The resolution of inflammation is an active process,guided by specialized proresolution lipid mediators(SPMs).These mediators originate from polyunsaturated fatty acids,such as omega-3.Sufficient evidence suggests tha...The resolution of inflammation is an active process,guided by specialized proresolution lipid mediators(SPMs).These mediators originate from polyunsaturated fatty acids,such as omega-3.Sufficient evidence suggests that the beneficial effects attributed to omega-3 are,at least in part,the result of the immunomodulatory action of the SPMs,which act systemically by overcoming inflammation and repairing tissue damage,without suppressing the immune response.Recent studies suggest that an imbalance in the synthesis and/or activity of these compounds may be associated with the pathogenesis of several inflammatory conditions,such as inflammatory bowel disease(IBD).Thus,this review highlights the advances made in recent years with regard to the endogenous synthesis and the biological role of lipoxins,resolvins,protectins,and maresins,as well as their precursors,in the regulation of inflammation;and provides an update on the participation of these mediators in the development and evolution of IBD and the therapeutic approaches that these immunomodulating substances are involved in this context.展开更多
Inflammation has been shown to play an important role in the progression of Alzheimer＇s disease （AD）. Recent epidemical study indicates that the incidence of AD in some populations is substantially influenced by th...Inflammation has been shown to play an important role in the progression of Alzheimer＇s disease （AD）. Recent epidemical study indicates that the incidence of AD in some populations is substantially influenced by the gene polymorphisms of the inflammation mediators. Meanwhile, an ensured risk factor, the ApoE ε4 allele is also reported to directly promote inflammation. Accordingly, it appears that an individual genetic background has partly determined his predisposition for AD by the extent of the inflammation response to the chronic stimulus by β-amyloid peptide （Aβ） deposits and other antigen stressor in the elderly. Hence we present a hypothesis that the inflammation genotypes may contribute to AD susceptibility. This may provide a new orientation both for future identification of individuals at risk and for personalized medication.展开更多
The purpose of this paper is to review current infor-mation about the role of inflammation caused by He-licobacter pylori(H. pylori) infection in neurological diseases such as Parkinson's disease, Alzheimer's ...The purpose of this paper is to review current infor-mation about the role of inflammation caused by He-licobacter pylori(H. pylori) infection in neurological diseases such as Parkinson's disease, Alzheimer's dis-ease, Guillain-Barré syndrome, multiple sclerosis, and other inflammatory diseases including ischemic stroke. Infection with H. pylori usually persists throughout life, resulting in a chronic inflammatory response with local secretion of numerous inflammatory mediators includ-ing chemokines [interleukin(IL)-8, macrophage che-motactic protein, growth-regulated oncogene(GRO)-α, chemokine(C-X-C motif) ligand 1] and cytokines [IL-1β, tumor necrosis factor-α, IL-6, IL-12, interferon-g], which can pass into the circulation and have a systemic effect. The persistence of detectable systemic and lo-cal concentrations of inflammatory mediators is likely to alter the outcome of neurological diseases. These proinflammatory factors can induce brain inflammation and the death of neurons and could eventually be asso-ciated to Parkinson's disease and also may be involved in the development of Alzheimer's disease. However,most neurological diseases are the result of a combina-tion of multiple factors, but the systemic inflammatory response is a common component and determinant in the onset, evolution, and outcome of diseases. How-ever, more studies are needed to allow understanding of the effects and mechanisms by which the inflamma-tory response generated by H. pylori infection affects neurological diseases.展开更多
AIM： To observe the apoptosis and oncosis of pancreatic acinar cells and secondary inflammatory reaction in pancreatic tissue from rats with acute pancreatitis （AP）, and the influences of artemisinin on them.METHOD...AIM： To observe the apoptosis and oncosis of pancreatic acinar cells and secondary inflammatory reaction in pancreatic tissue from rats with acute pancreatitis （AP）, and the influences of artemisinin on them.METHODS： AP was induced by 4 intraperitoneal iojections of caerulein at 1 h intervals. To induce apoptosis, solution of artemisinin （50 mg/kg） was given intraperitoneally 1, 12, 24 and 36 h after the last caerulein injection. Histological examination of impairment of pancreatic tissue and detection of serum amylase were performed to evaluate the severity of acute pancreatitis. Apoptosis and oncosis were detected with acridine orange （AO） and ethylene dibromide （EB） staining. Caspase-3 and myeloperoxidase （MPO） activity were measured by colorimetric assay. Nuclear factor-kappa B （NF-KB） activation was detected by flow cytometry. Macrophage inflammatory protein-lα（MIP-1α） protein was measured by Western blot. Interleukin- 1β（IL-1β） mRNA was detected by RT-PCR.RESULTS： Addition of artemisinin increased the number of apoptotic cells （11.7%±1.4% vs 6.3%± 0.7%, P 〈 0.05）, while reduced the number of oncotic cells （13.0% ±2.4% vs 17.5%±2.2%, P 〈 0.05）. The activity of caspase-3 speeded up （1.52±0.21 vs 1.03±0.08, P 〈 0.05）, the pancreas pathological impairment was relieved （3.0±0.5 vs 4.0± 0.5, P 〈 0.05） and the level of serum amylase decreased （5642±721 U/dL vs 7821±653 U/dL, P 〈 0.05）. The activation of NF-1α （29%±4.1% vs 42%±5.8%）, MIP-1α protein （3.7±0.5 vs 5.8±0.7）,MPO （0.52±0.06 U/g vs 0.68±0.09 U/g）, IL-1β mRNA （1.7 ±0.3 vs 2.4 ±0.4） in the apoptosis inducing group was obviously decreased （P 〈 0.05）.CONCLUSION： Inducing apoptosis can relieve pathological impairment and inflammatory reaction in AP rats.展开更多
The mast cell is an enigmatic cell type whose physiological function has preoccupied large numbers of investigators for decadest. Some have concluded that the absence of mast cells is incompatible with life, at least ...The mast cell is an enigmatic cell type whose physiological function has preoccupied large numbers of investigators for decadest. Some have concluded that the absence of mast cells is incompatible with life, at least in humans, because no human conditions have been documented where these cells are absent from the body. On the other hand, mice harboring specific mutations in certain growth factors, or their receptors, that展开更多
Due to persistent or low-intensity stimulation,tissue cells are in a state of injury for a long time,and the inflammatory state continues,eventually leading to nonresolving inflammation.In this nonresolving inflammati...Due to persistent or low-intensity stimulation,tissue cells are in a state of injury for a long time,and the inflammatory state continues,eventually leading to nonresolving inflammation.In this nonresolving inflammation,various inflammatory mediators and inflammatory cells act on tissue cells,and tumors are easily induced.Further,the unique microenvironment of the tumor further aggravates the development of uncontrolled inflammation.Eventually a vicious circle is formed.In this paper,we explored the mechanism of inflammatory mediators,inflammatory cells and tumors in nonresolving inflammation from the relationship between nonresolving inflammation and tumors,and provided some new ideas for the prevention and treatment of tumors.展开更多
Hexavalent chromium and its compounds are prevalent pollutants,especially in the work environment,pose a significant risk for multisystem toxicity and cancers.While it is known that chromium accumulation in the liver ...Hexavalent chromium and its compounds are prevalent pollutants,especially in the work environment,pose a significant risk for multisystem toxicity and cancers.While it is known that chromium accumulation in the liver can cause damage,the dose-response relationship between blood chromium(Cr)and liver injury,as well as the possible potential toxic mechanisms involved,remains poorly understood.To address this,we conducted a follow-up study of 590 visits from 305 participants to investigate the associations of blood Cr with biomarkers for liver injury,including serum alanine aminotransferase(ALT),aspartate aminotransferase(AST),total bilirubin(TBIL),and direct bilirubin(DBIL),and to evaluate the mediating effects of systemic inflammation.Platelet(PLT)and the platelet-to-lymphocyte ratio(PLR)were utilized as biomarkers of systemic inflammation.In the linear mixed-effects analyses,each 1-unit increase in blood Cr level was associated with estimated effect percentage increases of 0.82%(0.11%,1.53%)in TBIL,1.67%(0.06%,3.28%)in DBIL,0.73%(0.04%,1.43%)in ALT and 2.08%(0.29%,3.87%)in AST,respectively.Furthermore,PLT mediated 10.04%,11.35%,and 10.77%increases in TBIL,DBIL,and ALT levels induced by chromate,respectively.In addition,PLR mediated 8.26%and 15.58%of the association between blood Cr and TBIL or ALT.These findings shed light on the mechanisms underlying blood Cr-induced liver injury,which is partly due to worsening systemic inflammation.展开更多
Asthma is a disease characterized by airway chronic inflammation and bronchial hyperactivity, involving the imbalance of oxidative and antioxidative agents. There is an increased free radical generation and a decrease...Asthma is a disease characterized by airway chronic inflammation and bronchial hyperactivity, involving the imbalance of oxidative and antioxidative agents. There is an increased free radical generation and a decreased antioxidant enzyme activity, which correlate with the severity of the disease. The oxidative stress triggers specific physiopathological changes in the respiratory tract as a result of proinflammatory molecule formation, such as isoprostanes and PAF- like lipids. The synthesis of these mediators is dependent on the availability of lipid substrates, such as PUFAs, which are present in cell membranes. Therefore, lipid oxidation may have an important role in the perpetuation and amplification of the asthmatic inflammatory response. This article will make considerations about how oxidative stress contributes to asthma pathogenesis.展开更多
The main pathophysiological feature of sepsis is the uncontrollable activation of both pro-and anti-inflammatory responses arising from the overwhelming pro-duction of mediators such as pro-and anti-inflammatory cytok...The main pathophysiological feature of sepsis is the uncontrollable activation of both pro-and anti-inflammatory responses arising from the overwhelming pro-duction of mediators such as pro-and anti-inflammatory cytokines. Such an uncontrollable inflammatory response would cause many kinds of metabolic derangements. One such metabolic derangement is hyperglycemia. Accordingly, control of hyperglycemia in sepsis is considered to be a very effective therapeutic approach. However, despite the initial enthusiasm, recent studies reported that tight glycemic control with intensive insulin therapy failed to show a beneficial effect on mortality of patients with severe sepsis and septic shock. One of the main reasons for this disappointing result is the incidence of harmful hypoglycemia during intensive insulin therapy. Therefore, avoidance of hypoglycemia during intensive insulin therapy may be a key issue in effective tight glycemic control. It is generally accepted that glycemic control aimed at a blood glucose level of 80-100 mg/dL, as initially proposed by van den Berghe, seems to be too tight and that such a level of tight glycemic control puts septic patients at increased risk of hypoglycemia. Therefore, now many researchers suggest less strict glycemic control with a target blood glucose level of 140-180 mg/dL. Also specific targeting of glycemic control in diabetic patients should be considered. Since there is a significantcorrelation between success rate of glycemic control and the degree of hypercytokinemia in septic patients, some countermeasures to hypercytokinemia may be an important aspect of successful glycemic control. Thus, in future, use of an artificial pancreas to avoid hypoglycemia during insulin therapy, special consideration of septic diabetic patients, and control of hypercytokinemia should be considered for more effective glycemic control in patients with severe sepsis and septic shock.展开更多
Objective: To study the effect of decoy-oligodeoxynucleotides (decoy-ODNs) in dumbbell shape with the oligodeoxynucleotide sequence similar to nuclear factor kappa B (NF-κB) cis-elements on expression of inflammation...Objective: To study the effect of decoy-oligodeoxynucleotides (decoy-ODNs) in dumbbell shape with the oligodeoxynucleotide sequence similar to nuclear factor kappa B (NF-κB) cis-elements on expression of inflammation mediators in pMΦ cells from rats. Methods: With carriers of cationic liposomes, decoy-ODNs were transfected into pMΦ cells of rats. Then the inhibiting effects of the decoy-ODNs on tumor necrosis factor α (TNFα), interleukin-6 (IL-6) and IL-10 were analyzed. Results: Decoy-ODNs could decrease the expression of TNFα and IL-6 in dose-dependent fashion but had weaker inhibiting effect on IL-10. Conclusions: Decoy-ODNs targeting NF-κB can decrease the expression of inflammatory mediators in pMΦ cells from rats.展开更多
Objective Assessment of the comprehensive relationship among apolipoprotein CIII（apoCⅢ） levels, inflammation, and metabolic disorders is rare. Methods A total of 1455 consecutive patients not treated with lipid-low...Objective Assessment of the comprehensive relationship among apolipoprotein CIII（apoCⅢ） levels, inflammation, and metabolic disorders is rare. Methods A total of 1455 consecutive patients not treated with lipid-lowering drugs and undergoing coronary angiography were enrolled in this cross-sectional study. A mediation analysis was used to detect the underlying role of apoCⅢ in the association of inflammation with metabolic syndrome（MetS）. Results Patients with MetS showed higher levels of apoCⅢ [95.1（73.1-131.4） vs. 81.7（58.6-112.4） μg/mL, P 〈 0.001] and inflammatory markers [high sensitivity C-reactive protein, 1.7（0.8-3.4） vs. 1.1（0.5-2.2） mg/L; white blood cell count,（6.48 ± 1.68） vs.（6.11 ± 1.67） × 10~9/L]. The levels of apoCⅢ and inflammatory markers increased with the number of metabolic risk components（all P 〈 0.001）. Furthermore, apoCⅢ levels were associated with virtually all individual MetS risk factors and inflammatory markers（all P 〈 0.05）. Importantly, the prevalence of MetS in each metabolic disorder rose as apoCⅢ levels increased（all P 〈 0.05）. Mediation analysis showed that apoCⅢ partially mediated the effect of inflammation on MetS independently from triglycerides. Conclusion Plasma apoCⅢ levels were significantly associated with the development and severity of MetS, and a role of apoCⅢ in the effect of inflammation on the development of MetS was identified.展开更多
基金Supported by the National Council for Scientific and Technological Development(CNPq)for Leal RF(301388/2018-0)the Post-doctoral Scholarship from Funding for Education,Research and Extension Support(FAEPEX),University of Campinas for Pascoal LB+1 种基金the Undergraduate Scholarship from the CNPq(125138/2020-2)for Palma BBthe Undergraduate Scholarship from the São Paulo State Research Support Foundation(FAPESP)(2020/02571-9)for Damázio TA.
文摘The resolution of inflammation is an active process,guided by specialized proresolution lipid mediators(SPMs).These mediators originate from polyunsaturated fatty acids,such as omega-3.Sufficient evidence suggests that the beneficial effects attributed to omega-3 are,at least in part,the result of the immunomodulatory action of the SPMs,which act systemically by overcoming inflammation and repairing tissue damage,without suppressing the immune response.Recent studies suggest that an imbalance in the synthesis and/or activity of these compounds may be associated with the pathogenesis of several inflammatory conditions,such as inflammatory bowel disease(IBD).Thus,this review highlights the advances made in recent years with regard to the endogenous synthesis and the biological role of lipoxins,resolvins,protectins,and maresins,as well as their precursors,in the regulation of inflammation;and provides an update on the participation of these mediators in the development and evolution of IBD and the therapeutic approaches that these immunomodulating substances are involved in this context.
基金the National Basic Research Development Program of China (No. 2006cb500706)the National Natural Science Foundation of China (No. 30700251)+1 种基金Shanghai Key Project of Basic Science Research (No. 04DZ14005)the Program for Outstanding Medical Academic Leader (No. LJ 06003).
文摘Inflammation has been shown to play an important role in the progression of Alzheimer＇s disease （AD）. Recent epidemical study indicates that the incidence of AD in some populations is substantially influenced by the gene polymorphisms of the inflammation mediators. Meanwhile, an ensured risk factor, the ApoE ε4 allele is also reported to directly promote inflammation. Accordingly, it appears that an individual genetic background has partly determined his predisposition for AD by the extent of the inflammation response to the chronic stimulus by β-amyloid peptide （Aβ） deposits and other antigen stressor in the elderly. Hence we present a hypothesis that the inflammation genotypes may contribute to AD susceptibility. This may provide a new orientation both for future identification of individuals at risk and for personalized medication.
基金Supported by Hospital Infantil de México Federico Gómez,No.HIM/2012/018
文摘The purpose of this paper is to review current infor-mation about the role of inflammation caused by He-licobacter pylori(H. pylori) infection in neurological diseases such as Parkinson's disease, Alzheimer's dis-ease, Guillain-Barré syndrome, multiple sclerosis, and other inflammatory diseases including ischemic stroke. Infection with H. pylori usually persists throughout life, resulting in a chronic inflammatory response with local secretion of numerous inflammatory mediators includ-ing chemokines [interleukin(IL)-8, macrophage che-motactic protein, growth-regulated oncogene(GRO)-α, chemokine(C-X-C motif) ligand 1] and cytokines [IL-1β, tumor necrosis factor-α, IL-6, IL-12, interferon-g], which can pass into the circulation and have a systemic effect. The persistence of detectable systemic and lo-cal concentrations of inflammatory mediators is likely to alter the outcome of neurological diseases. These proinflammatory factors can induce brain inflammation and the death of neurons and could eventually be asso-ciated to Parkinson's disease and also may be involved in the development of Alzheimer's disease. However,most neurological diseases are the result of a combina-tion of multiple factors, but the systemic inflammatory response is a common component and determinant in the onset, evolution, and outcome of diseases. How-ever, more studies are needed to allow understanding of the effects and mechanisms by which the inflamma-tory response generated by H. pylori infection affects neurological diseases.
基金the Natural Science Foundation of Heilongjiang Province,China,No. D0227
文摘AIM： To observe the apoptosis and oncosis of pancreatic acinar cells and secondary inflammatory reaction in pancreatic tissue from rats with acute pancreatitis （AP）, and the influences of artemisinin on them.METHODS： AP was induced by 4 intraperitoneal iojections of caerulein at 1 h intervals. To induce apoptosis, solution of artemisinin （50 mg/kg） was given intraperitoneally 1, 12, 24 and 36 h after the last caerulein injection. Histological examination of impairment of pancreatic tissue and detection of serum amylase were performed to evaluate the severity of acute pancreatitis. Apoptosis and oncosis were detected with acridine orange （AO） and ethylene dibromide （EB） staining. Caspase-3 and myeloperoxidase （MPO） activity were measured by colorimetric assay. Nuclear factor-kappa B （NF-KB） activation was detected by flow cytometry. Macrophage inflammatory protein-lα（MIP-1α） protein was measured by Western blot. Interleukin- 1β（IL-1β） mRNA was detected by RT-PCR.RESULTS： Addition of artemisinin increased the number of apoptotic cells （11.7%±1.4% vs 6.3%± 0.7%, P 〈 0.05）, while reduced the number of oncotic cells （13.0% ±2.4% vs 17.5%±2.2%, P 〈 0.05）. The activity of caspase-3 speeded up （1.52±0.21 vs 1.03±0.08, P 〈 0.05）, the pancreas pathological impairment was relieved （3.0±0.5 vs 4.0± 0.5, P 〈 0.05） and the level of serum amylase decreased （5642±721 U/dL vs 7821±653 U/dL, P 〈 0.05）. The activation of NF-1α （29%±4.1% vs 42%±5.8%）, MIP-1α protein （3.7±0.5 vs 5.8±0.7）,MPO （0.52±0.06 U/g vs 0.68±0.09 U/g）, IL-1β mRNA （1.7 ±0.3 vs 2.4 ±0.4） in the apoptosis inducing group was obviously decreased （P 〈 0.05）.CONCLUSION： Inducing apoptosis can relieve pathological impairment and inflammatory reaction in AP rats.
基金Supported by the grants from the National Institutes of Health,USA (DK33491 and AT01180) and the Crohn's and Colitis Foundation of America
文摘The mast cell is an enigmatic cell type whose physiological function has preoccupied large numbers of investigators for decadest. Some have concluded that the absence of mast cells is incompatible with life, at least in humans, because no human conditions have been documented where these cells are absent from the body. On the other hand, mice harboring specific mutations in certain growth factors, or their receptors, that
文摘Due to persistent or low-intensity stimulation,tissue cells are in a state of injury for a long time,and the inflammatory state continues,eventually leading to nonresolving inflammation.In this nonresolving inflammation,various inflammatory mediators and inflammatory cells act on tissue cells,and tumors are easily induced.Further,the unique microenvironment of the tumor further aggravates the development of uncontrolled inflammation.Eventually a vicious circle is formed.In this paper,we explored the mechanism of inflammatory mediators,inflammatory cells and tumors in nonresolving inflammation from the relationship between nonresolving inflammation and tumors,and provided some new ideas for the prevention and treatment of tumors.
基金supported by the National Natural Science Foundation of China(Nos.82273603,82003427,U2004202)。
文摘Hexavalent chromium and its compounds are prevalent pollutants,especially in the work environment,pose a significant risk for multisystem toxicity and cancers.While it is known that chromium accumulation in the liver can cause damage,the dose-response relationship between blood chromium(Cr)and liver injury,as well as the possible potential toxic mechanisms involved,remains poorly understood.To address this,we conducted a follow-up study of 590 visits from 305 participants to investigate the associations of blood Cr with biomarkers for liver injury,including serum alanine aminotransferase(ALT),aspartate aminotransferase(AST),total bilirubin(TBIL),and direct bilirubin(DBIL),and to evaluate the mediating effects of systemic inflammation.Platelet(PLT)and the platelet-to-lymphocyte ratio(PLR)were utilized as biomarkers of systemic inflammation.In the linear mixed-effects analyses,each 1-unit increase in blood Cr level was associated with estimated effect percentage increases of 0.82%(0.11%,1.53%)in TBIL,1.67%(0.06%,3.28%)in DBIL,0.73%(0.04%,1.43%)in ALT and 2.08%(0.29%,3.87%)in AST,respectively.Furthermore,PLT mediated 10.04%,11.35%,and 10.77%increases in TBIL,DBIL,and ALT levels induced by chromate,respectively.In addition,PLR mediated 8.26%and 15.58%of the association between blood Cr and TBIL or ALT.These findings shed light on the mechanisms underlying blood Cr-induced liver injury,which is partly due to worsening systemic inflammation.
文摘Asthma is a disease characterized by airway chronic inflammation and bronchial hyperactivity, involving the imbalance of oxidative and antioxidative agents. There is an increased free radical generation and a decreased antioxidant enzyme activity, which correlate with the severity of the disease. The oxidative stress triggers specific physiopathological changes in the respiratory tract as a result of proinflammatory molecule formation, such as isoprostanes and PAF- like lipids. The synthesis of these mediators is dependent on the availability of lipid substrates, such as PUFAs, which are present in cell membranes. Therefore, lipid oxidation may have an important role in the perpetuation and amplification of the asthmatic inflammatory response. This article will make considerations about how oxidative stress contributes to asthma pathogenesis.
文摘The main pathophysiological feature of sepsis is the uncontrollable activation of both pro-and anti-inflammatory responses arising from the overwhelming pro-duction of mediators such as pro-and anti-inflammatory cytokines. Such an uncontrollable inflammatory response would cause many kinds of metabolic derangements. One such metabolic derangement is hyperglycemia. Accordingly, control of hyperglycemia in sepsis is considered to be a very effective therapeutic approach. However, despite the initial enthusiasm, recent studies reported that tight glycemic control with intensive insulin therapy failed to show a beneficial effect on mortality of patients with severe sepsis and septic shock. One of the main reasons for this disappointing result is the incidence of harmful hypoglycemia during intensive insulin therapy. Therefore, avoidance of hypoglycemia during intensive insulin therapy may be a key issue in effective tight glycemic control. It is generally accepted that glycemic control aimed at a blood glucose level of 80-100 mg/dL, as initially proposed by van den Berghe, seems to be too tight and that such a level of tight glycemic control puts septic patients at increased risk of hypoglycemia. Therefore, now many researchers suggest less strict glycemic control with a target blood glucose level of 140-180 mg/dL. Also specific targeting of glycemic control in diabetic patients should be considered. Since there is a significantcorrelation between success rate of glycemic control and the degree of hypercytokinemia in septic patients, some countermeasures to hypercytokinemia may be an important aspect of successful glycemic control. Thus, in future, use of an artificial pancreas to avoid hypoglycemia during insulin therapy, special consideration of septic diabetic patients, and control of hypercytokinemia should be considered for more effective glycemic control in patients with severe sepsis and septic shock.
基金ThisstudywassupportedbytheNationalNaturalScienceFoundationofChina (No .30 170 36 7),theTenth FiveYearPlanofMilitaryCommand (No .0 1MB113)andMajorBasicResearchDevelopmentProgramofChina (No .G19990 5 4 2 0 3)
文摘Objective: To study the effect of decoy-oligodeoxynucleotides (decoy-ODNs) in dumbbell shape with the oligodeoxynucleotide sequence similar to nuclear factor kappa B (NF-κB) cis-elements on expression of inflammation mediators in pMΦ cells from rats. Methods: With carriers of cationic liposomes, decoy-ODNs were transfected into pMΦ cells of rats. Then the inhibiting effects of the decoy-ODNs on tumor necrosis factor α (TNFα), interleukin-6 (IL-6) and IL-10 were analyzed. Results: Decoy-ODNs could decrease the expression of TNFα and IL-6 in dose-dependent fashion but had weaker inhibiting effect on IL-10. Conclusions: Decoy-ODNs targeting NF-κB can decrease the expression of inflammatory mediators in pMΦ cells from rats.
基金partially supported by the Capital Special Foundation of Clinical Application Research(Z121107001012015)the Capital Health Development Fund(2011400302,201614035)+1 种基金the Beijing Natural Science Foundation(7131014)CAMS Major Collaborative Innovation Project(2016-I2M-1-011)
文摘Objective Assessment of the comprehensive relationship among apolipoprotein CIII（apoCⅢ） levels, inflammation, and metabolic disorders is rare. Methods A total of 1455 consecutive patients not treated with lipid-lowering drugs and undergoing coronary angiography were enrolled in this cross-sectional study. A mediation analysis was used to detect the underlying role of apoCⅢ in the association of inflammation with metabolic syndrome（MetS）. Results Patients with MetS showed higher levels of apoCⅢ [95.1（73.1-131.4） vs. 81.7（58.6-112.4） μg/mL, P 〈 0.001] and inflammatory markers [high sensitivity C-reactive protein, 1.7（0.8-3.4） vs. 1.1（0.5-2.2） mg/L; white blood cell count,（6.48 ± 1.68） vs.（6.11 ± 1.67） × 10~9/L]. The levels of apoCⅢ and inflammatory markers increased with the number of metabolic risk components（all P 〈 0.001）. Furthermore, apoCⅢ levels were associated with virtually all individual MetS risk factors and inflammatory markers（all P 〈 0.05）. Importantly, the prevalence of MetS in each metabolic disorder rose as apoCⅢ levels increased（all P 〈 0.05）. Mediation analysis showed that apoCⅢ partially mediated the effect of inflammation on MetS independently from triglycerides. Conclusion Plasma apoCⅢ levels were significantly associated with the development and severity of MetS, and a role of apoCⅢ in the effect of inflammation on the development of MetS was identified.
