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 investigate the changes of interleukin-8 (IL-8), tumor necrosis factor-α(TNF-α) and phospholipase A2 (PLA2) in serum, bronchoalveolar lavage fluid (BALF) and lung tissue of COPD rats and the effects of tiotropium.To identify the anti-inflammatory function of tiotropium. MethodsRat COPD model was established by passive smoking as well as intratracheal instillation of lipopolysaccharide(LPS).Thirty male SD rats were randomly divided into a control group, a COPD group and a tiotropium bromide treatment group (n=10 in each group).The pathologic changes of the lung tissue and airway were observed by HE staining.The total and differential cell counts in BALF were observed.The levels of IL-8, TNF-α, PLA2 in serum, BALF and lung tissue were measured by enzyme-linked immunosorbent assay. ResultsHE staining revealed that the rat COPD model was successfully established.The COPD group appeared obvious emphysema, while the treatment group appeared mild emphysema.The total inflammatory cells, the proportion of neutrophils and lymphocyte, and the levels of IL-8, TNF-α, PLA2 in serum, BALF and lung tissue in the COPD group were obviously higher than those in the control group (P < 0.01).The total inflammatory cells, the proportion of neutrophils and lymphocyte, and the levels of IL-8, TNF-α, PLA2 in serum, BALF and lung tissue in the treatment group were significantly lower than those in the COPD group but higher than those in the control group (P < 0.01). ConclusionsTiotropium bromide can reduce the levels of IL-8, TNF-α, PLA2 in serum, BALF and lung tissue of COPD rats by reducing the leakage of inflammatory cells, and alleviate the airway inflammation and the degree of emphysema.
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.
ObjectiveTo isolate and identify the cartilage progenitor cells (CPCs) from normal cartilage, and to explore the influence of interleukin 1β (IL-1β) in different concentrations on its chondrogenesis. MethodsCPCs were isolated from normal cartilage of adult New Zealand white rabbit with the fibronectin adhesion assay;the cell phenotype was identified;and the cloning and differentiation of CPCs were observed. CPCs were incubated with H-DMEM in group A, with chondrogenic induced medium in group B, with chondrogenic induced medium+0.1 ng/mL IL-1β in group C and chondrogenic induced medium+1.0 ng/mL IL-1β in group D for 3 weeks. The histology, biochemistry, and real-time fluorescence quantitative PCR were performed to observe the effect of IL-1β on the chondrgenic differentiation. ResultsThe CPCs from normal cartilage expressed positively stem cell phenotype, which have similar ability of cloning and differentiation to stem cells. The cell pellets in groups C and D were significantly smaller than those in group B, and cell showed hypertrophic morphology change. There were more expressions of collagen type Ⅱ and collagen type X in group B than in group A, in group B than in groups C and D, and in group C than group D with Safranin O staining. The biochemistry results showed that collagen type Ⅱ content, glycosaminoglycan (GAG) content, and the ratio of GAG/DNA were significantly lower in groups C and D than in group B (P<0.05), and in group D than in group C (P<0.05);but the DNA content was significantly higher in groups C and D than in group B (P<0.05), and no significant difference between groups C and D (P>0.05). The real-time fluorescence quantitative PCR results showed that the relative mRNA expressions of collagen type Ⅱ, collagen type X, and Sox-9 were significantly lower in groups C and D than in group B (P<0.05), and in group D than in group C (P<0.05), but the relative mRNA expressions of Runx-2 and matrix metalloproteinase 13 were significantly higher in groups C and D than in group B (P<0.05), and in group D than in group C (P<0.05). ConclusionThere are CPCs having the character of stem cells in normal cartilage, and they have the capability of cloning and potential differentiation. IL-1β can inhibit the chondrogenesis of CPCs, and possibly promote the osteogenic differentiation.
Objective To investigate the changes and significance of serum inflammatory factors in coronary heart disease ( CHD) patients with obstructive sleep apnea-hypopnea syndrome ( OSAHS) , and the treatment effects of continuous positive airway pressure( CPAP) . Methods A total of 76 CHD patients in Renmin Hospital of Wuhan University from October 2007 to October 2008 were enrolled. Polysomnography ( PSG) was performed in these CHD patients to identify if they were complicated by OSAHS. The levels of inflammatory factors including TNF-α, IL-6, high sensitive C-reactive protein ( hs-CRP) in serum were determined in the CHD patients and 23 normal subjects. The CHD patients with moderate-severe OSAHS ( AHI≥15 episodes/hour) were treated by Auto-CPAP for 3 months and all parameters above were measured again. Results There were 41 /76 ( 53. 9% ) of CHD patients had moderate-severe OSAHS and were treated with CPAP. The levels of TNF-α, IL-6 and hs-CRP were significantly higher in the CHD patients than those in the normal controls ( all P lt; 0. 01) , and were significantly higher in moderate-severe OSAHS patients than those in the non-OSAHS CHD patients. Auto-CPAP ventilation significantly decreased the levels of inflammatory factors in the CHD patients with moderate-severe OSAHS. Conclusions An obvious proinflammatory state is detected in CHD patients, and is aggravated with OSAHS. CPAP is a useful treatment for CHD patients with mediate to severe OSAHS.
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 systematically review the data of peripheral inflammatory markers in patients with Alzheimer’s disease (AD) and vascular dementia (VaD) to further indicate pathogenesis and antidiastole.MethodsPubMed, EMbase, The Cochrane Library, CNKI, WanFang Data and VIP databases were electronically searched to collect studies on peripheral inflammatory markers in patients with AD and VaD from inception to July 2020. Two reviewers independently screened literature, extracted data, and assessed risk of bias of included studies, and meta-analysis was performed by using Stata 15.1SE software.ResultsA total of 30 studies involving 2 377 patients were included. The results of meta-analysis showed that the IL-6 level was higher in VaD group than that in AD group (SMD=−0.477, 95%CI −0.944 to −0.009, P=0.046). However, there were no statistical difference in peripheral IL-1β (SMD=−0.034, 95%CI −0.325 to 0.257, P=0.818), TNF-α (SMD=0.409, 95%CI −0.152 to 0.970, P=0.153) or CRP (SMD=0.277, 95%CI −0.228 to 0.782, P=0.282) levels.ConclusionsThese findings suggest that IL-6 may be sensitive markers to distinguish AD from VaD. Due to limited quality and quantity of the included studies, more high-quality studies are required to verify the conclusions.
ObjectiveTo evaluate the clinical effects of segmentectomy versus lobectomy under single utility port video-assisted thoracic surgery on inflammatory factors and immune cells in peripheral blood of non-small cell lung cancer patients, and to analyze the effect of changes of postoperative inflammatory factors and immune cells on the prognosis of the patients.MethodsThe clinical data of 256 patients who underwent segmentectomy or lobectomy under single utility port video-assisted thoracic surgery for non-small cell lung cancer in the First Affiliated Hospital of Hebei North University from January 2016 to October 2020 were retrospectively collected. According to the operation method, they were divided into a segmentectomy group (126 patients with 79 males and 47 females at an age of 63.4±6.2 years) and a lobectomy group (130 patients with 91 males and 39 females at an age of 62.9±5.6 years). The change of inflammatory factors (C reactive protein, interleukin-6, interleukin-8, tumor necrosis factor-α) and immune cells (CD4+T cells, CD8+T cells and natural killer cells) were recorded and analyzed before operation (T0) and 1 day (T1), 3 days (T2), 7 days (T3), 1 month (T4) after the operation between the two groups. According to postoperative recurrence situations, they were divided into a recurrence group and a non-recurrence group, multivariate logistic regression analysis was used to analyze the relationship between the change of postoperative inflammatory factors, immune cells, and the prognosis of patients with non-small cell lung cancer.Results(1) There was no statistical difference in sex ratio, underlying diseases, body mass index, levels of preoperative inflammatory factors or immune cells between the two groups (all P>0.05). (2) The changes of postoperative inflammatory factors in the segmentectomy group were significantly less than those in the lobectomy group at T1-T3 (all P<0.05), and the changes of postoperative immune cells in the segmentectomy group were significantly less than those in the lobectomy group at T1-T4 (all P<0.05). (3) The changes of postoperative inflammatory factors and immune cells on postoperative day 3 in the recurrence group were significantly more than those in the non-recurrence group (all P<0.05). (4) Multivariate logistic regression analysis showed that the changes of postoperative inflammatory factors and immune cells on postoperative day 3 may be the risk factors for postoperative recurrence and metastasis in patients with non-small cell lung cancer (all P<0.05).ConclusionSingle utility port video-assisted thoracic surgery segmentectomy for the treatment of non-small cell lung cancer can reduce the inflammatory response and protect body's immune function, and the change of postoperative inflammatory factors and immune cells in postoperative day 3 may be the risk factors for postoperative recurrence and metastasis in patients with non-small cell lung cancer.
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.
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.