Objective To assess the effect and safety of clinical nutritional supplementation with different patterns for treating systematic inflammatory response syndrome (SIRS). Methods Randomized controlled trials (RCTs) were identified from MEDLINE (1996 to Nov. 2004), EMBASE (1984 to Nov. 2002), Cochrane Controlled Trials Register (Issue 4, 2004), Chinese Cochrane Centre Database (Issue 4, 2004), CBMdisc (1978 to Nov. 2004). We handsearched related published and unpublished data and their references. All RCTs of nutritional interventions for SIRS were included. Data were extracted and evaluated by two reviewers independently with designed extraction form. RevMan 4.2.7 software was used for data analysis. Results Six RCTs involving 353 patients were included. All the results of meta-analysis were listed as the following: ① Mortality: compared with routine nutrition, one study showed that glutamine had a statistical difference with RR 0.67 and 95%CI 0.31 to 1.32. Compared with no treatment, one study showed selenium had a statistical difference with RR 1.19, 95%CI 0.59 to 2.41. ② Compared with routine nutrition, one study showed that glutamine had a statistical difference on reducing the ratio of nasocomial infection of SIRS with RR 0.5, 95%CI 0.27 to 0.91, but had no statistical difference on reducing the ratio of multiple organ dysfunction syndrome with RR 1.53, 95%CI 0.64 to 3.66. ③ Improvement of the critical condition of SIRS: compared with routine nutrition, one study showed that glutamine had a statistical differences with WMD 4.0, 95%CI 2.36 to 5.64; compared with high calorie intake, two studies showed low calorie intake had a statistical difference with WMD 4.9, 95%CI 1.76 to 8.04. ④ Reduction of the complication of hyperglycemia and hypertriglyceridemia: compared with high calorie intake, one study showed low calorie intake had statistical difference with WMD －0.70, 95%CI －1.20 to －0.20 and WMD －1.80, 95% CI －2.42 to －1.16 respectively and all P≤0.01. ⑤ Increasing of the plasma IgG concentration: compared with routine nutrition, two studies showed that glutamine had a statistical difference with WMD 4.20, 95% CI 2.23 to 6.16. ⑥ Increasing of the nitrogen balance, intestinal permeability, the level of plasma concentration of anlbumin, prealbumin and TRF: compared with control interventions, glutamine, low calorie intake, selenium supplementation and fructose-glucose-xylitol mixture showed no statistical difference. Conclusions Glutamine, low calorie intake, selenium supplementation, FGX mixture may decrease the complication of infection or metabolism and be better than the controlled interventions; but there is no benefit on reducing the rate of death result from SIRS compared with controlled interventions. The evidence of most RCTs with poor quality is too weak to draw a conclusion. More high quality trials are required.
Objective To explore the molecular mechanism of miR-515-5p in inhibiting chondrocyte apoptosis and alleviating inflammatory response in osteoarthritis (OA). Methods Human cartilage cell line C28/I2 was cultured in vitro and treated with 10 ng/mL interleukin 1β (IL-1β) for 24 hours to construct an in vitro OA model. C28/I2 cells were transfected with miR mimics, mimics negative control (NC), over expression (oe)-NC, and oe-Toll-like receptor 4 (TLR4), respectively, and then treated with 10 ng/mL IL-1β for 24 hours to establish OA model. Cell proliferation capacity was detected by cell counting kit 8 and 5-Ethynyl-2’-deoxyuridine, cell apoptosis and cell cycle were detected by flow cytometry, and B-cell lymphoma 2 protion (Bcl-2), Bcl-2-associated X protein (Bax), cleaved-Caspase-3, TLR4, myeloid differentiation primary response gene 88 (MyD88), p65 and phosphorylated p65 (p-p65) protein expression levels were detected by Western blot. Real-time fluorescence quantitative PCR was used to detect mRNA expression levels of miR-515-5p and TLR4, and ELISA was used to detect pro-inflammatory factor prostaglandin E2 (PGE2), tumor necrosis factor α (TNF -α), and IL-6 levels in cell supernatant. The potential binding sites between miR-515-5p and TLR4 were predicted by BiBiServ2 database, and the targeting relationship between miR-515-5p and TLR4 was verified by dual luciferase reporting assay. Results After the treatment of C28/I2 cells with IL-1β, the expressions of miR-515-5p and Bcl-2 protein and the proliferation ability of C28/I2 cells significantly reduced. The expression levels of Bax and cleaved-Caspase-3 protein, the levels of pro-inflammatory factors (PGE2, TNF-α, IL-6) in the supernatant of C28/I2 cells, and the apoptosis of C28/I2 cells significantly increased. In addition, the proportion of the cells at S phase and G2 phase decreased significantly, and the proportion of cells at G1 phase increased significantly, suggesting that the cell cycle was blocked after IL-1β treatment. After transfection with miR mimics, the expression level of miR-515-5p in the cells significantly up-regulated, partially reversing the apoptosis of OA chondrocytes induced by IL-1β, and alleviating the cycle arrest and inflammatory response of OA chondrocytes. After treating C28/I2 cells with IL-1β, the mRNA and protein levels of TLR4 significantly increased. Overexpression of miR-515-5p targeted inhibition of TLR4 expression and blocked activation of MyD88/nuclear factor κB (NF-κB) pathway. Overexpression of TLR4 could partially reverse the effect of miR mimics on IL-1β-induced apoptosis and inflammation of OA chondrocytes. ConclusionmiR-515-5p negatively regulates the expression of TLR4, inhibits the activation of MyD88/NF-κB pathway and apoptosis of OA chondrocytes, and effectively alleviates the inflammatory response of the cells.
Objective To investigate the clinical value of peripheral serum cell-free DNA/neutrophil extracellular traps (cf-DNA/NETs) level in diagnosis and severity assessment of sepsis patients. Methods Forty patients with sepsis and 40 patients with non-infectious systemic inflammatory response syndrome (nf-SIRS) were enrolled in this study. The cf-DNA/NETs level in serum of all subjects were measured. Receiver operating characteristic (ROC) curve was used to evaluate the diagnostic ability of the cf-DNA/NETs, white blood cell count (WBC), procalcitonin (PCT) and interleukin-6 (IL-6). The sepsis patients were stratified into a survival group and a death group according to the prognosis. Sequential organ failure (SOFA) score were recorded in the sepsis patients, and the correlations between SOFA and cf-DNA/NETs, PCT, WBC, IL-6 were analyzed. Results Compared with the nf-SIRS group, cf-DNA/NETs and PCT levels were significantly higher in the sepsis group (both P<0.05). WBC and IL-6 showed no significant differences between the two groups (bothP>0.05). The area under the ROC curve (AUC) of cf-DNA/NETs was 0.884 for diagnosis of sepsis, and it was higher than the AUC of PCT (0.803). The cf-DNA/NETs showed better sensitivity (81.2% and 79.2%) and specificity (81.0% and 82.4%) than PCT. cf-DNA/NETs and PCT were significantly higher in the death group than those in the survival group. Bivariate collection analysis revealed positive correlations between SOFA score and the two biomarkers of cf-DNA/NETs and PCT (r1=0.573, r2=0.518; both P<0.01). Conclusions cf-DNA/NETs and PCT have certain value in early diagnosis of sepsis, and cf-DNA/NETs shows better diagnostic value in distinguishing sepsis from nf-SIRS than PCT. cf-DNA/NETs can be used as a routine monitoring index to help assess disease severity in sepsis.
To evaluate the process from systemic inflammatory response syndrome (SIRS) to multiple organ dysfunction syndrome (MODS) and probe the therapeutic strategies for elderly patients, we retrospectively studied the clinical data of SIRS and MODS in 292 elderly patients with surgical abdominal emergency. Results: On admission, the morbidity rate of SIRS was 41.1%. Afterwards the morbidity rate of MODS was 14.2%, and the mortality rate of the elderly patients with SIRS was 11.7%. After 48 hours of therapy, MODS was developed in 40.5% of the cases also with SIRS. Of all the 292 elderly patients, 19 cases (6.5%) developed MODS and 16 patients (84.2%) died. Conclusion: The outcome of the patients with surgical abdominal emergency may be improved if SIRS is early diagnosed, the cause of SIRS after 48 hours therapy is well defined and the body inflammatory response is properly regulated.
Objective To investigate the feasibility of selenium-methylselenocysteine (SMC) to promote peripheral nerve regeneration and its mechanism of action. Methods Rat Schwann cells RSC96 cells were randomly divided into 5 groups, which were group A (without any treatment, control group), group B (adding 100 μmol/L H2O2), group C (adding 100 μmol/L H2O2+100 μmol/L SMC), group D (adding 100 μmol/L H2O2+200 μmol/L SMC), group E (adding 100 μmol/L H2O2+400 μmol/L SMC); the effect of SMC on cell proliferation was detected by MTT method, and the level of oxidative stress was detected by immunofluorescence for free radicals [reactive oxygen species (ROS)] after determining the appropriate dose group. Thirty-six 4-week-old male Sprague Dawley rats were randomly divided into 3 groups, namely, the sham operation group (Sham group), the sciatic nerve injury group (PNI group), and the SMC treatment group (SMC group), with 12 rats in each group; the rats in the PNI group were fed with food and water normally after modelling operation, and the rats in the SMC group were added 0.75 mg/kg SMC to the drinking water every day. At 4 weeks after operation, the sciatic nerves of rats in each group were sampled for neuroelectrophysiological detection of highest potential of compound muscle action potential (CMAP). The levels of inflammatory factors [interleukin 17 (IL-17), IL-6, IL-10 and oxidative stress factors catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA)] were detected by ELISA assay. The luxol fast blue (LFB) staining was used to observe the myelin density, fluorescence intensity of glial fibrillary acidic protein (GFAP) and myelin basic protein (MBP) was observed by immunofluorescence staining, and myelin morphology was observed by transmission electron microscopy with measurement of axon diameter. Western blot was used to detect the protein expressions of p38 mitogen-activated protein kinases (p38MAPK), phosphorylated p38MAPK (p-p38MAPK), heme oxygenase 1 (HO-1), and nuclear factor erythroid 2-related factor 2 (Nrf2). ResultsMTT assay showed that the addition of SMC significantly promoted the proliferation of RSC96 cells, and the low concentration could achieve an effective effect, so the treatment method of group C was selected for the subsequent experiments; ROS immunofluorescence test showed that group B showed a significant increase in the intensity of ROS fluorescence compared with that of group A, and group C showed a significant decrease in the intensity of ROS fluorescence compared with that of group B (P<0.05). Neuroelectrophysiological tests showed that the highest potential of CMAP in SMC group was significantly higher than that in PNI and Sham groups (P<0.05). ELISA assay showed that the levels of IL-6, IL-17, and MDA in PNI group were significantly higher than those in Sham group, and the levels of IL-10, SOD, and CAT were significantly lower; the levels of IL-6, IL-17, and MDA in SMC group were significantly lower than those in PNI group, and the levels of IL-10, SOD, and CAT were significantly higher (P<0.05). LFB staining and transmission electron microscopy showed that the myelin density and the diameter of axons in the SMC group were significantly higher than those of the PNI group and the Sham group (P<0.05). Immunofluorescence staining showed that the fluorescence intensity of GFAP and MBP in the SMC group were significantly stronger than those in the PNI group and Sham group (P<0.05). Western blot showed that the relative expressions of Nrf2 and HO-1 proteins in the SMC group were significantly higher than those in the PNI group and Sham group, and the ratio of p-p38MAPK/p38MAPK proteins was significantly higher in the PNI group than that in the SMC group and Sham group (P<0.05). Conclusion SMC may inhibit oxidative stress and inflammation after nerve injury by up-regulating the Nrf2/HO-1 pathway, and then inhibit the phosphorylation of p38MAPK pathway to promote the proliferation of Schwann cells, which ultimately promotes the formation of myelin sheaths and accelerates the regeneration of peripheral nerves.
ObjectiveTo investigate the feasibility and safety of non-intubation anesthesia in thoracic surgery.MethodsFrom September 2017 to December 2019, 296 patients were operated at department of thoracic surgery in our hospital. There were 167 males and 129 females with an average age of 50.69±12.95 years, ranging from 16 to 76 years. The patients were divided into two groups according to whether they were intubated: 150 patients were in a non-intubation group, including 83 males and 67 females with an average age of 49.91±13.59 years, ranging from 16 to 76 years, and 146 patients were in an intubation group including 84 males and 62 females with an average age of 51.49±12.26 years, ranging from 16 to 74 years. Intraoperative data, postoperative recovery, inflammatory response of the two groups were compared.ResultsThere was no statistical difference between the two groups in operation time, blood loss, the lowest oxygen saturation or other indicators (P>0.05). But the highest partial pressure of carbon dioxide of the non-intubation group was higher than that of the intubation group (P=0.012). The non-intubation group was superior to the intubation group in postoperative recovery and inflammatory response (P<0.05).ConclusionThe non-intubation anesthesia is safe and maneuverable in thoracic surgery, and it has some advantages in accelerating postoperative rehabilitation.
The synthesis and secretion of inflammatory cytokines in the monocytes of 68 cases of multiple system organ failure (MSOF) patients was investigated by the method of MTT stained in cytokines dependent defferential cell strain. The data showed that the serum levels of tumor necrosis factor, interleukine 1 and interleukine 6 were increased (Ｐ＜0.01) in the monocytes of MSOF patients. The synthesis and secretion of these inflammatory cytokines gradually increased in the monocytes after onset of MSOF. After 5 days of treatment with antibiotics and electrolytes intravenous infusion, the secretion of TNF, IL-1 and IL-6 were decreased respectively. These results suggested that the TNF, IL-1 and IL-6 are integrated into system inflammatory responese and caused the injury to the tissues and organs. The production levels of these cytokines can be regarded as the index of MSOF and its severity.
ObjectiveTo investigate the influence of endoplasmic reticulum stress (ERS) on smoking-induced nucleus pulposus cells apoptosis and inflammatory response.MethodsBetween October 2016 and October 2018, 25 patients with cervical disc herniation receiving discectomy were collected and divided into smoking group (14 cases) and non-smoking group (11 cases). The baseline data of age, gender, herniated segment, and Pfirrmann grading showed no significant difference between the two groups (P>0.05). The obtained nucelus pulposus tissues were harvested to observe the cell apoptosis via detecting the apoptosis-related proteins (Caspase-3 and PRAP) by TUNEL staining and Western blot test. The nucleus pulposus cells were isolated and cultured with enzyme digestion, of which the third generation cells were used in follow-up experiments. Then, the expressions of inflammatory factors [interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α)] were detected by ELISA; the nuclear translocation of P65 was monitored by cell immunofluorescence staining. Furthermore, ERS-related proteins (GRP78 and CHOP) were detected by Western blot; and endoplasmic reticulum ultrastructure was observed under transmission electron microscope. To verify the regulatory effect of ERS, cells were pretreated by ERS specific inhibitor (4-PBA), then cell apoptosis and inflammatory response were tested.ResultsThe nucleus pulposus tissue observation showed that the cell apoptotic rate and the expressions of apoptosis-related proteins (Caspase-3 and PARP) were obviously higher in smoking group than in non-smoking group (P<0.05). The nucleus pulposus cells observation indicated that the expressions of the inflammatory factors (IL-1β and TNF-α) and the ERS-related proteins (GRP78 and CHOP) were also higher in smoking group than in non-smoking group (P<0.05). The results of cell immunofluorescence staining further confirmed that smoking stimulated nuclear translocation of P65 in nucleus pulposus cells. The ERS injury was much more serious in smoking group than in non-smoking group. Furthermore, after 4-PBA inhibiting ERS, the expressions of GRP78, CHOP, IL-1β, TNF-α, and P65 were significantly decreased (P<0.05), and flow cytometry results showed that cell apoptotic rate in smoking group was decreased, showing significant difference compared with the non-smoking group (P<0.05).ConclusionSomking can stimulate cell apoptosis and inflammatory response in nucleus pulposus cells via ESR pathway. Suppressing ESR may be a novel target to suspend smoking-induced intervertebral disc degeneration.
ObjectiveTo investigate the changes of diamine oxidase(DAO) and endotoxin(ET) during the treatment of systemic inflammatory response syndrome with human growth hormone and the relationship between human growth hormone and intestinal mucosal barrier injury. MethodsOne hundred and fortysix patients with systemic inflammatory response syndrome were randomly divided into operative group and nonoperative group, which were again randomly divided into the study group and control group.Plasma concentration of DAO and ET were determined before the treatment and 1 week after the treatment.ResultsPlasma concentration of DAO and ET in study group decreased after treatment with significant difference (P＜0.05，P＜0.01).ConclusionHuman growth hormone can protect intestinal mucosa barrier.
【Abstract】ObjectiveThere are two main functions of gastrointestinal tract, digestion and absorption, and barrier function. The latter has an important defensive effect, which keeps the body away from the invading and damaging of bacteria and endotoxin. It maintains the systemic homeostasis. Intestinal dysfunction would happen when body suffers from diseases or harmful stimulations. The more serious intestinal disorders would harm the intestinal protective mechanism, or intestinal barrier function, and bacterial/endotoxin translocation, of intestinal failure (IF) would ensue. This article provides a critical review of the evidence indicating that an increase in bacterial translocation is associated with sepsis, and even the multiple organ failure syndrome in critically ill patients. The intransit microorganisms play an essential role in the homeostasis of local and systemic immunity. MethodsAll studies published from 2000 to June 2005 about intestinal permeability, bacterial translocation, and systemic inflammatory response syndrome were located by search of PubMed. ResultsClinical and experimental studies investigating the correlation between bacterial translocation and systemic inflammatory response syndrome, associated with the damage of the gut barrier function . To keep the mucosal barrier function intact is one of the main issues in the prevention of bacterial translocation. This could be achieved by the adequate delivery of oxygen and nutrient supplementation to the gut. Enteral nutrition, probiotic can be a good choice. ConclusionWith a better understanding of the bacteriahost interactions in health and the alterations induced by critical illness, new therapies that improve the environment of both may lead to better recovery rates in intensive care unit patients.