ObjectiveTo systematically review the effect of compound Danshen dripping pills combined with Western medicine on inflammatory factors and cardiac function after percutaneous coronary intervention (PCI) in patients with acute myocardial infarction.MethodsDatabases including CNKI, WanFang Data, VIP, CBM, PubMed, Web of Science, EMbase and The Cochrane Library were searched for randomized controlled trials of compound Danshen dripping pills combined with Western medicine in the treatment of acute myocardial infarction after PCI. The retrieval time was from the establishment of the databases to June 11th, 2020. Two reviewers independently screened literature, extracted data and evaluated the risk bias of included studies. RevMan 5.3 software was used for meta-analysis.ResultsA total of 16 studies were included, involving 2 069 patients. The results of the meta-analysis showed that the combination of compound Danshen dripping pills could increase the left ventricular ejection fraction (MD =−4.74, 95%CI 4.07 to 5.42, P<0.01), decrease the B-type natriuretic peptide (SMD=−3.81, 95%CI −5.06 to −2.57, P<0.01), the level of interleukin-6 (SMD=−3.20, 95%CI −4.54 to −1.86, P<0.01) and level of tumor necrosis factor-a (SMD=−4.96, 95%CI −7.03 to −2.89, P<0.01).ConclusionsCurrent evidence suggests that the combination of compound Danshen dropping pills has potential benefits in inhibiting inflammation and improving cardiac function after PCI. Due to the limited quality and quantity of the included studies, more high-quality studies are required to verify the above conclusions.
Objective To investigate the protective effect of annexin A1 (ANXA1) derived from human umbilical cord mesenchymal stem cells (HucMSCs) on lipopolysaccharide (LPS) -induced acute lung injury (ALI). Methods Six-week-old male C57BL/6 mice were randomly divided into a sham group, a LPS group, a LPS+HucMSC-cm (LPS+cm) group, a LPS+nc-cm group, and a LPS+si-cm group, with 6 mice in each group. LPS (5 mg/kg) was intratracheally injected to induce ALI model. Then, normal saline, HucMSC-cm (HucMSC conditioned medium), HucMSC-nc-cm (normal ANXA1 expression) and HucMSC-si-cm (knockout of ANXA1) were injected intratracheally with 50 μL each after LPS treatment for 4 hours. After 72 hours of LPS administration, the mice were killed, and the blood and lung tissues were retained. After corresponding treatment, the blood and lung tissues were preserved. The expression of IL-6 in peripheral blood of mice was detected by enzyme-linked immunosorbnent assay, the pathological changes of lung tissues were observed by hematoxylin-eosin staining, and the expressions of interleukin-6 (IL-6) and vascular cell adhesion molecule-1 (VCAM-1) in lung tissues of each group were detected by Western blot and immunohistochemistry. Results Compared with the sham group, the lung histopathology of mice in the LPS group showed significantly increased inflammatory factor infiltration, alveolar collapse, and lung tissue structure destruction as well as lung tissue injury score and wet/dry weight ratio (W/D) increased (all P<0.05). Accordingly, IL-6 and VCAM-1 protein levels in lung tissue and IL-6 expression in peripheral blood were increased (all P<0.05). Compared with the LPS group, the pathological injury of lung tissue in the LPS+cm group was improved, the lung tissue injury score and the W/D ratio decreased while IL-6, VCAM-1 protein levels in lung tissue and IL-6 expression in peripheral blood were decreased (all P<0.05). But there were no significant differences between the LPS+cm group and the LPS+ nc-cm group (all P>0.05). Compared with the LPS+nc-cm group, lung tissue pathological injury was aggravated again, lung tissue injury score and W/D were also increased in the LPS+si-cm group (all P<0.05). IL-6 and VCAM-1 protein levels in lung tissue and IL-6 expression in peripheral blood were increased again (all P<0.05). Conclusion ANXA1 derived from HucMSCs has certain protective effect in LPS-induced ALI model.
A new independent subtype CD4+ T cell which massively secreted interleukin-17 (IL-17) was found at the beginning of the 21st century, and thus it was named as T helper cell 17 (Th17 cell). With the progress of the research in recent years, Th17 cells were found to be widely involved in a variety of the human diseases such as autoimmune diseases, infections and tumors through secretion of IL-17. The relationship between Th17 cells, IL-17 and the occurrence, development and prognosis of lung cancer was reviewed.
Objective To study the effect of nontypeable Hemophilus influenzae(NTHi) strain ATCC49247 on proinflammatory cytokines expression of human A549 lung epithelial cell line. Methods Confluent A549 cells were co-incubated with NTHi, NTHi+Erythromycin(10 mg/L), NTHi+Gentamicin(100 mg/L), and NTHi+Dexamethasone(100 μmol/L),and nuclear factor kappa B(NF-κB) inhibitor primed cells were co-incubated with NTHi for 24 h. Then levels of interleukin-8（IL-8） and tumor necrosis factor-α(TNF-α) in the supernatant was assayed by enzyme-linked immunosorbent assay(ELISA) and the expression of intercellular adhesion molecule-1(ICAM-1) in cells was detected by immunohistochemistry staining. Results A549 cells were transformed and died after co-intubated with NTHi for 24 h. NTHi induced A549 cells to release significantly greater amounts of IL-8, which was inhibited by NF-κB inhibitor pyrrolidine dithiocarbamate（PDTC）. Incubating of A549 cells with NTHi significantly induced release of IL-8 and the expression of ICAM-1, which was blocked by erythromycin and dexamethasone and not by gentamicin. TNF-α was not detected in all circumstances. Conclusions NTHi can increase significantly the release and expression of proinflammatory cytokines through NF-κB pathway. Antibacterial drug erythromycin also has anti-inflammatory effect.
Objective To introduce the inflammatory microenvironment and epithelial-mesenchymal transition process of hepatocellular carcinoma, and review the relationship between them. Methods Domestic and international literatures were collected to summary the relationship between epithelial-mesenchymal transition and the inflammatory microenvironment of hepatocellular carcinoma. Result Many inflammatory factors and viral gene encoding proteins in the inflammatory microenvironment play an important role in the process of epithelial-mesenchymal transition in hepatocellular carcinoma. Conclusions The inflammatory microenvironment of hepatocellular carcinoma is an indispensable role in the process of epithelial-mesenchymal transition. The inhibition and treatment of inflammatory microenvironment may play a more active role in the control of tumor invasion and metastasis.
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 investigate the effects of melatonin (MT) on bone mass and serum inflammatory factors in rats received ovariectomy (OVX) and to investigate the effects of MT on the levels of inflammatory factors in culture medium and osteogenic ability of bone marrow mesenchymal stem cells (BMSCs) stimulated by lipopolysaccharide. Methods Fifteen 12-week-old Sprague Dawley (SD) rats were randomly divided into 3 groups. The rats in Sham group only received bilateral lateral abdominal incision and suture, the rats in OVX group received bilateral OVX, and the rats in OVX+MT group received 100 mg/(kg·d) MT oral intervention after bilateral OVX. After 8 weeks, the levels of serum inflammatory factors [interleukin-1β (IL-1β), IL-6, and tumor necrosis factor α (TNF-α)] were detected using ELISA assay. Besides, the distal femurs were detected by Micro-CT to observe changes in bone mass and microstructure, and quantitatively measured bone volume fraction, trabecular thickness, and trabecular number. The BMSCs were extracted from the femurs of three 3-week-old SD rats using whole bone marrow culture method and passaged. The 3rd-5th passage BMSCs were cultured with different concentrations of MT (0, 1, 10, 100, 1 000 µmol/L), and the cell viability was then detected using cell counting kit 8 (CCK-8) to select the optimal concentration of MT for subsequent experiments. Cells were devided into osteogenic induction group (group A) and osteogenic induction+1/5/10 μg/mL lipopolysaccharide group (group B-D). The levels of inflammatory factors (IL-1β, IL-6 and TNF-α) in cell culture medium were detected using ELISA assay after corresponding intervention. According to the results of CCK-8 method and ELISA detection, the cells were intervened with the most significant concentration of lipopolysaccharide for stimulating inflammation and the optimal concentration of MT with osteogenic induction, defining as group E, and the cell culture medium was collected to detect the levels of inflammatory factors by ELISA assay. After that, alkaline phosphatase (ALP) staining and alizarin red staining were performed respectively in groups A, D, and E, and the expression levels of osteogenic related genes [collagen type Ⅰ alpha 1 chain (Col1a1) and RUNX family transcription factor 2 (Runx2)] were also detected by real time fluorescence quantitative PCR (RT-qPCR). ResultsELISA and Micro-CT assays showed that compared with Sham group, the bone mass of the rats in the OVX group significantly decreased, and the expression levels of serum inflammatory factors (IL-1β, IL-6, and TNF-α) in OVX group significantly increased (P<0.05). Significantly, the above indicators in OVX+MT group were all improved (P<0.05). Rat BMSCs were successfully extracted, and CCK-8 assay showed that 100 µmol/L was the maximum concentration of MT that did not cause a decrease in cell viability, and it was used in subsequent experiments. ELISA assays showed that compared with group A, the expression levels of inflammatory factors (IL-1β, IL-6, and TNF-α) in the cell culture medium of groups B-D were significantly increased after lipopolysaccharide stimulation (P<0.05), and in a concentration-dependent manner. Moreover, the expression levels of inflammatory factors in group D were significantly higher than those in groups B and C (P<0.05). After MT intervention, the expression levels of inflammatory factors in group E were significantly lower than those in group D (P<0.05). ALP staining, alizarin red staining, and RT-qPCR assays showed that compared with group A, the percentage of positive area of ALP and alizarin red and the relative mRNA expressions of Col1a1 and Runx2 in group D significantly decreased, while the above indicators in group E significantly improved after MT intervention (P<0.05). ConclusionMT may affect the bone mass of postmenopausal osteoporosis by reducing inflammation in rats; MT can reduce the inflammation of BMSCs stimulated by lipopolysaccharide and weaken its inhibition of osteogenic differentiation of BMSCs.
Objective To observe the changes of soluble triggering receptor expressed on myeloid cell-1 ( sTREM-1) and inflammatory mediators levels in plasma of severe pneumonia patients, and explore the significance of systemic inflammatory response state.Methods Plasma levels of sTREM-1, tumor necrosis factor-α ( TNF-α) and interleukin-10 ( IL-10) were examined in 40 patients with severe pneumonia, 25 patients with uncomplicated pneumonia, and 15 healthy volunteers. Plasma levels of TNF-α,IL-10 and sTREM-1 in survival and non-survival severe pneumoniawere observed on days 1,4, 7 and the day of discharge or death.Results Plasma levels of TNF-α, IL-10, and sTREM-1 [ ( 44. 25 ±10. 81) pg/mL,( 58. 21 ±16. 41) pg/mL, ( 51. 75 ±18. 51) pg/mL, respectively] in the patients with severe pneumonia were higher than those with uncomplicated pneumonia [ ( 24.6 ±6. 45) pg/mL, ( 24. 56 ±7. 1) pg/mL,( 25. 55 ±7. 72) pg/mL, respectively] and the normal controls [ ( 13. 82 ±4. 04) pg/mL, ( 15. 30 ±4. 45)pg/mL, ( 14. 37 ±4. 82) pg/mL, respectively] ( P lt;0. 001) . Plasma levels of TNF-α, IL-10, and sTREM-1 were gradually decreased in the survivors, while maintained at high levels or increased in the non-survivors.The levels of these mediators were all significantly higher in the non-survivors than the survivors at all time points. The ratio of TNF-α/ IL-10 level was higher in the severe pneumonia patients than the uncomplicated pneumonia patients and the control subjects ( 1. 286 ±0. 177 vs. 1. 077 ±0. 410 and 0. 932 ±0. 154) on day 1.The ratio of TNF-α/IL-10 level was higher in the non-survivors than the survivors at all time points. There was negative correlation between plasma levels of sTREM-1 and TNF-αon day 1 ( r = - 0. 479, P =0. 002) ,and positive correlation between plasma levels of sTREM-1 and IL-10 on day 1 ( r = 0. 326, P = 0. 040) .Conclusions There are excessive release of inflammatory mediators and unbalanced systemic inflammatory response in patients with severe pneumonia, especially in non-survivors. sTREM-1, TNF-α and IL-10 are involved in the inflammatory response, and their levels may reflect the prognosis.
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.