scholarly journals Kiwi Root Extract Inhibits the Development of Endometriosis in Mice by Downregulating Inflammatory Factors

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Tingting Liao ◽  
Shenzhi Zhao ◽  
Tong Zhou ◽  
Jiajia Song ◽  
Xianping Huang ◽  
...  
Keyword(s):  
Gelatin Zymography ◽  
Angiogenic Factor ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Root Extract ◽  
Lesion Volume ◽  
Ectopic Tissue ◽  
Tnf Α ◽  
Mrna And Protein Expression ◽  
Ep2 Receptor

Purpose. To determine whether the kiwi root extract inhibits the development of endometriosis in mice by suppressing inflammatory factors. Materials and Methods. The mouse model of endometriosis was induced by surgery after which the mice were continuously injected with the drug for 14 days. On the 14th day, the mice were sacrificed, and the peritoneal fluid was obtained for enzyme-linked immunosorbent assay. Endometrial ectopic tissue was weighed and analyzed by tissue immunochemistry, RT-PCR, western blotting, and gelatin zymography experiment. Results. Kiwi root extract significantly reduced endometriotic lesion volume and downregulated the proinflammatory cytokines IL-6, IL-8, IL-1β, and TNF-α, as well as the angiogenic factor VEGF-A. It also inhibited the mRNA and protein expression of COX-1 and COX-2, IL-6, TGF-β1, EP2 receptor, and ER-β in endometriotic lesions but did not affect the expression of MMP-9 and MMP-2. Conclusions. Kiwi root extract could significantly inhibit the growth of surgery-induced endometriosis in mice. Our results suggest that the kiwi root extract may inhibit the development and progression of ectopic endometrium through disruption of neovascularization and reducing inflammation, which may be beneficial in treating this common gynecological disease.

scholarly journals Effects of Shugan-Jianpi Recipe on the Expression of the p38 MAPK/NF-κB Signaling Pathway in the Hepatocytes of NAFLD Rats

Medicines ◽  
2018 ◽  
Vol 5 (3) ◽  
pp. 106 ◽  
Author(s):  
Yuanjun Deng ◽  
Kairui Tang ◽  
Runsen Chen ◽  
Yajie Liu ◽  
Huan Nie ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
P38 Mapk ◽  
Low Dose ◽  
Serum Levels ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
High Dose ◽  
Model Group ◽  
Necrosis Factor Alpha ◽  
Tnf Α

Background: In traditional Chinese medicine, the Shugan-Jianpi recipe is often used in the treatment of nonalcoholic fatty liver disease (NAFLD). This study aimed to explore the mechanism of the Shugan-Jianpi recipe in relation to rats with NAFLD induced by a high-fat diet. Methods: Rats were randomly divided into eight groups: normal group (NG), model group (MG), low-dose Chaihu–Shugan–San group (L-CG), high-dose Chaihu–Shugan–San group (H-CG), low-dose Shenling–Baizhu–San group (L-SG), high-dose Shenling–Baizhu–San group (H-SG), low dose of integrated-recipes group (L-IG), and high dose of integrated-recipes group (H-IG). After 26 weeks, a lipid profile, aspartate, and alanine aminotransferases in serum were detected. The serum levels of inflammatory factors including interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) were analyzed using the enzyme linked immunosorbent assay (ELISA) method. Hepatic pathological changes were observed with hematoxylin-eosin (HE) and oil red O staining. The expression of the p38 mitogen-activated protein kinases (MAPK)/nuclear factor-κB (NF-κB) pathway was detected by quantitative real-time PCR and Western blotting. Results: A pathological section revealed that NAFLD rats have been successfully reproduced. Compared with the model group, each treatment group had different degrees of improvement. The Shugan-Jianpi recipe can inhibit the serum levels of IL-1β, IL-6, and TNF-α in NAFLD rats. The expression of mRNA and a protein related to the p38 MAPK/NF-κB signaling pathway were markedly decreased as a result of the Shugan-Jianpi recipe. Conclusions: The Shugan-Jianpi recipe could attenuate NAFLD progression, and its mechanism may be related to the suppression of the p38 MAPK/NF-κB signaling pathway in hepatocytes.

scholarly journals The neuroprotective effect of pretreatment with carbon dots from Crinis Carbonisatus (carbonized human hair) against cerebral ischemia reperfusion injury

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Yue Zhang ◽  
Suna Wang ◽  
Fang Lu ◽  
Meiling Zhang ◽  
Hui Kong ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Carbon Dots ◽  
Ischemia Reperfusion Injury ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Inflammatory Factors ◽  
Lesion Volume ◽  
Ischemic Lesion ◽  
Tnf Α

Abstract Background Cerebral infarction and cerebral hemorrhage, also known as “stroke”, is one of the leading cause of death. At present, there is no real specific medicine for stroke. Crinis Carbonisatus (named Xue-yu-tan in Chinese), produced from carbonized hair of healthy human, and has been widely applied to relieve pain and treat epilepsy, stroke and other diseases in China for thousands of years. Results In this work, a new species of carbon dots derived from Crinis Carbonisatus (CrCi-CDs) were separated and identified. And the neuroprotective effect of carbon dots from CrCi were evaluated using the middle cerebral artery occlusion (MCAO) model. Neurological deficit score and infarction volume was assessed, evans blue content of ischemic hemispheres was measured, the concentrations of inflammatory factors, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) in the cortex were measured, and the levels of neurotransmitters in the brain were determined. Preconditioning of CrCi-CDs significantly reduced ischemic lesion volume and blood–brain-barrier (BBB) permeability, improved neurologic deficits, decreased the level of TNF-α and IL-6 in MCAO rats, inhibited excitatory neurotransmitters aspartate (Asp) and glutamate (Glu), and increased the level of 5-hydroxytryptamine (5-HT). The RNA-Sequencing results reveal that further potential mechanisms behind the activities may be related to the anti-inflammation effects and inhibition of neuroexcitatory toxicity. Conclusion CrCi-CDs performs neuroprotective effect on cerebral ischemia and reperfusion injury, and the mechanisms may correlate with its anti-inflammatory action, which suggested that CrCi-CDs have potential value in clinical therapy on the acute apoplexy cases in combination with thrombolytic drugs. Graphic abstract

Evaluation of angiogenis activation during interleukin-2 infusion in patients with renal cell cancer (RCC)

2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 14640-14640
Author(s):  
C. Simonelli ◽  
R. Talamini ◽  
A. Bearz ◽  
M. Berretta ◽  
P. Monini ◽  
...  
Keyword(s):  
Cell Cancer ◽  
Interleukin 2 ◽  
Angiogenesis Inhibitors ◽  
Angiogenic Factor ◽  
Inflammatory Factors ◽  
Cytokine Network ◽  
Tnf Α ◽  
Ifn Γ ◽  
Few Data ◽  
Factor Release

14640 It is well known that during IL-2 administration a complex activation of the cytokine network is on going, but few data are available about the effect of this activation on angiogenesis. In our Institution all patients with metastatic RCC undergo to the following schedule of IL-2 infusion: IL-2 10 MIU continuous infusion (ci) 5/7 days, one week off followed by IL-2 10 MIU ci 5/7 days, 4 week off (1 cycle); for a total number of 2 cycles. We evaluated the activation of angiogenesis measuring the plasma level of VEGF MMP2 and MMP9 before, during and after the 5 days IL-2 ci. In 13 patients analysed, before IL-2 ci, we have the following median level of plasma VEGF (773+ 378 pg/ml), MMP2 (55.9 + 19.9 ng/ml) and MMP9 (1146+498 ng/ml). The baseline median values of VEGF MMP-9 showed a trend to correlate with the number of metastasis before therapy. During 3 days of IL-2 ci we did not observed any significant increase of VEGF MMP2 and MMP9 as well as after 24 hours from the end of the 5 days ci. On the contrary, at the same time-points, during and after IL-2 ci, we observed the activation of pro-inflammatory cytokines network, measured by the statistically significant increased levels of neopterin IFN-γ and TNF-α and sIcam.This preliminary observation demonstrated that IL-2 ci, even if it highly activates the release of pro-inflammatory factors, does not affect the release of angiogenic surrogate markers such as VEGF MMP2 and MMP9. On the basis of our experience we can suggest that the most suitable time to test angiogenesis inhibitors during IL-2 therapy appear to be the intervals between IL-2 administration and not during IL-2 infusion when the most severe side effects occur and it is not observed a significant increase of angiogenic factor release. No significant financial relationships to disclose.

Correlation between Depression, Posttraumatic Stress Disorder, and Inflammatory Factors in Patients with Severe Burn Injury

2018 ◽  
Vol 84 (8) ◽  
pp. 1350-1354 ◽  
Author(s):  
Donglin Jiang ◽  
Shengyang Jiang ◽  
Fang Gong ◽  
Fenglai Yuan ◽  
Peng Zhao ◽  
...  
Keyword(s):  
Posttraumatic Stress Disorder ◽  
Posttraumatic Stress ◽  
Stress Disorder ◽  
Burn Injury ◽  
Self Report ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Severe Burn ◽  
Tnf Α ◽  
Severe Burn Injury

We aim to investigate the relation between depression, posttraumatic stress disorder (PTSD), and inflammatory factors in patients with severe burn injury. Psychological assessment was carried out using PTSD checklist (PCL) involving a 17-item self-report questionnaire (PCL-17) and the Hamilton Rating Scale for depression (HAMD-24). The serum IL-1β, IL-6, IL-8, and tumor necrosis factor-α (TNF-α) were determined using enzyme-linked immunosorbent assay. Correlation analysis was performed to analyze the correlation between the factors and scores of PTSD and depression. Compared with the PCL-17 score, HAMD-24 score, and inflammatory factors at month 3, a significant decrease was noticed in the PCL-17 score, HAMD-24 score, and inflammatory factors at months 6 and 9 (P < 0.01). For the HAMD-24 score, significant improvements were noticed in the anxiety/somatization, cognitive disorder, blocking, sleep disorders, and depression at months 3, 6, and 9. The levels of IL-1β, IL-8, and TNF-α were positively correlated with the PCL-17 score (P < 0.05). The levels of IL-1β, IL-6, IL-8, and TNF-α were positively correlated with the HAMD-24 score (P < 0.05). Patients with severe burn injury showed obvious stress alternation displaying specific depression-related characteristics, and inflammation may involve in the pathogenesis of PTSD and depression in burn patients.

scholarly journals Acupuncture Can Regulate the Peripheral Immune Cell Spectrum and Inflammatory Environment of the Vascular Dementia Rat, and Improve the Cognitive Dysfunction of the Rats

2021 ◽  
Vol 13 ◽  
Author(s):  
Pan Pan ◽  
Zhinan Ma ◽  
Zhen Zhang ◽  
Zhenzhen Ling ◽  
Yao Wang ◽  
...  
Keyword(s):  
Immune Function ◽  
Vascular Dementia ◽  
Cognitive Dysfunction ◽  
Peripheral Blood ◽  
Acupuncture Treatment ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Spatial Learning And Memory ◽  
Tnf Α ◽  
Cox 2

ObjectiveThe aim of this study is to analyze the effects of acupuncture on peripheral immune function, inflammation, and cognitive impairment in vascular dementia (VD) rats.MethodsIn this study, 2-month-old healthy male Wistar rats (260–280 g) were assigned to the groups as follows: normal group (Gn, n = 10), sham-operated group (Gs, n = 10), and operated group (Go, n = 45). The Go group was established by permanent, bilateral common carotid artery occlusion (BCCAO). Two months after operation, the operated rats were screened by hidden platform trial and the rats with cognitive dysfunction were further randomly divided into impaired group (Gi), acupoint group (Ga), and non-acupoint group (Gna) with 10 rats in each group. The Ga group was given acupuncture treatment for 14 days with a rest for every 7 days. After treatment, the Morris water maze (MWM) test was performed to evaluate the spatial learning and memory abilities of rats. The lymphocyte subsets in peripheral blood and spleen of rats were measured by flow cytometry. The levels of cytokines [i.e., interleukin (IL)-1β, IL-2, IL-4, IL-10, tumor necrosis factor-α (TNF-α), and interferon-γ (INF-γ)], chemokines (i.e., macrophage inflammatory protein-2 (MIP-2)), and other inflammatory mediators (i.e., cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS)) in peripheral blood and hippocampus were measured by enzyme linked immunosorbent assay (ELISA).ResultsCompared with the Gn group, the Gi rats presented long escape latencies to find the platform. After acupuncture treatment, the escape latencies of the Ga group were rescued markedly when compared with the Gi group (P &lt; 0.05). The proportion of CD4 + T lymphocytes in both spleen and peripheral blood in the Ga group increased (P &lt; 0.05) in comparison with the Gi group. There is an obvious reduction in IL-1β (P &lt; 0.05), IL-2 (P &lt; 0.05), TNF-α (P &lt; 0.01), INF-γ (P &lt; 0.01), MIP-2 (P &lt; 0.05), and iNOS (P &lt; 0.01), coming along with the increased levels of IL-4 and IL-10 (P &lt; 0.01) in the Ga group when compared with the Gi group. In addition, the hippocampus proinflammatory factors IL-1β (P &lt; 0.01), IL-2 (P &lt; 0.01), TNF-α (P &lt; 0.05), INF-γ (P &lt; 0.05), MIP-2 (P &lt; 0.05), iNOS (P &lt; 0.01), and COX-2 decreased in the Ga group, whereas the anti-inflammatory factors IL-4 and IL-10 (P &lt; 0.01) increased.ConclusionThere are abnormal immune function and peripheral inflammation in VD rats. Acupuncture can regulate the peripheral immune function and inflammation of the VD rats and can improve the cognitive dysfunction of the rats.

scholarly journals Effects of Ropivacaine Hydrochloride on the Expression of Type I Interferon and Its Receptor in SH-SY5Y Cells

2020 ◽  
pp. 1-10
Author(s):  
Xianjie Wen ◽  
Zhaoxia Wu ◽  
Weidong Lin ◽  
Yiqun Li ◽  
Xiaoping Wang
Keyword(s):  
Cell Viability ◽  
Local Anesthetics ◽  
Type I Interferon ◽  
Inflammatory Factors ◽  
Type I ◽  
Apoptosis Rate ◽  
Tnf Α ◽  
Mrna And Protein Expression ◽  
Ropivacaine Hydrochloride

Nerve injury caused by local anesthetics is a hot issue that people pay close attention to, and its mechanism has not been fully clarified. Type I interferon (I-IFN) is an important factor in regulating inflammatory response. In this study, SH-SY5Y cells were injured by ropivacaine hydrochloride in vitro. The cell viability, apoptosis rate, mRNA and protein expression of I-IFN and its receptor IFNAR, as well as the contents of inflammatory cytokines TNF-α, IL-6 and IL-10 were detected to explore the correlation between I-IFN and neurotoxicity induced by ropivacaine hydrochloride. The results showed that after treated with ropivacaine hydrochloride, the cell viability was decreased, the apoptosis rate was increased, the mRNA and protein expressions of IFN-α, IFN-β, IFNAR1 and IFNAR2 were up-regulated, and the contents of inflammatory factors TNF - α, IL-6 and IL-10 were increased. These results suggest that type I interference and its receptor are associated with neurotoxicity of local anesthetics.

scholarly journals Imbalance of Th22/Treg cells causes microinflammation in uremic patients undergoing hemodialysis

2019 ◽  
Vol 39 (10) ◽  
Author(s):  
Tingting Ren ◽  
Jingyuan Xiong ◽  
Guangliang Liu ◽  
Shaoyong Wang ◽  
Zhongqi Tan ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Serum Levels ◽  
Treg Cells ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Dialysis Adequacy ◽  
Th22 Cells ◽  
Tnf Α ◽  
Uremic Patients ◽  
Dialysis Time

Abstract Background: Regulatory T (Treg) cells are of critical functionality in immune activation and inflammation in uremic patients undergoing hemodialysis (HD). A disruption in balance of Treg cells has potency to elicit infectious disease progression. Here, we examined possible association between ratio imbalance of Th22/Treg cells and microinflammation in uremic patients undergoing HD. Methods: Peripheral blood mononuclear cells (PBMCs) were isolated to allow measurement of the percentage of Th22 cells and Treg cells using flow cytometry. Subsequently, serum levels of related cytokines, interleukin (IL) 22 (IL-22) and IL-10 and inflammatory factors, C-reactive protein (CRP), (TNF-α), IL-6 were determined via enzyme-linked immunosorbent assay (ELISA). Then relationships among dialysis time, microinflammation status (CRP) and dialysis adequacy (immunoreactive parathyroid hormone (iPTH), urea clearance index (Kt/V), β2-MG, serum calcium, and serum phosphorus) were evaluated. Finally, correlation between microinflammation status and dialysis adequacy was analyzed with Pearson’s correlation coefficient. Results: An increased percentage of Th22 and a decreased percentage of Treg cells were evident in uremic patients undergoing HD. Serum levels of IL-22, CRP, TNF-α, and IL-6 were increased, while IL-10 serum level was reduced. An imbalance of Th22/Treg cells was associated with microinflammation status in uremic patients undergoing HD. Furthermore, prolongation of the dialysis time, the microinflammation status and dialysis adequacy were changed. Increased dialysis adequacy was observed to correlate with alleviated microinflammation of uremic patients undergoing HD. Conclusions: Conjointly, an imbalance of Th22/Treg cells may be a potential cause responsible for uremia occurrence, which in turn indicates that uremia could be effectively alleviated by altering the ratio of Th22/Treg cells.

scholarly journals Effect of Curcumin and N-Acetylcysteine on Brain Histology and Inflammatory Factors (MMP-2, 9 and TNF-α) in Rats Exposed to Arsenic

2018 ◽  
Vol 24 (4) ◽  
pp. 264-272 ◽  
Author(s):  
Mostafa Fallah ◽  
Najmeh Moghble ◽  
Iraj Javadi ◽  
Hossein Bahadoran ◽  
Alireza Shahriary
Keyword(s):  
Single Dose ◽  
Gelatin Zymography ◽  
White Matter Lesions ◽  
Pyramidal Cells ◽  
Inflammatory Factors ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Ca1 ◽  
Tnf Α ◽  
Ca1 Area ◽  
Factor Α

Background: Arsenic is a toxic element that widely widespread in environment. Inflammation is now considered as one of the major mechanisms implicated in arsenic poisoning. Curcumin (Cur) and N-acetylcysteine (NAC) are potential antioxidants that protect cells against inflammation. This study aimed to compare the protective effect of Cur and NAC on brain histology and inflammatory factors, including matrix metalloproteinases-2, -9 (MMP-2, 9) and tumor necrosis factor-α (TNF-α) in rats exposed to single dose of arsenic. Methods: Rats were exposed to single dose of arsenic (20mg/kg, by gavage) for 30 days and then treated with 300mg/kg NAC (by gavage) and 100mg/kg Cur (by gavage), individually. Serum level of TNF-α was measured using specific ELISA kits. MMP2 and MMP9 contents were measured using Gelatin Zymography method. Brain samples were collected for histopathological and morphological examinations. Results: Arsenic treatment induced white matter lesions and cellular damages at hippocampal CA1 area of the brain. The number of hippocampal CA1 pyramidal cells was significantly declined in arsenic exposed rats (p<0.05). Treatment with NAC and Cur improved these abnormalities. The mean levels of MMP2, MMP9 and TNF-α inflammatory biomarkers were slightly declined after treatment with NAC and Cur (p>0.05). Conclusion: NAC and Cur play an important role in protecting the hippocampal CA1 cells injury induced by arsenic.

scholarly journals FM0807 decelerates experimental arthritis progression by inhibiting inflammatory responses and joint destruction via modulating NF-κB and MAPK pathways

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
Nanwen Zhang ◽  
Zhiwei Liu ◽  
Hongbin Luo ◽  
Weifang Wu ◽  
Kaimei Nie ◽  
...  
Keyword(s):  
Synovial Fluid ◽  
Inflammatory Responses ◽  
Mapk Pathway ◽  
Joint Destruction ◽  
Mitogen Activated Protein Kinase ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Therapeutic Effects ◽  
Dependent Manner ◽  
Tnf Α

Abstract Background: Rheumatoid arthritis (RA) is a chronic articular synovial inflammatory disease. The precise etiology underlying the pathogenesis of RA remains unknown. We aimed to investigate the inhibitory effect of curcumin analog FM0807 (curcumin salicylate monoester, 2-hydroxy-, 4-[(1E,6E)-7-(4-hydroxy-3-methoxyphenyl)-3,5-dioxo-1,6-heptadien-1-yl]-2-methoxyphenyl ester) on experimental RA and investigate its possible mechanisms of action. Method: Rats with Freund’s complete adjuvant (FCA)-induced arthritis (AIA) were administered aspirin (0.1 mmol.kg−1), curcumin (0.1 mmol.kg−1), FM0807 (0.1, 0.2 mmol.kg−1) and vehicle via gastric gavage, from days 7 to 21, once daily. The hind paw volume and arthritis index (AI) were measured, and radiographic and histological examinations were performed. Twenty-one days later, the animals were killed and left ankle joints were removed to measure protein expression of the elements of the nuclear factor κB (NF-κB) and mitogen-activated protein kinase (MAPK) pathway by Western blot analysis. The enzyme-linked immunosorbent assay (ELISA) was employed to measure synovial fluid levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, IL-1β and IL-10. Results: Compared with AIA group, FM0807 reduced the AI and swelling of the injected hind paw in a dose-dependent manner, and inhibited increases in inflammatory cell infiltration, pannus formation and cartilage destruction. FM0807 also potently attenuated the increase in the expression of inflammatory factors TNF-α, IL-6 and IL-1β in synovial fluid, while IL-10 levels were also elevated. FM0807 significantly suppressed phosphorylation of extracellular-signal-regulated kinase (ERK) 1/2 (ERK1/2), c-Jun-N-terminal kinase (JNK) 1/2 (JNK1/2), p38MAPK, inhibitor of NF-κB kinase (IKK), IκB and NF-κB p65 protein, (all P<0.05), which displayed more potential effects compared with those of the aspirin and curcumin groups. Conclusion: FM0807 exerts its therapeutic effects on RA by inhibiting cartilage degeneration. FM0807 treatment might be an effective therapeutic approach for RA.

scholarly journals Association between serum sST2 levels and CD4+T cells in patients with organ failure: a pilot study

2021 ◽  
Author(s):  
qisong Peng ◽  
guoyou Shi ◽  
hongxiang lu
Keyword(s):  
T Cells ◽  
T Cell ◽  
Organ Failure ◽  
Normal Control ◽  
Cd4 T Cells ◽  
Cd4 T Cell ◽  
Inflammatory Factors ◽  
Enzyme Linked Immunosorbent Assay ◽  
Tnf Α ◽  
Normal Controls

Background: The importance of sST2 has been increasingly appreciated because of its associated with the development of heart failure and related diseases. Objective: The aim of this study was to evaluate the association of sST2 with CD4+T cells in patients with organ failure. Methods: 100 (M:F=60:40) organ failure patients aged (mean±SD=69.08±16.68) and 30 (M:F=14:16) normal control aged (mean±SD=60.23±13.99) serum sST2 were detected by chemiluminescence assay (CLIA) and the expression of serum IL-1, IL-6 and TNF-α were analyzed by enzyme-linked immunosorbent assay (ELISA). The proportion of CD4+T cells in peripheral blood was determined by flow cytometry (FCM). Association of sST2 with CD4+T cells in organ failure patents were analyzed by SPASS. Results: The expression of sST2 in organ failure patients (107.4±5.79ng/mL) was significantly higher than normal control (8.57±0.35ng/mL). Inflammatory factors IL-1 and IL-6 in patients were also increased than normal controls (IL-1: 0.33±0.04pg/mL vs 0.14±0.02pg/mL. IL-6: 165.7±10.53pg/mL vs 95.33±7.42pg/mL. TNF-α: 1.57±0.14pg/mL vs 6.11±0.77pg/mL). In patients, the results showed CD4+T cells were reduced compare with normal control (238.3±13.67/μL vs 1081±39.13/μL). Additionally, sST2 was found to be inversely associated with CD4+T cell in patients with organ failure. Conclusion: sST2 level was closely related to the development of organ failure and sST2 was obviously correlated with CD4+T cell in patients with organ failure.

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