 5 (GSTM5) on the inflammation and oxidative stress. Methods16HBE cells were treated with TNF-α (10 ng/mL, 24 h) in the absence or presence of the constructed GSTM5 eukaryotic expression vector (1 μg/mL). The concentration of malondialdehyde (MDA) and total antioxidation capacity (T-AOC) were detected by colorimetric method. The survival rate of cells was assessed by the methyl thiazolyl tetrazolium (MTT) assay. The transcription level of NADPH oxidase-1 (NOX1), NOX2, NOX3, NOX4, NOX5, dual oxidase-1 (DUOX1) and DUOX2 were evaluated by RT-PCR. Western blot was performed to investigate the protein levels of NOX1 and NOX2. ResultsTNF-α simulation significantly increased the level of MDA in cells, and decreased the level of T-AOC and survival rate of 16HBE. When transfected with the GSTM5 eukaryotic expression vector, the concentration of MDA significantly decreased (P < 0.05), and the activation of T-AOC increased dramatically (P < 0.05). Consequently, the survival rate of 16HBE in the GSTM5 group improved (P < 0.05). The 16HBE cells transfected with the constructed GSTM5 eukaryotic expression vector had a lower transcription and protein levels of NOX1 and NOX2 (all P < 0.01). There were no significant changes in the mRNA expressions of NOX3, NOX4, NOX5, DUOX1 or DUOX2. ConclusionGSTM5 may down-regulate the transcription level of NOX1 and NOX2 to reduce the inflammation and oxidative stress induced by TNF-α.
ObjectiveTo observe the protective effect of Zhicao Tea Mixture on Müller cells and the expression of inflammatory factors in mice with diabetic retinopathy.MethodsSeventy-five C57BL/6J mice were randomly divided into the normal control group, diabetes mellitus (DM) group, low concentrations group, medium concentrations group and high concentrations group, with 16 mice in each group. The diabetes model of mice in all groups except the normal control group were established by intraperitoneal injection of STZ (60 mg/kg). Four weeks after the successful modeling, the Zhicao Tea Mixture with low (30 ml/kg), medium (60 ml/kg) and high concentrations (120 ml/kg) were respectively administered by gavage. Weight and blood glucose of mice in each group were measured every two weeks. After 8 weeks, Western blot method was used to detect the mice retina Müller cells activation marker gelatinous fibrous acidic protein (GFAP). Immunofluorescence was performed to detect the expression GFAP and glutamine synthetase (GS). Real-time quantitative PCR (RT-qPCR) and ELISA were used to determine the mRNA and protein expression levels of mouse retinal VEGF, TNF-α, IL-1β and IL-6 respectively.ResultsThe weight of mice in the DM group was lower than that of the normal control group, and the blood glucose was increased. Zhicao Tea Mixture had no effect on the weight of DM mice, but had a significant hypoglycemic effect. The GFAP expression (t=38.318, P＜0.001) in the retina of mice in the DM group was increased and GS expression (t=29.737, P＜0.001) was decreased compared with the control group. The GFAP expression (t=13.677, 19.387, 16.305; P＜0.05) in the retina of mice in the low, medium and high concentrations group were decreased and GS expression (t=5.170, 19.399, 6.705; P＜0.05) were increased compared with the DM group. The expressions of retinal inflammatory factors VEGF, TNF-α, IL-1β and IL-6 in DM group all increased, while the expressions of the above-mentioned inflammatory factors in the retina of mice decreased in the low, medium and high concentrations group.ConclusionZhicao Tea Mixture can decrease the blood glucose of DM mice and reduces the diabetic retinal inflammatory response.
Objective To systematically review the efficacy of different exercises on inflammatory cytokines in individuals with overweight or obesity. Methods The CNKI, WanFang Data, VIP, PubMed, EBSCO, Cochrane Library, Web of Science and Embase databases were electronically searched to collect randomized controlled trials (RCTs) on the efficacy of exercise on inflammatory cytokines in individuals with overweight or obesity from January, 2000 to April, 2021. Two reviewers independently screened the literature, extracted data, and assessed the risk of bias of the included studies. The network meta-analysis was then performed using Stata 16.0 software. Results A total of 63 RCTs were included, 49 of which reported the changes in IL-6, 47 of which reported the changes in TNF-α, and 16 of which reported the changes in IL-10. The results of the network meta-analysis found that compared with those in the control group, aerobic exercise (AE) (SMD=−0.9, 95%CI −1.4 to −0.5, P<0.01) and high-intensity interval training (HIIT) (SMD=−1.3, 95%CI −2.3 to −0.3, P=0.011) significantly reduced IL-6. AE (SMD=−1.3, 95%CI −1.7 to −0.9, P<0.01), combined exercise (COM) (SMD=−0.7, 95%CI −1.3 to −0.1, P=0.02), and HIIT (SMD=−1.8, 95%CI −2.6 to −0.9, P<0.01) significantly reduced TNF-α; AE (SMD=0.8, 95%CI 0.1 to 1.5, P=0.03) significantly increased IL-10. The cumulative probability ranking results showed that HIIT was the most effective in reducing IL-6 and TNF-α and increasing IL-10, followed by AE and COM, and resistance training (RT) was the least effective. Conclusion Different exercise types have different effects on improving inflammation in individuals with overweight or obesity. HIIT can be suggested as the best exercise program to improve chronic inflammation in individuals with overweight or obesity. Due to the limited quantity and quality of the included studies, more high-quality studies are needed to verify the above conclusion.
Age-related macular degeneration (AMD) is one of the leading irreversible causes of blindness in China. The pathogenesis of AMD is not fully understood at present. Under various stress conditions, cellular senescence is activated, characterized by telomere shortening, mitochondrial dysfunction, DNA damage, and the release of various senescence-related secretory phenotype factors. Senescence is implicated in the pathogenesis of AMD through multiple pathways, contributing to chronic inflammation and the onset and progression of AMD. Mechanisms such as oxidative stress, lipofuscin, β amyloid protein and the membrane attack complex have become hotspots of study in the pathogenesis of AMD. The cyclic guanosine phosphate - adenosine synthase - interferon stimulating factor synthase-stimulator of interferon gene pathway has emerged as a critical signaling pathway in the early development of AMD, providing direction for further research on AMD. Currently, senolytics, selective agents targeting the induction of senescent cell apoptosis, show significant potential in the treatment of AMD. The integration of new technologies with cellular senescence may offer a novel approach to AMD treatment, and intervening in the AMD treatment through anti-cellular senescence pathways holds promising prospects.
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.
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.
Febrile seizures (FS) are one of the most common neurological disorders in pediatrics, commonly seen in children from three months to five years of age. Most children with FS have a good prognosis, but some febrile convulsions progress to refractory epilepsy (RE). Epilepsy is a common chronic neurological disorder , and refractory epilepsy accounts for approximately one-third of epilepsies. The etiology of refractory epilepsy is currently complex and diverse, and its mechanisms are not fully understood. There are many pathophysiological changes that occur after febrile convulsions, such as inflammatory responses, changes in the blood-brain barrier, and oxidative stress, which can subsequently potentially lead to refractory epilepsy, and inflammation is always in tandem with all physiological changes as the main response. This article focuses on the pathogenesis of refractory epilepsy resulting from post-febrile convulsions.