ObjectiveTo bioinformatically analyze the gene chip data of chondrocytes from osteoarthritis patients from the Gene Expression Omnibus (GEO) database, and explore the molecular mechanisms of osteoarthritis.MethodsWe searched the GEO database (up to April 23rd, 2021) for data of chondrocytes and gene expression profiling in human knee osteoarthritis via the key words of “osteoarthritis OR cartilage OR chondrocyte*”. Then, we selected the samples by our inclusion criteria. The data were normalized before analysis. After differentially expressed genes were identified, Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, Search Tool for the Retrival of Interacting Genes/Proteinsm, R language, Perl language, Cytoscape software, and DAVID database were used to perform differentially expressed gene analysis, functional annotation, and enrichment analysis.ResultsThe differentially expressed genes were mostly enriched in cell components and some extracellular regions, which participated in cell division, mitosis, cell proliferation and inflammatory response mainly via the regulation of protein kinase activity. The differentially expressed genes were mainly involved in the cell proliferation signaling pathway, mitogen-activated protein kinase signaling pathway, oocyte meiosis, cell cycle and so on.ConclusionsMultiple signaling pathways are involved in the changes of chondrocytes in human knee osteoarthritis, mainly about cell cycle and protein metabolism genes/pathways. Inflammatory factors and cytokines may be the most important links in the pathogenesis of osteoarthritis.
ObjectiveTo systematically review the influence of dexmedetomidine on early postoperative cognitive dysfunction (POCD) and serum inflammatory factors in elderly patients.MethodsWe searched PubMed, EMbase, The Cochrane Library, CBM, CNKI, WanFang Data and VIP databases from inception to April 2017, to collect randomized controlled trials (RCTs) about dexmedetomidine for early POCD in elderly patients. Two reviewers independently screened literature, extracted data, and assessed the risk of bias of included studies. Then, meta-analysis was performed by RevMan 5.3 software.ResultsA total of 23 RCTs, including 2 026 patients were enrolled. The results of meta-analysis showed that, the incidence of POCD in the dexmedetomidine group was lower than that in the control group (the first day: RR=0.40, 95%CI 0.30 to 0.53, P<0.000 01; the third day: RR=0.33, 95%CI 0.23 to 0.48,P<0.000 01; the seventh day: RR=0.42, 95%CI 0.22 to 0.78,P=0.006). Meanwhile, compared with the control group, the dexmedetomidine group significantly decreased the serum levels of TNF-α (immediately after operation: MD=–5.43, 95%CI –7.44 to –3.42, P<0.000 01; 1 h after operation: MD=–4.64, 95%CI –6.92 to –2.36,P<0.000 1; 24 h after operation: MD=–3.27, 95%CI –4.92 to –1.63,P<0.000 1) and IL-6 (immediately after operation: MD=–30.69, 95%CI –41.39 to –20.00,P<0.000 01; 1h after operation: MD=–20.84, 95%CI –28.87 to –12.80,P<0.000 01; 24 h after operation: MD=–13.42, 95%CI –19.90 to –6.94,P<0.000 1).ConclusionCurrent evidence indicates that dexmedetomidine could relief early POCD in elderly patients, in which the reduction of serum inflammatory factors alleviate inflammation response may play a vital role. Due to the limited quality and quantity of included studies, more high quality RCTs are required to verify the above conclusion.
Objective To investigate the influence of proteasome inhibitorMG-132 on inflammatory factors in COPD rats and its potential mechanism. Methods The COPD rat model was established by instillation of lipopolysaccharide and exposure to cigarette smoke. Then the rats were randomly divided into 4 groups( n = 12 in each group) , ie. a COPD model group, a COPD + MG-132 low concentration group ( 0. 05 mg·kg- 1·d - 1 ) , a COPD + MG-132 high concentration group( 0. 1 mg· kg- 1 · d - 1 ) , and a normal control group. The rats were injected intraperitoneally with different dose of MG-132 or normal saline. After 1 week and 4 weeks, 6 rats in each group were sarcrificed. Then the following parameters were determined including histopathological changes of lung tissue, and the concentrations of IL-1β, IL-6, IL-8 in serum and diaphragm via ELISA. Results The lung histopathological examination showed obvious emphysema and inflammatory infiltration in the COPD rats. These pathological changes were obviously ameliorated in two MG-132 treatment groups. The IL-1β, IL-6, and IL-8 levels in serumand diaphragmin the COPD model group were all significantly increased from1 week and 4 week than those in the normal control group( P lt;0. 05) .MG-132 down-regulated the expression of these inflammatory factors in a time-and dosedependent manner. The IL-1β, IL-6, and IL-8 levels in serum and diaphragm in the MG-132 low concentration group and high concentration group were all decreased compared with the COPD model group ( P lt; 0. 05) . Conclusion COPD is a systemic inflammatory disease which can be inhibited by the proteasome inhibitor MG-132 through suppressing inflammatory factors.
ObjectiveThis study applied Mendelian randomization to explore the potential causal relationship between inflammatory factors and diabetic nephropathy. MethodsSummary-level data from genome-wide association studies of inflammatory factors and diabetic nephropathy were used, and inverse variance weighted analysis was used as the primary analytical method, complemented by results from weighted median, MR-Egger regression, simple model, and median model approaches. Sensitivity analysis was used to test the reliability of the MR analysis results. ResultsIn the inverse variance weighted method, stem cell factor (OR=1.28, 95%CI 1.04 to 1.58, P=0.020) and interferon-γ (OR=1.36, 95%CI 1.10 to 1.70, P=0.005) were positively correlated with diabetic nephropathy, and diabetic nephropathy was positively correlated with interferon-inducible protein 10 (OR=0.90, 95%CI 0.83 to 0.98, P=0.012) were negatively correlated with diabetic nephropathy. Sensitivity analysis showed that MR analysis was reliable. ConclusionStem cell factors and interferon-γ are associated with an increased risk of developing diabetic nephropathy, and diabetic nephropathy decreases the expression of interferon-inducible protein 10 in vivo. Our results demonstrate a potential causal relationship between inflammatory factors and the development of diabetic nephropathy. This finding is of clinical significance for the pre-diagnosis and treatment of diabetic nephropathy.
This study aims to investigate the protective effect of resveratrol against liver injury in hindlimb unloading rats. Thirty 2-month-old male SD rats were randomly divided into normal group (Control), hindlimb unloading model group (Model), and hindlimb unloading+resveratrol administration group (Model+Res). The Model + Res group was injected intraperitoneally with 30 mg/kg of resveratrol, and the Control and Model groups were injected intraperitoneally with an equal volume of 0.9% NaCl. Liver tissues were collected after 28 days and analyzed for oxidative stress, inflammatory factors, energy metabolism indices, Na+-K+-ATPase and Ca2+-Mg2+-ATPase activity, and morphological changes were observed by hematoxylin-eosin staining. The protein expression levels of Bax, Bcl-2, p-PI3K, PI3K, p-AKT, and AKT were detected by Western blotting. Compared with the Control group, hepatocytes in the Model group showed swelling, abnormal morphology, nuclear consolidation, and cell membrane disruption. Oxidative stress, inflammatory factor levels, hepatic glycogen accumulation, and energy metabolism were increased in the liver tissues of the Model group, while resveratrol treatment significantly reversed these changes. The results of Western blotting showed that resveratrol significantly reduced the expression of Bax and increased the expression levels of Bcl-2, and the proteins of p-PI3K/PI3K and p-AKT/AKT expression levels. It is suggested that 28 days of hindlimb unloading treatment could lead to liver tissue injury in rats, which is manifested as oxidative stress, inflammatory response, energy metabolism disorder and increased apoptosis level, and resveratrol has a certain mitigating effect on this.
Objective To investigate the effect of sodium hyaluronate (SH) intra-articular injection on the treatment of knee osteoarthritis (OA), andto compare the contents of free radicals and inflammatory factors in joint fluids of pre-and pro-treatment as to explore the treatment mechanism of SH. Methods Ninety-two patients (111 knees) with mild(51)，moderate(35) and serious(25) knee OA were treated with intra-articular injections of SH (20 mg once a week for 5 weeks). According to Lysholm scoring, clinical signs such aspain, swelling,and the ability to walk, squat, run, go upstairs and downstairs were assessed before and after the treatment, and the contents of nitric oxide (NO), superoxide dismutase(SOD), malonic dialdehyde(MDA) and IL-1β、TNF-α in joint fluids from the OA joints before 1st,2nd, and 5th injection and 3 months after each injection were observed. Results All cases were followed up for 3 months. The improvements in the signs and function of knees were excellent in 42 knees, good in 38 knees, fair in 21 knees and poor in 10 knees, with 72.1% excellent and good results. The lighter the illness was, the better the improvement was: the rate of the excellent and good was 92.1% in mild group, 68.6% in moderate group and 42.9% in serious group. The contents of oxygen free radicals and IL-1β、TNF-α of the patients with mild and moderate OA decreasedmarkedly after being treated with SH（Plt;0.05）, but these decreased lightlyin serious OA group（Pgt;0.05）. SH had mild effect on the contents of NO. Three months after treatment, only in mild OA group the contents of NO significantly decreased（Plt;0.05）, and no significant change in moderate and serious groups was observed（Pgt;0.05）. Conclusion SH intraarticular injection has a positive effect on the relief of clinical symptoms and on the improvement of articular function of knee OA. The therapeutical effect of SH on OA is achieved possibly by decreasing the contents of free radicals especially oxygen free radicals and inflammatory factors in joint fluids.
ObjectiveTo summarize the clinical usage of modified ultrafiltration in pediatric cardiopulmonary bypass. MethodsWe selected 40 infants with congenital heart defects as our study subjects between January 2010 and February 2012. They were randomly divided into two groups. One group used modified ultrafiltration, while the other did not, during the operation with cardiopulmonary bypass. The different perioperative changes of pulmonary pressure and the tumor necrosis factor (TNF) and interleukin-8 (IL-8) concentration in plasma were observed in both the two groups. ResultsNo complication relative to modified ultrafiltration was found. After the operations began, TNF and IL-8 concentration in the two groups rose fast; at the end of operations and 2 hours after operation, the pulmonary pressure and TNF and IL-8 concentration in the two groups decreased, and the decrease in the modified ultrafiltration group was faster. ConclusionThe use of modified ultrafiltration during operations with cardiopulmonary bypass can reduce residual water within the body in a short period and decrease the concentration of inflammatory factors, which is helpful for postoperative recovery of the cardiac and lung functions.
ObjectiveTo investigate the effects of continuous positive airway pressure (CPAP) ventilation on blood pressure and related inflammatory factors in patients with obstructive sleep apnea hypopnea syndrome (OSAHS) and refractory hypertension, and explore the correlation between respiratory function and related inflammatory factors.MethodsPatients with OSAHS and refractory hypertension who visited Shenzhen Nanshan People’s Hospital between January 2014 and September 2018 were randomly divided into a CPAP group and a control group. The control group received routine treatment. The CPAP group received CPAP on the basis of conventional treatment. Each intervention lasted for 7 days. The changes of systolic and diastolic blood pressure were measured before and after 1, 3, 5, and 7 days, respectively. The respiratory function and related inflammatory factors were measured after 7 days of intervention.ResultsAfter 7 days of treatment in the CPAP group, the levels of apnea hyperpnoea index (AHI), lowest oxygen saturation and oxygen desaturation index were significantly better than those before intervention, with the improvement of respiratory function significantly higher than that of the control group after 7 days. Meanwhile the systolic and diastolic blood pressure levels were significantly lower in the CPAP group than those of the control group at 1, 3, 5, and 7 days, and lower than the pre-intervention after 7 days of intervention. After 7 days of intervention, the inflammatory factors in both groups were significantly improved (all P<0.05). However, the serum levels of high sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and endothelin-1 (ET-1) in the CPAP group were significantly lower than those of the control group after 7 days of treatment (P<0.05). There was a significant positive correlation between AHI level and hs-CRP, IL-6, TNF-α and ET-1 in the CPAP group after intervention (P<0.001).ConclusionsCPAP can significantly improve the blood pressure of patients with OSAHS and refractory hypertension. CPAP may improve the related inflammatory factors by improving the respiratory function of patients, thus reduce the patient’s blood pressure.
ObjectiveTo observe the relationship between the serum level changes of high-sensitivity C-reactive protein (hsCRP), interleukin (IL)-18, intercellular adhesion molecule-1(ICAM1), matrix metalloproteinase (MMP)-9 and lipoprotein-associated phospholipase A2(Lp-PLA2), and the multiple factors of acute cerebral infarction (ACI). MethodsWe chose 76 patients with ACI treated between July 2012 and June 2014 as our study subjects.On the second day (acute phase) and the 15th day (recovery phase) after onset, we checked the patients for their serum levels of hsCRP, IL-18, ICAM1, MMP-9 and Lp-PLA2.Then, multiple linear regression analysis was performed to observe the correlation of the serum level change degree of inflammatory factors with hypertension, diabetes, coronary heart disease, smoking history, carotid atherosclerotic plaque, lipid levels, infarct size and National Institute of Health Stroke Scale (NIHSS) score. ResultsThe changes of all the inflammatory factors in the acute phase and the recovery phase of cerebral infarction were not significantly related to smoking history, hypertension, coronary heart disease, low-density lipoprotein and NIHSS scores (P > 0.05).The changes of hsCRP and ICAM1 had significant correlation with cerebral infarct size, diabetes mellitus and carotid atherosclerotic plaque (P < 0.05), and the change level of Lp-PLA2 was related to diabetes mellitus, and carotid atherosclerotic plaque (P < 0.05).MMP-9 serum level change had correlation with only cerebral infarct size (P < 0.05). ConclusionsSerum level changes of inflammatory factors are related to various factors of cerebral infarction.The main factors that affecting the serum level changes are cerebral infarction area, diabetes mellitus and carotid atherosclerosis.
Objective To explore the role of macrophage-stimulating protein ( MSP) and receptor tyrosine kinase RON in the airway inflammation of chronic obstructive pulmonary disease( COPD) , and investigate its possible mechanism. Methods The rat COPDmodel was established by exposing the rats to cigarette smoke daily for three months. Rat alveolar macrophages ( AMs) were isolated in vivo and cultured,and then challenged with different concentrations of MSP for 24 hours. The concentrations of MSP in broncho-alveolar lavage fluid ( BALF) and serum, and the levels of IL-1β, TNF-α, IL-8, and IL-10 in the supernatants were measured by ELISA. The expression of RONmRNA in lung tissue was assessed by reverse transcription-polymerase chain reaction. The levels of RON protein in the lung tissue and AMs cultured in vitro were observed by immunohistochemistry. The activity of superoxide dismutase ( SOD) and malondialdehyde ( MDA) content in the culture solution were measured with chromatometry method. Results Compared with the control group, the concentrations of MSP in serum and BALF of the COPD rats were significantly higher ( P lt;0. 01) . The levels of RONmRNA and RON protein in the COPD rats were also upregulated significantly ( P lt; 0. 01) . MSP evoked the AMs isolated from the normal and COPD rats to generate more content of MDA and caused a reduction in activity of SOD. In addition, MSP stimulated TNF-α, IL-8, IL-1βand IL-10 release fromAMs of the normal and COPD rats dose-dependently. The levels of TNF-α, IL-8, and IL-1βwere higher, while the level of IL-10 and the SOD activity were lower in AMs of the COPD group than those of the control group in the same dose of MSP ( P lt;0. 01) . The more significant increase in the levels of TNF-α, IL-8, IL-1β, and the more notable decrease in the activity of SOD was found in the COPD group compared with the control group. But the degree of increasing MDA and IL-10 in the AMs of the COPD group was lower than that in the control group. Linear correlation analysis showed that the MSP concentration and the RON protein level in the COPD rats were positively associated with the total cellcounts and AM counts in BALF, and were related to the indexes for pulmonary emphysema. Conclusions There is a close correlation between the MSP and receptor tyrosine kinase RON with the airway inflammation of COPD. The mechanism might be that MSP promote the macrophages release inflammatory factors and increase the production of oxygen free radicals.