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OBJECTIVE To study the ameliorative effect and potential mechanism of curcumin on diabetes model rats with depression based on cAMP response element binding protein （CREB）/brain-derived neurotrophic factor （BDNF） signaling pathway. METHODS The diabetes model rat with depression was established by high fat and high sugar diet+intraperitoneal injection of streptozotocin+chronic unpredictable stress-induced depression. The successfully modeled rats were randomly divided into model group， positive control group （0.18 g/kg metformin and 1.8 mg/kg fluoxetine， gavage）， curcumin low-dose and high-dose groups （30， 60 mg/kg， gavage） and curcumin high-dose+CREB inhibitor group [60 mg/kg curcumin （gavage）+5 mg/kg CREB inhibitor 666-15 （intraperitoneal injection）]， with 12 rats in each group. Another 12 healthy rats were selected as the normal group. Each group was given a corresponding intervention for 4 weeks， the fasting blood glucose level of rats was detected， and the depression of rats was assessed. The levels of corticosterone （CORT） and inflammatory factors [tumor necrosis factor-α （TNF-α）， interleukin- 1β （IL-1β）， IL-6] in serum， and the levels of norepinephrine （NE） and 5-hydroxytryptamine （5-HT） in hippocampal tissue were determined. The pathological changes and neuronal apoptosis were observed in the hippocampal tissue of rats in each group； the expression levels of CREB， BDNF mRNA and protein in hippocampal tissue were detected. RESULTS Compared with the normal group， the hippocampal tissue of rats in the model group was severely damaged， and neurons were scattered， while the fasting blood glucose， the forced swimming immobility time， the tail suspension immobility time， serum levels of CORT， TNF-α， IL-1β and IL-6， and neuron apoptosis indexes were all increased or prolonged significantly （P＜0.05）. The levels of NE and 5-HT， the number of surviving neurons， and the expression levels of CREB and BDNF mRNA and protein in hippocampal tissue were decreased significantly （P＜0.05）. Compared with the 的model group， the damage to hippocampal tissue was relieved in the positive control group and curcumin groups， while the above indexes were improved significantly （P＜0.05）. The improvement effect of curcumin high-dose group was better than that of curcumin low-dose group （P＜0.05）. CREB inhibitor could significantly reverse the ameliorative effect of high-dose curcumin on the model rats （P＜0.05）. CONCLUSIONS Curcumin can improve the depression of diabetes model rats with depression， and relieve neuronal damage and inflammatory response， the mechanism of which may be associated with activating CREB/BDNF signaling pathway.
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Peritoneal adhesion (PA) is a high morbidity complication after surgical procedures, with serious clinical consequences and requiring substantial medical expenditure. The pathogenesis of PA is complex and is still not very clear. Clinically, it is mainly treated by optimizing surgical protocols, using anti-adhesion drugs and biomaterial barriers. Although these methods have shown certain preventive effects, the effectiveness needs to be further improved. Elucidating the mechanism of PA formation is the basis and premise for preventing its occurrence. In the process of PA formation, a variety of inflammatory cells, inflammatory factors play important roles. In this paper, the mechanism of inflammation and immunoregulatory responses in the formation of adhesions in the peritoneal cavity was reviewed, in order to provide a reference for the improvement of PA prevention strategies.
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The COVID-19 pandemic has caused numerous deaths around the world. A growing body of evidence points to the important role of overwhelming inflammatory responses in the pathogenesis of COVID-19 and the effectiveness of anti-inflammation therapy against COVID-19 is emerging. In addition to affecting the lungs, COVID-19 can be a severe systemic inflammatory disease that is related to endothelial dysfunction. We are calling for closer attention to endothelial dysfunction in COVID-19 not only for fully revealing the pathogenic mechanism of COVID-19 but also for properly adjusting the strategy of clinical intervention.
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Humans , COVID-19 , Endothelium , Inflammation , Pandemics , SARS-CoV-2ABSTRACT
OBJECTIVE： To investigate the improvement effects of water extract of Astragalus membranaceus on chronic renal failure （CRF） model rats and its effects on MAPK signaling pathway， and to investigate possible mechanism. METHODS： Male SD rats were randomly divided into control group （10 rats） and model group （50 rats）. CRF model was established by intragastric administration of 25％ Adenine suspension 200 mg/kg （once a day， for consecutive 28 d）. After modeling， modeling group was randomly divided into model group， benazepril group （positive control， 2 mg/kg）， A. membranaceus water extract low-dose， medium-dose and high-dose groups （1.5， 3， 6 g/kg，by crude drug）， with 10 rats in each group. Control group and model group were given constant volume of normal saline intragastrically， and administration groups were given relevant medicine intragastrically， once a day， for consecutive 28 d. Twelve hours after last medication， the contents of serum renal function indexes （serum creatinine， urea nitrogen， uric acid） were determined by colorimetry. ELISA method was used to detect the levels of serum inflammatory factors （IL-1β， IL-6 and TNF-α）. The activity or content of oxidative stress related indexes （SOD， CAT and MDA）in renal tissue of rats were determined by hydroxylamine method， visible spectrophotometry method and thiobarbituric acid method. The mRNA expression of apoptosis-related factors （Bax， Bcl-2， Caspase-3） in renal tissue， MAPK signaling pathway-related regulatory protein p38 MAPK， phosphorylated p38 MAPK（p-p38 MAPK）， ERK1/2， phosphorylated ERK1/2 （p-ERK1/2）， JNK and phosphorylated JNK （p-JNK） were determined by real- time PCR and Western blotting assay. RESULTS： Compared with control group， the contents of renal function indexes and the levels of inflammatory factors in serum， MDA content， mRNA expression ratio of Bax and Bcl-2 （Bax/Bcl-2）， mRNA related expression of Caspase-3， related expression of phosphorylation product of MAPK signaling pathway-related regulatory proteins （p-p38 MAPK， p-JNK， p-ERK1/2） in renal tissue were increased significantly in model group， while the activities of SOD and CAT were decreased significantly in renal tissue （P＜0.01）. Compared with model group， the contents of renal function indexes and the levels of inflammatory factors in serum， Bax/Bcl-2， related expression of phosphorylation product of MAPK signaling pathway-related regulatory proteins in renal tissue were decreased significantly in administration groups as well as MDA content and mRNA related expression of Caspase-3 were decreased significantly in benazepril group and A. membranaceus water extract medium-dose and high-dose groups； the activities of SOD and CAT in renal tissue were increased significantly in benazepril group and A. membranaceus water extract medium-dose and high-dose groups （P＜0.05 or P＜0.01）. MDA content and Bax/Bcl-2 of benazepril group were significantly lower than those of A. membranaceus water extract high-dose group （P＜0.05）. CONCLUSIONS： A. membranaceus water extract has a certain improvement effect on CRF model rats， and inhibit its inflammatory reaction， oxidant stress and cell apoptosis， the mechanism of which may be associated with inhibiting the expression of MAPK signaling pathway-related regulatory proteins.
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OBJECTIVE： To observe the improvement effects of ethanol extract of the root of Anacyclus pyrethrum （EEAP） on cough variant asthma （CVA） model rats. METHODS： Male SD rats were randomly divided into control group， model group， prednisone acetate group （positive control， 250 mg/kg）， EEAP low-dose， medium-dose and high-dose groups （160， 320， 640 mg/kg， by the weight of EEAP）， with 10 rats in each group. Except for control group， other group was given 1 mg/mL ovalbumin （OVA）-Freunds adjuvant complete solution subcutaneously， and aerosol inhalation of 1％ OVA-normal saline （once a day， 20 min each time， 15 d） to induce CVA. After last inhalation， control group and model group were given constant volume of water intragastrically； administration groups were given relevant medicine intragastrically， once a day， for consecutive 30 d. General symptoms of rats were observed in each group during experiment. The airway sensitivity of rats in each group was investigated by capsaicin cough provocation test， and the cough times were recorded. The contents of SOD and TNF-α in serum were determined by ELISA. The morphological characteristics of lung tissue were observed by HE staining. The number of eosinophils and leucocytes in alveolar lavage fluid was recorded by Rayleigh staining. RESULTS： Rats in the control group breathed smoothly， responded quickly and had glossy coat. The rest of the groups showed restlessness， cough， shortness of breath and other symptoms after antigen stimulation. Compared with control group， the congestion and edema of bronchial wall and infiltration of inflammatory cells in the lung tissue were observed in model group； the cough times increased significantly； serum content of TNF-α， eosinophil and leukocyte counts in alveolar lavage fluid increased significantly， and serum content of SOD decreased significantly （P＜0.05）. After treatment， above symptoms of rats were alleviated to varying degrees in administration groups， and the cough times were significantly reduced； the serum contents of TNF-α as well as eosinophil and leukocyte counts in alveolar lavage fluid were significantly reduced； the serum contents of SOD was increased significantly， but the cough times of EEAP groups were significantly higher than that of prednisone acetate group （P＜0.05）. CONCLUSIONS： EEAP may show the anti-inflammatory and antiasthmatic effects by inhibiting the secretion of TNF-α， increasing the content of SOD and inhibiting inflammatory cell infiltration.
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To explore the mechanism of acupoint embedding for obesity based on the western pathological mechanism of chronic low inflammatory response inducing the imbalance between"promoting inflammation"and"anti-inflammation"in immune reaction, and the pathological nature of deficient healthy and state of evil domination in the TCM theory induced by the"stagnation heat, phlegm heat, dampness heat, stasis heat"on the basis of deficiency. The mechanism may be improving the secretory disorder of adipose tissue and metabolic inflammatory response by the enhanced anti-inflammatory phagocytosis clearance ability in the immune system which is caused by the new inflammatory reaction under the stimulation of innate immune response pattern. The model of"inhibiting chronic low inflammation reaction through the innate immunity"may be an important mechanism of acupoint embedding for obesity.
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Humans , Acupuncture Points , Adipose Tissue , Immunity, Innate , Inflammation , Therapeutics , Medicine, Chinese Traditional , Obesity , TherapeuticsABSTRACT
Objective To evaluate the effect and mechanism of ginkgolide injection combined with edaravone on acute cerebral infarction.Methods 120 acute cerebral infarction patients were divided into observation group and control group,60 cases in each group.The control group was treated with edaravone,and the observation group was treated with ginkgolide injection combined with edaravone.The neuron specific enolase (NSE),S100β,tumor necrosis factor-α (TNF-α),interleukin-6 (IL-6),C reactive protein (CRP),National Institutes of Health stroke scale(NIHSS) and clinical efficacy were compared between the two groups.Results After treatment,the levels of NSE,S100β,CRP,IL-6 and TNF-α of the observation group were (7.1 ± 1.5) μg/L,(0.2 ±0.1) μg/L,(14.5 ± 3.7) mg/L,(20.9 ± 5.3) ng/L and (11.2 ± 3.0)μg/L,respectively,which of the control group were (8.9 ± 2.0) μg/L,(0.4 ± 0.2) μg/L,(21.3 ± 4.2) mg/L,(29.7 ± 3.2) ng/L and (18.8 ± 3.6) μg/L,respectively,those of the observation group were significantly lower than comrol group (t =2.898,2.894,3.012,2.998,3.025,all P ＜0.05).After treatment for 7d and 14d,the NIHSS scores of the observation group were (11.8 ± 3.0) points and (7.3 ±2.2) points,respectively,which of the control group were (15.2 ± 3.9) points and (10.5 ± 3.0) points,respectively,the observation group were significantly lower than control group(t =2.984,3.037,all P ＜ 0.05).The clinical efficacy of the observation group was significantly better than that of the control group (83.3 ％ vs.61.7％) (x2 =7.064,P ＜0.05).Conclusion Ginkgolide injection combined with edaravone in the treatment of acute cerebral infarction caninhibit inflammation reaction,alleviate nerve function damage,its effect is better than edaravone.
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OBJECTIVE:To investigate the effects of intensive atorvastatin therapy on postoperative blood lipid,inflammation reaction and major adverse cardiac events (MACE) in non-ST segment elevation myocardial infarction (NSTEMI) patients before PCI.METHODS:A total of 120 NSTEMI patients underwent selective PCI were randomly divided into control group (60 cases) and observation group (60 cases).Both groups were given Aspirin enteric-coated tablet 0.3 g orally,once a day+Clopidogrel sulfate tablet 300 mg orally,once a day,immediately after admission.After operation,they were given medicine continuously for consecutive 12 weeks.Control group was given Atorvastatin calcium tablet 80 mg orally,immediately after operation,and then was given 40 mg,once a day,for consecutive 12 weeks.Observation group was additionally given Atorvastatin calcium tablet 40 mg orally 6 h before operation on the basis of control group.The levels of TG,TC,HDL-C,LDL-C,hs-CRP,TNF-αt and IL-10 before and after PCI,the incidence of postoperative MACE,postoperative re-hospitalization rate and the occurrence of ADR were observed in 2 groups.RESULTS:There was no statistical significance in the levels of TG,TC,HDL-C or LDL-C between 2 groups before and after operation (P＜0.05).After operation,the levels of hs-CRP,TNF-α and IL-10 in 2 groups were significantly higher than before operation,and the observation group was significantly lower than the control group,with statistical significance (P＜ 0.05).There was no statistical significance in the incidence of postoperative MACE,postoperative re-hospitalization rate or the incidence of ADR between 2 groups (P＞0.05).CONCLUSIONS:Intensive atorvastatin therapy before PCI can effectively reduce the levels of inflammatory response in NSTEMI patients,but have no significant changes in blood lipid levels and MACE risk,without increasing the incidence of ADR.
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Objective To compare the clinical efficacy and serum levels of IL-35 and NF-κB of rosuvastatin and atorvastatin in patients with coronary heart disease.Methods i00 patients with coronary heart disease were selected,they were divided into two groups according to different statins.The control group (49 cases) was given atorvastatin calcium tablets.The observation group (51 cases) was given rosuvastatin calcium tablets.The effect of different statins in treatment of coronary heart disease was evaluated by lipid levels,IL-35,NF-κB level before and after treatment,adverse reaction during treatment.Results Before treatment,The TG,TC,LDL-C,HDL-C levels of two groups had no significant difference.After treatment,the TG,TC,LDL-C levels of two groups were decreased,and the LDL-C level in the observation group was lower than that of the control group (P ＜ 0.05).The TG,TC level had no significant differences between two groups.After treatment,the HDL-C levels were increased in two groups.There were no significant differences between groups.Before treatment,there were no statistical significance on serum IL-35,NF-κB level.After treatment,the IL-35 level was increased and NF-κB was decreased in two groups (P ＜ 0.05).And the IL-35 level was higher than that of the control group,the NF-κB level was lower than that the control group (P ＜ 0.05).During treatment,there was no statistical significance on adverse reaction between two groups.Conclusion Rosuvastatin and Atorvastatin have good lipid-lowering effect on coronary heart disease.Rosuvastatin can reduce the LDL-C obviously.These drugs can control the inflammation reaction,with less adverse reaction.It is the ideal lipid-lowering drug in clinical treatment of coronary heart disease.
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Objective To compare the clinical efficacy and serum levels of IL-35 and NF-κB of rosuvastatin and atorvastatin in patients with coronary heart disease.Methods i00 patients with coronary heart disease were selected,they were divided into two groups according to different statins.The control group (49 cases) was given atorvastatin calcium tablets.The observation group (51 cases) was given rosuvastatin calcium tablets.The effect of different statins in treatment of coronary heart disease was evaluated by lipid levels,IL-35,NF-κB level before and after treatment,adverse reaction during treatment.Results Before treatment,The TG,TC,LDL-C,HDL-C levels of two groups had no significant difference.After treatment,the TG,TC,LDL-C levels of two groups were decreased,and the LDL-C level in the observation group was lower than that of the control group (P ＜ 0.05).The TG,TC level had no significant differences between two groups.After treatment,the HDL-C levels were increased in two groups.There were no significant differences between groups.Before treatment,there were no statistical significance on serum IL-35,NF-κB level.After treatment,the IL-35 level was increased and NF-κB was decreased in two groups (P ＜ 0.05).And the IL-35 level was higher than that of the control group,the NF-κB level was lower than that the control group (P ＜ 0.05).During treatment,there was no statistical significance on adverse reaction between two groups.Conclusion Rosuvastatin and Atorvastatin have good lipid-lowering effect on coronary heart disease.Rosuvastatin can reduce the LDL-C obviously.These drugs can control the inflammation reaction,with less adverse reaction.It is the ideal lipid-lowering drug in clinical treatment of coronary heart disease.
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Objective To compare the lipoprotein(a) (Lp-a) and lipid metabolism level in rheumatoid arthritis(RA) patients and control group (healthy subjects),and evaluate the correlation between Lp-a levels and systemic inflammation in patients with RA.Methods Blood samples from 30 RA patients with positive rheumatoid factor and 30 healthy controls were collected,with same distribution of gender and age in both groups.Lipid metabolism level such as Lp-a,triglyceride(TG),total cholesterol(TC),high-density lipoprotein cholesterol (HDL-C),low-density lipoprotein cholesterol (LDL-C),very low-density lipoprotein cholesterol (VLDL-C) and inflammation markers such as tumor necrosis factor α (TNF-α),interleukin 6 (IL-6) and C reactive protein (CRP) were detected and analyzed statistically.Results LP-a levels were higher in RA patients than that of control group(P＜0.001),HDL-C levels were lower in RA group (P＜0.05),while TC,TG,LDL-C and VLDL-C levels showed no difference (P＞0.05).The TNF-α、IL-6 and CRP levels of RA patients were higher than that of control group(P＜0.05),and the association between higher Lp-a level and TNF-α were confirmed (r=0.753,P＜0.001).Conclusions High levels of Lp-a are often observed in RA patients,and a rising Lp-a level are associated with systematic inflammation reaction.Lp-a may be a risk factor for RA progress.
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Objective To observe the influence of different level of hyperhomocysteinemia on mRNA and protein expressions of KV1 .3 ,CaN,NFAT,IL-6 and TNF-αin lymphocytes of patients with acute ST-segment elevation myocardial infarction (STEMI).Methods We selected 90 STEMI patients and divided them into three groups according to the level of plasma homocysteine:the first experimental group (STEMI group,Hcy30 μmol/L,n=30 ).Another 30 healthy examined people were selected as control group (n=3 0 ).Peripheral lymphocytes were isolated by Ficoll density gradient centrifugation.The Hcy in the plasma was measured with the IMX assays.Real-time quantitative PCR (RT-PCR)was used to detect mRNA expressions of KV1.3,CnAα,NFAT1,IL-6 and TNF-αand Western blot technique was used to detect the expressions of KV1.3,CnAαand NFAT1.Results The mRNA and protein expression levels of KV1.3,CnAαand NFAT1 in each experimental group were significantly higher than those in control group (P<0 .0 5 or P<0 .0 1 ).Multiple comparison in each experimental group showed that compared with that in the first experimental group,the expression level of the second experimental group increased (P<0.05 or P<0.01)and compared with first and second experimental groups,the expression level of the third experimental group increased (P<0.05 or P<0.01).The mRNA expression levels of IL-6 and TNF-αin each experimental group were significantly higher than those in control group (P<0.05 or P<0.01 ).Multiple comparison in each experimental group showed that compared with that in the first experimental group,the expression level of the second experimental group increased (P<0 .0 5 or P<0 .0 1 )and compared with first and second experimental groups,the expression level of the third experimental group increased (P<0.01).Plasma total Hcy levels were positively correlated with mRNA and protein expressions of KV1.3 in all observed groups (r=0.503 P=0.000,r=0.726 P=0.000).Conclusion The higher level of Hcy in plasma,the higher mRNA and protein expression levels of KV1.3,CnAα,NFAT1 and the higher mRNA expression levels of IL-6,TNF-αin the lymphocyte of STEMI patients,which may be one mechanism for Hcy exacerbating the inflammatory reaction of STEMI.
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Objective Acute pancreatitis (AP) is a common acute abdomen which is widely discussed by scientists for its fast onset,acute progress and accompanied complications including SIRS and MODS.Although the therapeutic efficacy of AP was improved with the improvements in critical care,the incidence and mortality of AP remains high worldwide.The precise mechanism of AP is complicated and still controversial up to now.Recently,the regulatory mechanism of renin angiotensin system (RAS) and nuclear factor-kappa B (NF-κB) on AP has drawn attention of people.And the research could provide crucially important theoretical basis for clinical treatment.In this article,the latest research about the connection among RAS,NF-κB and AP were reviewed.
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Objective:To study the inflammation stress reaction between laparoscopic operation and open operation in treating hysteromyoma.Methods: hysteromyoma patients in our hospital from January 2011 to December 2012 were enrolled and randomly divided into observation group given laparoscopic operation and control group given open operation. Then inflammatory factors levels were detected, operation trauma index were observed and the correlation were analyzed.Results: (1)After treatment, inflammatory factor levels of two groups were higher than those before treatment and IL-1(t=5.892,P0.05), intraoperative bleeding volume(t=7.842,P<0.05), postoperative anal exhaust time(t=7.283,P<0.05), bed time(t=8.213,P<0.05) and NRS pain scores(t=7.883,P<0.05) of observation group were lower than control group(P<0.05); (3) Intraoperative bleeding volume, postoperative anal exhaust time, bed time and NRS pain scores were positively correlated with IL-1,r2 were separately 0.485, 0.521, 0.442, 0.451; and positively correlated with TNF-α levels,r2 were separately 0.556, 0.513, 0.423, 0.458, the difference was statistical significance(P<0.05).Conclusion: Laparoscopic operation is helpful to reduce the operation wound and relieve postoperative inflammatory reaction; and there was close correlation between inflammatory stress and operation trauma.
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Objective To investigate the expression of p38 MAPK gene and p38 MAPK protein,and explore the effect of p38 MAPK in inflammation reaction of severe acute pancreatitis.Methods 48 cases with severe acute pancreatitis were chosen as research group,and another 48 healthy cases as control group.The expression of p38 MAPK gene were investigated by RT-PCR,and the expression of p38 MAPK and P-p38 MAPK protein were investigated by western blot. Results The expression of p38 MAPK mRNA,p38 MAPK protein and P-p38 MAPK protein in research group were higher than that in control group,the differences were all statistically significant(P<0.05 ).Conclusion The expression of p38 MAPK gene and p38 MAPK protein were significantly increased in patients with severe acute pancreatitis,which showed that p38 MAPK played an important role in inflammation reaction.
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This article was aimed to determine effects of Jia-Shen prescription (JSP) on infarct size (IS), cardiac function and myocardial cytokine in the early phase of myocardial infarction (MI) in rats. Acute MI models were induced by the ligation of left anterior descending coronary artery in Sprague-Dawley (SD) rats. The rats were ran-domly divided into five groups, which were the sham-operated group, model group, JSP-3 g (3 g·kg-1·day-1) group, JSP-6 g (6 g·kg-1·day-1) group, and the losartan (10 mg·kg-1·day-1) group. IS was determined by Evans blue and 2,3,5-Triphenyltetrazolium chloride (TTC) 3 days after MI. The left ventricular structure and contractility were measured by echocardiography performed 7 days after MI. And contents of myocardial inflammatory mediators in-cluding tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), and monocyte chemoattractant protein-1 (MCP-1) were measured by ELISA. The results showed that compared with the model group, treatment with JSP at the dose of 6 g significantly reduced myocardial IS (P<0.05);left ventricular end diastolic diameter (LVEDD) and left ventricu-lar end systolic diameter (LVESD) were significantly decreased (P<0.05); left ventricular ejection fraction (LVEF) and left ventricular fraction shortening (LVFS) were significantly increased (P<0.05).The results were similar as the losartan group. Compared with the model group, JSP can significantly reduce the production of TNF-α, IL-1βand MCP-1 in cardiac tissues (P<0.05). Except TNF-α, these effects of JSP were in a dose-dependent manner. JSP (6 g) had equal effectiveness with losartan. It was concluded that consistent with losartan-induced cardioprotection, JSP administered after MI reduced myocardial IS, improved cardiac function, and decreased inflammatory mediators in ischemic myocardium. The data indicated that JSP exerted its cardioprotection possibly via inhibiting inflammatory response.
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Objective To explore the relation between plasmocytoid dentritic cells (pDCs) and cerebral immune-inflammation reaction following ischemic stroke. Methods Circulating pDCs were measured by flow cytometry in 62 patients with acute ischaemic stroke (AIS), 26 healthy controls, 12 patients with asymptomatic cerebral infarction stenosis (ACI-S), and 14 patients with transient ischaemic attack (TIA). The sizes of infarct lesions were assessed by DWI scanning. AIS group was further divided into lacunar infarction group, small infarction group,and large infarction group according to the infarction area. The correlation between the number of pDCs and NHISS score and CRP level was also analyzed in AIS group. Results The labsolute number of pDCs and the percentage of pDCPs to circulating blood white cells were significantly lower in AIS group than in the healthy control group (P<0.001). As compared with lacunar infarction group, the number of pDCPs decreased significantly in large infarction group. The number of pDCPs was negatively correlated with the levels of CRP and the NIHSS score. Conclutions Patients with AIS has a decreased level of circulating pDCs, which may be involved in the gathering of circulating pDCs in the infarcted brain to trigger cerebral immune reaction.
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Objective: To investigate the effect of lethal Vibrio vulnificus infection on the blood system and the pathology changes of the major organs in mice, and to explore the possible mechanism of the related death. Methods: Lethal Vibrio vulnificus-infection model was established with mice. The model mice were divided into two groups: a control group and an infection group. ELISA was used to examine the serum levels of TNF-α, IL-1β, and TF. Serum total bilirubin (TBIL), creatinine (Cre), and blood urea nitrogen (BUN) were analyzed using automatic biochemical analyzer; whole blood cell analysis was also performed. The pathological changes of the heart, lung, liver, spleen, and kidney were observed under electron and light microscopes. Results: Compared with the control group, the serum levels of TNF-α, IL-1β, and TF were significantly increased in mice after infection with Vibrio vulnificus (P < 0.05); the serum levels of BUN, Cre, TBIL, diastase and alanine aminotransferase (ALT) were significantly increased (P < 0.05). The ratios of WBC, platelet, and lymphocytes were all significantly decreased after infection compared with the control group (P<0.05). The ratios of red blood cells, monocytes, and Hb level were significantly increased compared with the control group (P<0.05). The pathological changes of major organs included hyperaemia, edema, inflammatory cell infiltration, and apoptosis. Conclusion: Lethal infection with Vibrio vulnificus can initiate super-inflammation reaction in mice; it can also activate the blood coagulation system and induce systemic tissue injury, finally leading to death.
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Objective To investigate the role of nuclear factor ?B activation in the onset of acute coronary syndrome(ACS).Methods 76 patients with acute myocardial infraction(AMI),41 patients with unstable angina pectoris(UAP),43 patients with stable angina pectoris(SAP)and 20 normal controls were enrolled.NF-?B activation in monocytes in peripheral blood monocyte was determined by ELISA with the NF-?B p65 Kit the at 3 and 5 days after admission.Results The activity of NF-?B in monocytes of peripheral blood in AMI patients and UAP patients was significantly higher than that in SAP patients and normal controls(P