Effects of Wuwei Xiaodu Decoction on Uterine Energy Metabolism and Serum Inflammatory Factors in Rats with Acute Pelvic Inflammatory Disease

[Objectives]To observe the effects of Wuwei Xiaodu Decoction on uterine energy metabolism and serum inflammatory factors in the acute pelvic inflammatory disease(APID)model.[Methods]75 Wistar rats(females)were randomly divided into control group,model group and Wuwei Xiaodu Decoction low,medium and high dose groups(n=15).Except for the control group,the rat APID model was established by right uterine inoculation.On the fifth day after inoculation,the low,medium and high dose groups of Wuwei Xiaodu Decoction were administered at 4,8 and 16 g/kg,and the control group and model group received normal saline.Rats were killed 12 h after nondose administration,blood was collected from the abdominal aorta and measured by ELISA for serum interleukin-6(interleukin-6,IL-6),IL-8,and C-reactive proteins(CRP);the right uterus of rats was tested for high-energy phosphate adenosine phosphate(AMP),adenosine diphosphate(ADP),adenosine triphosphate(ATP)and total adenine nucleotides(TAN)level to evaluate the uterine energy metabolism.[Results]AMP,ADP,ATP and TAN were significantly higher in the Wuwei Xiaodu Decoction of low,medium and high dose than the model group,while the serum IL-6,IL-8 and CRP were significantly lower than the model group,and the difference between the low,medium and high doses(P<0.05).[Conclusions]The Wuwei Xiaodu Decoction can dose-dependent promote uterine energy metabolism and inhibit inflammatory response in APID model rats.

The effect of Huanglian Jiedu Decoction on inflammatory factors and oxidative stress in patients with acute ischemic stroke

Objective:To study the clinical efficacy of Huanglian Jiedu decoction in treating acute ischemic stroke(AIS)and its effects on inflammatory factors and oxidative stress.Method:A total of 53 patients with AIS were recruited as the study subjects and randomly divided into a control group and a treatment group using a random number table method.The control group consisted of 26 patients and the treatment group consisted of 27 patients.The control group received conventional Western medicine treatment.The control group received routine Western medicine treatment,while the treatment group received Huanglian Jiedu decoction based on the control group,with 14 days as a course of treatment.The effects of Huanglian Jiedu decoction on neurological function and activities of daily living were evaluated using the National Institute of Health stroke scale(NIHSS)and activities of daily living(ADL)scores.The effects of Huanglian Jiedu decoction on inflammatory reactions and oxidative stress were evaluated by detecting interleukin-4(IL-4),interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),transforming growth factorβ(TGF-β),total antioxidative capacity(T-AOC),malondialdehyde(MDA),superoxide dismutase(SOD),and catalase(CAT)levels.Results:After treatment with Huanglian Jiedu Decoction,the ALD scores of AIS patients in both groups increased,while the NISHH scores decreased,suggesting that Huanglian Jiedu Decoction has therapeutic effects on AIS patients.It also reduces the levels of serum IL-6,TNF-α,MDA in AIS patients and increases the levels of IL-4,TGF-β,CAT,SOD,T-AOC,suggesting that Huanglian Jiedu decoction can improve the anti-inflammatory and antioxidant abilities of AIS patients.Conclusion:Huanglian Jiedu decoction can help AIS patients recover their neurological function,increase their capacity for self-care in daily life,and strengthen the body’s anti-inflammatory and antioxidant defenses.

Inflammatory mediators and microcirculatory disturbance in acute pancreatitis

BACKGROUND: Inflammatory mediators are not only initiation factors of acute pancreatitis (AP) but also key factors causing pancreatic hemorrhage and necrosis, which damage important organs such as the heart, brain, liver, kidney and lung. Microcirculatory disturbance in AP has attracted widespread attention. In order to provide a theoretical basis for clinical therapy of AP, it is very important to explore the effect of inflammatory mediators on microcirculatory disturbance in this disease. DATA SOURCES: In this review, the impact of inflammatory mediators on microcirculatory disturbance in AP was reviewed according to the literature, especially the articles indexed in PubMed and books published in China and reports from websites. RESULTS: At present, inflammatory mediation and microcirculatory disturbance are the two major hypotheses to explain the development of AP. Although experimental studies have shown that inflammatory mediators induce or aggravate microcirculatory disturbance, the clinical application of these findings is still difficult because the inflammatory mediators are diverse and their research is not comprehensive and thorough. CONCLUSION: It is very important to explore the influence of inflammatory mediators on microcirculatory disturbance in AP.

Systemic inflammatory response following acute myocardial infarction

Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Iuflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction （AMI）, Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes （such as death, recurrent myocardial in- farction, and heart failure） in patients with AMI.

Effect of resveratrol on activation of nuclear factor kappa-B and inflammatory factors in rat model of acute pancreatitis

AIM: To observe the effect of resveratrol on nuclear factor Kappa-B (NF-κB) activation and the inflammatory response in sodium taurocholate-induced pancreatitis in rats. METHODS: Seventy-two male SD rats were randomly divided into three groups: sham operation group (control), severe acute pancreatitis (SAP) group, and severe acute pancreatitis group treated with resveratrol (RES). A SAP model was established by injecting 4% sodium taurocholate 1 mL/kg through puncturing the pancreatic duct. In Res group, Res was given at 30 mg/kg b.m. intraperitoneally after the SAP model was successfully established. Eight animals from each group were sacrificed at 3, 6 and 12 h after modeling. The expression of NF-κB activation of pancreas was detected by irnmunohistochemical staining, whereas the levels of TNF-α and IL-8 in pancreatic tissues were estimated by radioimrnunoassay. The pathological changes of pancreas and lungs were examined microscopically. RESULTS: Much less hyperemia, edema, dust-colored necrotic focus and soaps were noticed in pancreas in RES group than in SAP group. In RES group, hemorrhage, exudates and infiltration of inflammatory cells in pancreas and interstitial edema, destruction of alveolar wall in lung were significantly less than in SAP group. In the SAP group, the activation of NF-κB in pancreatic tissues was enhanced significantly at any measure point compared with control group (64.23±10.72% vs 2.56±0.65%, 55.86±11.34% vs 2.32±0.42%, 36.23±2.30% vs 2.40±0.36%,P<0.01), TNF-α, IL-8 were also increased and reached their peak at 6 h and then declined. The activation of NF-κB and the levels of TNF-α and IL-8 in RES group were significantly lower than those in SAP group (P<0.01): activation (52.63±9.45% vs 64.23±10.72%, 40.52±8.40% vs 55.86±11.34%, 29.83±5.37% vs 36.23±2.30%), TNF-α (132.76±15.68 pg/mL vs 158.36±12.58 pg/mL, 220.32±23.57 pg/mL vs 247.67± 11.62 pg/mL, 175.68±18.43 pg/mL vs 197.35±12.57 pg/mL) and IL-8 (0.62±0.21 μg/L vs 0.83±0.10 μg/L, 1.10±0.124 μg/L vs1.32±0.18 μg/L, 0.98±0.16 μg/L vs 1.27±0.23μg/L). CONCLUSION: The activation of NF-KB is involved in the inflammatory response of rats with SAP. Resveratrol could effectively inhibit the expression of NF-κB activation, alleviate the severity of SAP through its anti-inflammatory effects and regulate the inflammatory mediators.

Effects of large dose of dexamethasone on inflammatory mediators and pancreatic cell apoptosis of rats with severe acute pancreatitis

AIM: To investigate the influence of high dose of dexamethasone on inflammatory mediators and apoptosis of rats with severe acute pancreatitis (SAP). METHODS: SAP rats were randomly assigned to the model group and treatment group while the normal rats were assigned to the sham operation group. The mortality,ascite volumes,ascites/body weight ratio and pancreas pathological changes of all rats were observed at 3,6 and 12 h after operation. Their contents of amylase and endotoxin in plasma and contents of tumor necrosis factor (TNF-α),phospholipase A2 (PLA2) and IL-6 in serum were also determined. The microarray sections of their pancreatic tissues were prepared,terminal transferase dUTP nick end labeling (TUNEL) staining was performed and apoptotic indexes were calculated. RESULTS: There was no marked difference between treatment group and model group in survival. The contents of amylase and endotoxin in plasma and contents of TNF-α,PLA2 and IL-6 in serum,ascite volumes,ascites/body weight ratio and pancreas pathological scores were all lower in treatment group than in model group to different extents at different time points P < 0.05,58.3 (26.4) ng/L vs 77.535 (42.157) ng/L in TNF-α content,8.00 (2.00) points vs 9.00 (2.00) points in pathological score of pancreas respectively; P < 0.01,0.042 (0.018) EU/mL vs 0.056 (0.0195) EU/mL in endotoxin content,7791 (1863) U/L vs 9195 (1298) U/L in plasma amylase content,1.53 (0.79) vs 2.38 (1.10) in ascites/body weight ratio,8.00 (1.00) points vs 11.00 (1.50) points in pathological score of pancreas; P < 0.001,3.36 (1.56) ng/L vs 5.65 (1.08) ng/L in IL-6 content,4.50 (2.00) vs 7.20 (2.00),4.20 (1.60) vs 6.40 (2.30),3.40 (2.70) vs 7.90 (1.70) in ascite volumes,respectively. The apoptotic indexes of pancreas head and pancreas tail were all higher in treatment group than in model group at 6 h P < 0.01,0.00 (2.00)% vs 0.00 (0.00)%,0.20 (1.80) vs 0.00 (0.00) in apoptosis indexes,respectively. CONCLUSION: The mechanism of dexamethasone treatment in acute pancreatitis is related to its inhibition of inflammatory mediator generation and induction of pancreatic acinar cell apoptosis.

Inflammatory role of the acinar cells during acute pancreatitis

Pancreatic acinar cells are secretory cells whose main function is to synthesize, store and f inally release digestive enzymes into the duodenum. However, in response to noxious stimuli, acinar cells behave like real inflammatory cells because of their ability to activate signalling transduction pathways involved in the expression of inflammatory mediators. Mediated by the kinase cascade, activation of Nuclear factor-κB, Activating factor-1 and Signal transducers and activators of transcription transcription factors has been demonstrated in acinar cells, resulting in overexpression of inflammatory genes. In turn, kinase activity is down-regulated by protein phosphatases and the f inal balance between kinase and phosphatase activity will determine the capability of the acinar cells to produce inflammatory factors. The kinase/ phosphatase pair is a redox-sensitive system in which kinase activation overwhelms phosphatase activity under oxidant conditions. Thus, the oxidative stress developed within acinar cells at early stages of acute pancreatitis triggers the activation of signalling pathways involved in the up-regulation of cytokines, chemokines and adhesion molecules. In this way, acinar cells trigger the release of the f irst inflammatory signals which can mediate the activation and recruitment of circulating inflammatorycells into the injured pancreas. Accordingly, the role of acinar cells as promoters of the inflammatory response in acute pancreatitis may be considered. This concept leads to amplifying the focus from leukocyte to acinar cells themselves, to explain the local inflammation in early pancreatitis.

Monocytes in systematic inflammatory response syndrome:Differences between sepsis and acute pancreatitis

AIM: To unravel the differences between systematic in- flammatory response syndrome (SIRS) of acute pancre- atitis compared to the same syndrome in sepsis. METHODS: Twenty-five patients were enrolled, 12 with sepsis and 13 acute pancreatitis. After diagnosis 20 ml blood was sampled. Half were assayed for isolation of monocytes and 10 ml was centrifuged for serum test of tumor necrosis factor alpha (TNFα) and interleukin-6 (IL-6). Half of monocytes were incubated in the presence of patients’ serum and supernatants were collected. The other half was treated for estimation of optical photom- etry under caspase-3 inhibition. TNFα and IL-6 were es- timated by an enzyme immunoassay. RESULTS: median ± SE of serum IL-6 in septic patients and acute pancreatitis patients was 192.30 ± 35.40 ng/L and 21.00 ± 16.05 ng/L, respectively (P < 0.01). Re- spective values of caspase-3 were 0.94 ± 0.17 pmol/min 104 cells and 0.34 ± 0.09 pmol/min 104 cells (P < 0.05). IL-6 of monocyte supernatants of patients with sepsis was significantly increased after addition of patients’ serum, while that of patients with acute pancreatitis did not show significant difference. CONCLUSION: The data have shown that monocyte activity is different between acute pancreatitis and sepsis. This phenomenon might be explained as a different pathway to the pro-inflammatory cytokines release or could be a novel anti-inflammatory response in acute pancreatitis.

Effect of Sheng-jiang powder on multiple-organ inflammatory injury in acute pancreatitis in rats fed a high-fat diet

BACKGROUND Obesity worsens inflammatory organ injury in acute pancreatitis(AP), but there is no effective preventive strategy. Sheng-jiang powder(SJP) has been shown to alleviate multiple-organ inflammatory injury in rats with high-fat diet-induced obesity. Hence, SJP is supposed to have an effect on multiple-organ inflammatory injury in AP in rats fed a high-fat diet.AIM To explore how obesity may contribute to aggravating inflammatory organ injury in AP in rats and observe the effect of SJP on multiple-organ inflammatory injury in AP in rats fed a high-fat diet.METHODS Rats were randomly assigned to a control group(CG), an obese group(OG), and an SJP treatment group(SG), with eight rats per group. The rats in the OG and SG were fed a high-fat diet. From the third week, the rats in the SG were given oral doses of SJP(5 g/kg of body weight). After 12 wk, AP was induced in the three groups. Serum amylase level, body weight, Lee's index, serum biochemistry parameters, and serum inflammatory cytokine and tissue cytokine levels were assessed, and the tissue histopathological scores were evaluated and compared.RESULTS Compared with the CG, serum triglyceride, total cholesterol, interleukin-6, and interleukin-10 levels were significantly higher in the OG, and serum high-density lipoprotein cholesterol level was significantly lower in the OG. Moreover,enhanced oxidative damage was observed in the pancreas, heart, spleen, lung,intestine, liver, and kidney. Evidence of an imbalanced antioxidant defense system, especially in the pancreas, spleen, and intestine, was observed in the obese AP rats. Compared with the OG, serum high-density lipoprotein cholesterol, interleukin-10, and superoxide dismutase expression levels in the pancreas, spleen, and intestine were increased in the SG. Additionally, SJP intervention led to a decrease in the following parameters: body weight; Lee's index; serum triglyceride levels; serum total cholesterol levels; malondialdehyde expression levels in the pancreas, heart, spleen, lung, and liver; myeloperoxidase expression levels in the lung; and pathological scores in the liver.CONCLUSION Obesity may aggravate the inflammatory reaction and pathological multipleorgan injury in AP rats, and SJP may alleviate multiple-organ inflammatory injury in AP in rats fed a high-fat diet.

Diagnosis and treatment of acute pulmonary inflammation in critically ill patients: The role of inflammatory biomarkers

Pneumonia and acute respiratory distress syndrome are common and important causes of respiratory failure in the intensive care unit with a significant impact on morbidity, mortality and health care utilization despite early antimicrobial therapy and lung protective mechanical ventilation. Both clinical entities are characterized by acute pulmonary inflammation in response to direct or indirect lung injury. Adjunct anti-inflammatory treatment with corticosteroids is increasingly used, although the evidence for benefit is limited. The treatment decisions are based on radiographic, clinical and physiological variables without regards to inflammatory state. Current evidence suggests a role of biomarkers for the assessment of severity, and distinguishing sub-phenotypes (hyperinflammatory versus hypo-inflammatory) with important prognostic and therapeutic implications. Although many inflammatory biomarkers have been studied the most common and of interest are C-reactive protein, procalcitonin, and pro-inflammatory cytokines including interleukin 6. While extensively studied as prognostic tools (prognostic enrichment), limited data are available for the role of biomarkers in determining appropriate initiation, timing and dosing of adjunct anti-inflammatory treatment (predictive enrichment)

Low-dose dopamine reduces inflammatory factors of acute pancreatitis in rats

BACKGROUND: Acute pancreatitis, especially acute necrotizing pancreatitis (ANP), is a serious disease with a high morbidity because of multiorgan dysfunction. Recent studies have indicated that during the pathogenesis of ANP, changes of the microcirculation play an important role in the worsening of the disease. This study based on a. model of acute pancreatitis in Wistar rats was to determine the effect of treatment with low-dose dopamine on acute pancreatitis by the dynamic measurement of serum levels of inflammatory factors IL-6 and TNF-alpha. METHODS: Fifty Wistar rats were randomly divided into two groups, and a model of ANP was set up by injecting sodium taurocholate into the pancreatic duct. Rats in the dopamine group (treatment group) were given dopamine by vein and those in the acute pancreatitis group (control group) were given normal saline. To assess the effect of low-dose doparnine (5 mu g . kg(-1) . min(-1)) on induced acute pancreatitis, the antibody sandwich ELISA method was used to measure the serum levels of IL-6 and TNF-alpha at different times before and after the induction of ANP. RESULTS: The serum levels of IL-6 and TNF-alpha in the treatment and control groups before and after ANP induction were significantly different. There was a markedly significant difference in the comparison of the two groups after ANP induction (P<0.01), but no significant difference in the comparison before the induction (P>0.05). Postoperative pancreatic histopathologic changes in the treatment group were more marked than those in the control group. CONCLUSIONS: Low-dose dopamine is effective in treating ANP by alleviating inflammatory reactions. This effect may be related to the fact that low-dose doparnine not only can increase the blood flow of the pancreatic microcirculation but also reduce its permeability.

The role of inflammatory mediators in severe acute pancreatitis and regulation of glucocorticoids

OBJECTIVE: To investigate the effect of glucocorticoids on systemic inflammatory mediator release in rats with acute pancreatitis and the outcome of dexamethasone in treatment of acute pancreatitis. METHODS: Sixty-eight Wistar rats were divided into sham, acute pancreatitis, and treatment (intravenous dexamethasone 0.5 mg/kg) groups. Experimental acute pancreatitis was induced by the injection of 5% sodium taurocholate (0.1 ml/100 mg body weight) into the pancreatic-biliary duct. The bIood samples were obtained and examined for 6-keto-PGI_1α, TXB_2 and IL-6 postoperatively at 3,6 and 12 hours, respectively. The pancreatic samples were evaluated by a blinded method. Twelve-hour survival rate was determined and compared between the groups. RESULTS: The high serum concentrations of 6-keto-PGI_1α, TXB_2 and IL-6 were noted in the rats with acute pancreatitis associated with pancreatic hemorrhage and necrosis. Their 12-hour survival rate was 42.9%. The rats in the treatment group survived with significantly reduced serum concentrations of 6-keto-PGI_1α, TXB_2 and IL-6 (P<0.05). Their pancreatic morphology was normal. CONCLUSION: Dexamethasone may reduce the serum concentration of 6-keto-PGI_1α, TXB_2, and IL-6, and the severity of acute pancreatitis while increasing the survival rate of rats with acute pancreatitis.

Expression and Significance of Toll-like Receptor 2,4 of Peripheral Blood Mononuclear Cells in Acute Abdomen Patients Associated with Systemic Inflammatory Response Syndrome

The changes of Toll-like receptor （TLR） 2, 4 of peripheral blood mononuclear cells （PBMCs） in the acute abdomen patients associated with systemic inflammatory response syndrome （SIRS） and their potential significance were explored. A clinical study was performed on 103 acute abdomen patients in whom 65 were associated with SIRS. Forty healthy individuals served as normal controls. The mRNA expression of TLR2, 4 was detected by RT-PCR, and the expression of TNF-α and IL-6 by ELISA. The level of plasma endotoxin, hospital stay and mortality were measured. It was found that the endotoxin level was increased to varying degrees in all the acute abdomen patients, and the endotoxin level was and hospital stay longer in SIRS group than in non-SIRS group （P〈0.01）. TLR2 mRNA, TLR4 mRNA, IL-6 and TNF-ct could be detected with low value in normal controls, but they were up-regulated markedly on the 1 st day after admission. Then TLR4 mRNA, IL-6 and TNF-α were decreased gradually, but TLR2 mRNA maintained at a high level till the 5th day. These indexes above in SIRS group were higher than those in non-SIRS group （P〈0.01）. The results of correlation analysis revealed the expression of TLR2, 4 mRNA was positively correlated with the levels of TNF-α and IL-6, and the hospital stay, The results of Logistic regression demonstrated that overexpression of TLR2, 4 mRNA might result in higher risk of multiple organ dysfunction syndrome （MODS）. It was concluded that in the acute abdomen patients associated with SIRS, the expression of TLR2, 4 in PBMCs was increased markedly, suggesting that TLR might play an important role in the pathogenesis of acute abdomen associated with SIRS.

Comparative transcriptomic analysis reveals the molecular changes of acute pancreatitis in experimental models

BACKGROUND Acute pancreatitis(AP)encompasses a spectrum of pancreatic inflammatory conditions,ranging from mild inflammation to severe pancreatic necrosis and multisystem organ failure.Given the challenges associated with obtaining human pancreatic samples,research on AP predominantly relies on animal models.In this study,we aimed to elucidate the fundamental molecular mechanisms underlying AP using various AP models.AIM To investigate the shared molecular changes underlying the development of AP across varying severity levels.METHODS AP was induced in animal models through treatment with caerulein alone or in combination with lipopolysaccharide(LPS).Additionally,using Ptf1αto drive the specific expression of the hM3 promoter in pancreatic acinar cells transgenic C57BL/6J-hM3/Ptf1α(cre)mice were administered Clozapine N-oxide to induce AP.Subsequently,we conducted RNA sequencing of pancreatic tissues and validated the expression of significantly different genes using the Gene Expression Omnibus(GEO)database.RESULTS Caerulein-induced AP showed severe inflammation and edema,which were exacerbated when combined with LPS and accompanied by partial pancreatic tissue necrosis.Compared with the control group,RNA sequencing analysis revealed 880 significantly differentially expressed genes in the caerulein model and 885 in the caerulein combined with the LPS model.Kyoto Encyclopedia of Genes and Genomes enrichment analysis and Gene Set Enrichment Analysis indicated substantial enrichment of the TLR and NOD-like receptor signaling pathway,TLR signaling pathway,and NF-κB signaling pathway,alongside elevated levels of apoptosis-related pathways,such as apoptosis,P53 pathway,and phagosome pathway.The significantly elevated genes in the TLR and NOD-like receptor signaling pathways,as well as in the apoptosis pathway,were validated through quantitative real-time PCR experiments in animal models.Validation from the GEO database revealed that only MYD88 concurred in both mouse pancreatic tissue and human AP peripheral blood,while TLR1,TLR7,RIPK3,and OAS2 genes exhibited marked elevation in human AP.The genes TUBA1A and GADD45A played significant roles in apoptosis within human AP.The transgenic mouse model hM3/Ptf1α(cre)successfully validated significant differential genes in the TLR and NOD-like receptor signaling pathways as well as the apoptosis pathway,indicating that these pathways represent shared pathological processes in AP across different models.CONCLUSION The TLR and NOD receptor signaling pathways play crucial roles in the inflammatory progression of AP,notably the MYD88 gene.Apoptosis holds a central position in the necrotic processes of AP,with TUBA1A and GADD45A genes exhibiting prominence in human AP.

Early selective enteral feeding in treatment of acute pancreatitis: A case report

BACKGROUND Early initiation of enteral feeding is recognized to play a crucial role in improving the outcomes of treatment of acute pancreatitis.However,the method of adminis-tration of enteral nutrition remains debatable.We present the experience of treating a patient with moderate-severe acute pancreatitis,at high risk of progressing to a severe or fatal condition,using a novel method of selective feeding with duodenal isolation.CASE SUMMARY A 27-year-old female patient presented to the emergency unit of the hospital with a typical manifestation of acute pancreatitis.Despite a conventional treatment,the patient’s condition deteriorated by day 2 of hospitalization.Using an endoscopic approach,a novel catheter PandiCathffwas placed to the duodenum of the patient,isolating its segment between the duodenal bulb and the ligament of Treitz.In the isolated area created,a negative pressure was applied,followed by introduction of early selective enteral feeding.The patient’s condition subsequently improved in a rapid manner,and no complications often associated with moderate-to-severe acute pancreatitis developed.CONCLUSION Within 48 h of starting treatment with the novel method,it can prevent the development of multiple organ failure and,when combined with minimally invasive drainage methods,help prevent infection.

Exploring the mechanism of electroacupuncture at different acupoints on acute colitis rats based on JAK2/STAT3/SOCS1 signaling pathway

Objective:To investigate the mechanism of JAK2/STAT3/SOCS1 signaling pathway in electroacupuncture of different acupoints on acute colitis rats.Methods:36 SPF SD rats were randomly divided into 6 groups,with 6 rats in each group.The rat model of acute colitis was prepared by enema with glacial acetic acid solution.After the model was established,electroacupuncture was given to each acupoint group,with density wave,frequency 2Hz-50 Hz,intensity 2 mA,muscle tremor as the degree 20 min/time,1 time/day,for 3 consecutive days.Observe the general condition of rats;the pathological changes of colonic mucosa in rats were observed by HE method.The contents of serum interleukin-4(IL-4)and interleukin-8(IL-8)were detected by ELISA.Western blot and RT-PCR were used to detect the expression of JAK2,STAT3,SOCS1 protein and mRNA in rat colon tissue.Results:In contrast to the normal group,the overall condition of the model group was worse,the colonic mucosa was severely damaged,even necrotic,and the ulcer surface was obvious.The content of IL-4 in serum was obviously reduced,and the content of IL-8 was obviously go up(P<0.01).The protein content of JAK2,STAT3 and the expression of JAK2,STAT3 mRNA in colon tissue of rats were obviously go up,while the protein content of SOCS1 and the expression of SOCS1 mRNA were obviously reduced(P<0.01).In contrast to the model group,the general condition of rats in each acupoint group was significantly improved,the damage and necrosis of colonic mucosa and ulcer surface were obviously alleviated,the content of IL-4 in serum was obviously go up,and the content of IL-8 was significantly decreased(P<0.01).The protein content of JAK2,STAT3 and the expression of JAK2,STAT3 mRNA in colon tissue of rats were obviously reduced,while the protein content of SOCS1 and the expression of SOCS1 mRNA were obviously go up(P<0.05,P<0.01).Comparison of different acupoint groups,the colonic mucosal injury in the Zusanli group was significantly reduced,the content of serum IL-4 was significantly increased,and the content of IL-8 was significantly decreased(P<0.05,P<0.01).The protein content and mRNA expression of JAK2 and STAT3 in colon tissue were significantly down-regulated,while the protein content and mRNA expression of SOCS1 were significantly go up(P<0.05,P<0.01).Conclusion:Electroacupuncture at each acupoint can improve the damage of colonic mucosa and reduce the inflammatory response.The therapeutic effect of Zusanli(ST36)is better than that of Tianshu(ST25),Dachangshu(BL25)and Shangjuxu(ST37).The mechanism may be related to the regulation of JAK2/STAT3/SOCS1 signaling pathway related proteins and inflammatory cytokines IL-4 and IL-8.

Research Progress on the Pathogenesis of Acute Lung Injury(ALI)

In this review,the databases searched were PubMed and Web of Science.It is believed that the main causes of acute lung injury(ALI)and acute respiratory distress syndrome(ARDS)are inflammatory response disorders,excessive oxidative stress,cell death,endoplasmic reticulum stress,coagulation dysfunction,and weakened aquaporin function.

Effects of Intravenous Thrombolytic Therapy with Alteplase on Neurological Function,Coagulation Function and Serum Inflammatory Factors in Patients with Acute Cerebral Infarction

Objective:To investigate the effects of intravenous thrombolysis therapy with alteplase on neurological function,coagulation function and serum inflammatory factors in patients with acute cerebral infarction.Methods:A total of 96 patients with acute cerebral infarction admitted to our hospital from September 2017 to October 2019 were randomly divided into two groups,with 48 patients in each group.The control group(n=48)received routine treatment,and the observation group received intravenous thrombolysis therapy with alteplase on the basis of routine treatment.The neurological deficit score,prothrombin time(PT),activated partial thromboplastin time(APTT),tumor necrosis factor-a level(TNF-α),and high-sensitivity C-reactive protein(hs-CRP)were compared between the two groups after 15 days of treatment.Results:After treatment,NIHSS scores in both groups were lower than those before treatment;PT levels were increased,while APTT,TNF-αand hs-CRP levels were all decreased in both groups,and the changes in the observation group were greater than those in the control group,with statistically significant difference(P<0.05).Conclusions:Intravenous thrombolysis therapy with alteplase can improve the neurological function,coagulation function and serum levels of inflammatory factors in patients with acute cerebral infarction,which is worthy of clinical application.

Effect of oral mesalamine on inflammatory response in acute uncomplicated diverticulitis

AIM: To evaluate the impact of mesalamine administration on inflammatory response in acute uncomplicated diverticulitis.METHODS: We conducted a single centre retrospective cohort study on patients admitted to our surgical department between January 2012 and May 2014 with a computed tomography-confirmed diagnosis of acute uncomplicated diverticulitis. A total of 50 patients were included in the analysis, 20(study group) had received 3.2 g/d of mesalamine starting from the day of admission in addition to the usual standard treatment, 30(control group) had received standard therapy alone. Data was retrieved from a prospective database. Our primary study endpoints were: C reactive protein mean levels over time and their variation from baseline(ΔCRP) over the first three days of treatment. Secondary end points included: mean white blood cell and neutrophile count over time, time before regaining of regular bowel movements(passing of stools), time before reintroduction of food intake, intensity of lower abdominal pain over time, analgesic consumption and length of hospital stay.RESULTS: Patients characteristics and inflammatoryparameters were similar at baseline in the two groups. The evaluation of CRP levels over time showed, in treated patients, a distinct trend towards a faster decrease compared to controls. This difference approached statistical significance on day 2(mean CRP 6.0 +/- 4.2 mg/d L and 10.0 +/- 6.7 mg/d L respectively in study group vs controls, P = 0.055). ΔCRP evaluation evidenced a significantly greater increment of this inflammatory marker in the control group on day 1(P = 0.03). A similar trend towards a faster resolution of inflammation was observed evaluating the total white blood cell count. Neutrophile levels were significantly lower in treated patients on day 2 and on day 3(P < 0.05 for both comparisons). Mesalamine administration was also associated with an earlier reintroduction of food intake(median 1.5 d and 3 d, study group vs controls respectively, P < 0.001) and with a shorter hospital stay(median 5 d and 5.5 d, study group vs controls respectively, P = 0.03).CONCLUSION: Despite its limitations, this study suggests that mesalamine may allow for a faster recovery and for a reduction of inflammatory response in acute uncomplicated diverticulitis.

Effect of glutamine nutrition support on the intestinal mucosal barrier function and inflammatory response in patients with severe acute pancreatitis

Objective:To study the effect of glutamine nutrition support on the intestinal mucosal barrier function and inflammatory response in patients with severe acute pancreatitis.Methods:Patients with severe acute pancreatitis who were treated in Pengzhou People's Hospital between May 2014 and November 2016 were selected as the research subjects and randomly divided into two groups, control group received conventional symptomatic treatment and conventional enteral nutrition intervention, and Gln group received conventional symptomatic treatment and glutamine enteral nutrition intervention. The contents of intestinal mucosal barrier damage markers and inflammatory mediators in serum as well as the expression of inflammatory signaling molecules in peripheral blood were detected before and after treatment;the number of intestinal flora was detected after treatment.Results:After treatment, LPS, DAO, HBD2, TNF-α, sTREM-1, IL-1β and IL-6 levels in serum as well as TLR4, NF-kB, MyD88 and p38MAPK mRNA expression in peripheral blood mononuclear cells of both groups of patients were significantly lower than those before treatment, LPS, DAO, HBD2, TNF-α, sTREM-1, IL-1β and IL-6 levels in serum as well as TLR4, NF-kB, MyD88 and p38MAPK mRNA expression in peripheral blood mononuclear cells of Gln group after treatment were significantly lower than those of control group, and the number of lactobacillus, bifidobacterium and bacteroides were significantly higher than those of control group while the number of escherichia coli and enterococcus were significantly lower than those of control group.Conclusion: Glutamine nutrition support for severe acute pancreatitis can reduce the intestinal mucosal barrier function injury and inhibit the inflammatory response activation.