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| 1 | Ulinastatin for acute lung injury and acute respiratory distress syndrome: A systematic review and meta-analysis显示文摘AIM: To investigate the efficacy and safety of ulinastatin for patients with acute lung injury(ALI) and those with acute respiratory distress syndrome(ARDS).METHODS: A systematic review of randomized controlled trials(RCTs) of ulinastatin for ALI/ARDS was conducted. Oxygenation index, mortality rate [intensive care unit(ICU) mortality rate, 28-d mortality rate] and length of ICU stay were compared between ulinastatin group and conventional therapy group. Meta-analysis was performed by using Rev Man 5.1.RESULTS: Twenty-nine RCTs with 1726 participants were totally included, the basic conditions of which were similar. No studies discussed adverse effect. Oxygenation index was reported in twenty-six studies(1552 patients). Ulinastatin had a significant effect in improving oxygenation [standard mean difference(SMD) = 1.85, 95%CI: 1.42-2.29, P < 0.00001, I2 = 92%]. ICUmortality and 28-d mortality were respectively reported in eighteen studies(987 patients) and three studies(196 patients). We found that ulinastatin significantly decreased the ICU mortality [I2 = 0%, RR = 0.48, 95%CI: 0.38-0.59, number needed to treat(NNT) = 5.06, P < 0.00001], while the 28-d mortality was not significantly affected(I2 = 0%, RR = 0.78, 95%CI: 0.51-1.19, NNT = 12.66, P = 0.24). The length of ICU stay(six studies, 364 patients) in the ulinastatin group was significantly lower than that in the control group(SMD =-0.97, 95%CI:-1.20--0.75, P < 0.00001, I2 = 86%). CONCLUSION: Ulinastatin seems to be effective for ALI and ARDS though most trials included were of poor quality and no information on safety was provided. | Yu-Xin Leng Shu-Guang Yang Ya-Han Song Xi Zhu Gai-Qi Yao | 2014 | World Journal of Critical Care Medicine2014，3，1： | 61 |
| 2 | Efficacy of prone position in acute respiratory distress syndrome patients: A pathophysiology-based review显示文摘Acute respiratory distress syndrome(ARDS) is a syndrome with heterogeneous underlying pathological processes. It represents a common clinical problem in intensive care unit patients and it is characterized by high mortality. The mainstay of treatment for ARDS is lung protective ventilation with low tidal volumes and positive end-expiratory pressure sufficient for alveolar recruitment. Prone positioning is a supplementary strategy available in managing patients with ARDS. It was first described 40 years ago and it proves to be in alignment with two major ARDS pathophysiological lung models; the 'sponge lung'- and the 'shape matching'-model. Current evidence strongly supports that prone positioning has beneficial effects on gas exchange, respiratory mechanics, lung protection and hemodynamics as it redistributes transpulmonary pressure, stress and strain throughout the lung and unloads the right ventricle. The factors that individually influence the time course of alveolar recruitment and the improvement in oxygenation during prone positioning have not been well characterized. Although patients' response to prone positioning is quite variable and hard to predict, large randomized trials and recent meta-analyses show that prone position in conjunction with a lung-protective strategy, when performed early and in sufficient duration, may improve survival in patients with ARDS. This pathophysiology-based review and recent clinical evidence strongly support the use of prone positioning in the early management of severe ARDS systematically and not as a rescue maneuver or a last-ditch effort. | Vasilios Koulouras Georgios Papathanakos Athanasios Papathanasiou Georgios Nakos | 2016 | World Journal of Critical Care Medicine2016，5，2： | 39 |
| 3 | Andrographolide sulfonate ameliorates lipopolysaccharide-induced acute lung injury in mice by down-regulating MAPK and NF-κB pathways显示文摘Acute lung injury(ALI) or acute respiratory distress syndrome(ARDS) is a severe, lifethreatening medical condition characterized by widespread inflammation in the lungs, and is a significant source of morbidity and mortality in the patient population. New therapies for the treatment of ALI are desperately needed. In the present study, we examined the effect of andrographolide sulfonate, a water-soluble form of andrographolide(trade name: Xi-Yan-Ping Injection), on lipopolysaccharide(LPS)-induced ALI and inflammation. Andrographolide sulfonate was administered by intraperitoneal injection to mice with LPS-induced ALI. LPS-induced airway inflammatory cell recruitment and lung histological alterations were significantly ameliorated by andrographolide sulfonate. Protein levels of pro-inflammatory cytokines in bronchoalveolar lavage fluid(BALF) and serum were reduced by andrographolide sulfonate administration. m RNA levels of pro-inflammatory cytokines in lung tissue were also suppressed. Moreover, andrographolide sulfonate markedly suppressed the activation of mitogen-activated protein kinase(MAPK) as well as p65 subunit of nuclear factor-κB(NF-κB). In summary, these results suggest that andrographolide sulfonate ameliorated LPS-induced ALI in mice by inhibiting NF-κB and MAPK-mediated inflammatory responses. Our study shows that water-soluble andrographolide sulfonate may represent a new therapeutic approach for treating inflammatory lung disorders. | Shuang Peng Nan Hang Wen Liu Wenjie Guo Chunhong Jiang Xiaoling Yang Qiang Xu Yang Sun | 2016 | Acta Pharmaceutica Sinica B2016，6，3： | 38 |
| 4 | 肺泡上皮细胞功能特性与内毒素性急性肺损伤显示文摘 | 张秋金 李银平 黎檀实 | 2005 | 中国危重病急救医学2005，17，6： | 24 |
| 5 | Activation of SIRT1 ameliorates LPS-induced lung injury in mice via decreasing endothelial tight junction permeability显示文摘The integrity of the endothelial barrier is a determinant of the prognosis of lipopolysaccharide (LPS)-induced acute lung injury (ALI). In this study, we investigated whether and how Sirtuin 1 (SIRT1) maintained the vascular integrity during ALI. An experimental model of ALI was established in mice through intratracheal administration of LPS (10 mg/kg). LPS stimulation significantly increased the pulmonary permeability and decreased the expression of SIRT1 and tight junction proteins (TJs), including occludin, claudin-5, tight junction protein 1 and tight junction protein 2. Morphological studies showed that LPS induced obvious lung injury with inammatory cell infiltration in the interstitial and alveolar space, hemorrhage, edema, and the thickened alveolar wall compared to the control mice. Intratracheal administration of the selective SIRT1 activator SRT1720 (6.25 mg/kg) significantly attenuated LPS- induced lung injury, lung hyper-permeability and increased TJs expression, whereas intratracheal administration of the selective SIRT1 inhibitor EX527 (6.25 mg/kg) aggravated LPS-induced ALI. Similar protective effects of SIRT1 on pulmonary cellular permeability were observed in primary human pulmonary microvascular endothelial cells treated with LPS (2 mg/mL) in vitro. We further demonstrated that the RhoA/ROCK signaling pathway was activated in SIRT1 regulation of tight junction permeability. The RhoA/ROCK inhibitor Y-27632 (10 μM) increased the expression of TJs and reversed LPS- or EX527-induced hyper-permeability. In conclusion, SIRT1 ameliorates LPS-induced lung injury via decreasing endothelial tight junction permeability, possibly via RhoA/ ROCK signaling pathway. This finding may contribute to the development of new therapeutic approaches for lung injury. | Cui-ping Fu Sheng-yu Hao Xiao-bo Xu Jian Zhou Zi-long Liu Huan Lu Li-min Wang Wei-zhong Jin Shan-qun Li | 2019 | Acta Pharmacologica Sinica2019，40，5： | 22 |
| 6 | Effect of intestinal ischemia-reperfusion on expressions of endogenous basic fibroblast growth factor and transforming growth factor β in lung and its relation with lung repair显示文摘AIM To study the changes of endogenoustransforming growth factor β(TGFβ)and basicfibroblast growth factor(bFGF)in lung followingintestinal ischemia and reperfusion injury andtheir effects on lung injury and repair.METHODS Sixty Wistar rats were divided intofive groups,which underwent sham-operation,ischemia(45 minutes),and reperfusion(6,24and 48 hours,respectively)after ischemia(45minutes).Immunohistochemical method wasused to observe the localization and amounts ofboth growth factors.RESULTS Positive signals of both growthfactors could be found in normal lung,mainly inalveolar cells and endothelial cells of vein.Afterischemia and reperfusion insult,expressions ofboth growth factors were increased and theiramounts at 6 hours were larger than those ofnormal control or of 24 and 48 hours after insult.CONCLUSION The endogenous bFGF and TGF βexpression appears to be up-regulated in thelung following intestinal ischemia andreperfusion,suggesting that both growth factorsmay be involved in the process of lung injury andrepair. | Xiao Bing Fu Yin Hui Yang Tong Zhu Sun Xiao Man Gu Li Xian Jiang Xiao Oing Sun Zhi Yong Sheng Research Laboratory,304th Hospital of PLA,Beijing 100037,China | 2000 | World Journal of Gastroenterology2000，6，3： | 21 |
| 7 | Brain-lung crosstalk: Implications for neurocritical care patients显示文摘Major pulmonary disorders may occur after brain injuries as ventilator-associated pneumonia, acute respiratory distress syndrome or neurogenic pulmonary edema. They are key points for the management of brain-injured patients because respiratory failure and mechanical ventilation seem to be a risk factor for increased mortality, poor neurological outcome and longer intensive care unit or hospital length of stay. Brain and lung strongly interact via complex pathways from the brain to the lung but also from the lung to the brain. Several hypotheses have been proposed with a particular interest for the recently described 'double hit' model. Ventilator setting in brain-injured patients with lung injuries has been poorly studied and intensivists are often fearful to use some parts of protective ventilation in patients with brain injury. This review aims to describe the epidemiology and pathophysiology of lung injuries in brain-injured patients, but also the impact of different modalities of mechanical ventilation on the brain in the context of acute brain injury. | Ségolène Mrozek Jean-Michel Constantin Thomas Geeraerts | 2015 | World Journal of Critical Care Medicine2015，4，3： | 20 |
| 8 | Pathogenesis of acute lung injury in rats with severe acute pancreatitis显示文摘BACKGROUND: Acute lung injury (ALI) is the most common and severe complication of severe acute pancreatitis (SAP). The elucidation of the mechanism of ALI contributes to the diagnosis and treatment of the illness. In this study, we studied the pathogenesis of ALI in rats with severe acute pancreatitis. METHODS: The rats were sacrificed at 1, 3, 5, 6, 9 and 12 hours after the establishment of the model of SAP. Pancreas and lung tissues were obtained for pathological study, and examination of microvascular permeability and myeloperoxidase (MPO) examination. The gene expressions of tumor necrosis factor-α (TNF-α) and intercellular adhesion molecule-1 (ICAM-1) in the pancreas and lung tissues were detected by reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS: After the establishment of the SAP model, the degree of pancreatic and lung injury increased gradually along with the gradual increase of MPO activity and micro-vascular permeability. Gene expressions of TNF-α and ICAM-1 in the pancreas rose at 1 hour and peaked at 7 hours. In contrast, their gene expression in the lungs rose slightly at 1 hour and peaked at 9-12 hours. CONCLUSION: An obvious time window existed between SAP and lung injury, which is beneficial to the early prevention of the development of ALI. | Xue-Min Liu, Jun Xu and Zi-Fa Wang Department of Hepatobiliary Surgery, First Hospital, Xi’an Jiaotong University, Xi’an 710061 , China | 2005 | Hepatobiliary & Pancreatic Diseases International2005，4，4： | 18 |
| 9 | Strategies to reduce pulmonary complications after esophagectomy显示文摘Esophagectomy,the surgical removal of all or part of the esophagus,is a surgical procedure that is associated with high morbidity and mortality.Pulmonary complications are an especially important postoperative problem.Therefore,many perioperative strategies to prevent pulmonary complications after esophagectomy have been investigated and introduced in daily clinical practice.Here,we review these strategies,including improvement of patient performance and technical advances such as minimally invasive surgery that have been implemented in recent years.Furthermore,interventions such as methylprednisolone,neutrophil elastase inhibitor and epidural analgesia,which have been shown to reduce pulmonary complications,are discussed.Benefits of the commonly applied routine nasogastric decompression,delay of oral intake and prophylactic mechanical ventilation are unclear,and many of these strategies are also evaluated here.Finally,we will discuss recent insights and new developments aimed to improve pulmonary outcomes after esophagectomy. | Teus J Weijs Jelle P Ruurda Grard AP Nieuwenhuijzen Richard van Hillegersberg Misha DP Luyer | 2013 | World Journal of Gastroenterology2013，19，39： | 17 |
| 10 | N-acetylcysteine inhibits activation of toll-like receptor 2 and 4 gene expression in the liver and lung after partial hepatic ischemia-reperfusion injury in mice显示文摘BACKGROUND:Toll-like receptor 2 and 4(TLR2/4)may play important roles in ischemia-reperfusion(I/R)injury, and N-acetylcysteine(NAC)can prevent the generation of reactive oxygen species(ROS)induced by I/R injury.This study aimed to investigate the changes in TLR2/4 gene expression in the liver and lung after I/R injury with or without NAC pretreatment. METHODS:BALB/c mice were used in a model of partial hepatic I/R injury and randomly assigned to a sham-operated control group(SH),a hepatic ischemia/ reperfusion group(I/R)or a NAC pretreated,hepatic I/R group(I/R-NAC).The levels of TNF-αin the portal vein and plasma alanine aminotransferase(ALT)were measured at 1 and 3 hours after reperfusion.The lung wet-to-dry ratio was measured,and the expression of TLR2/4 mRNA and protein in the liver and lung were assessed with RT-PCR and Western blotting at the same time points. RESULTS:Compared with the I/R group,the expression of TLR2/4 mRNA and protein in the liver and lung in the I/R-NAC group was decreased at the same time point (P<0.05).The levels of portal vein TNF-αand plasma ALT increased continuously in the I/R group at 1 and 3 hours of reperfusion compared with the SH group;however,they declined significantly in the group pretreated with NAC (P<0.05).The extent of lung edema was relieved in the I/ R-NAC group compared with the I/R group(P<0.05).CONCLUSIONS:TLR2/4 was activated in the liver and lung in the process of partial hepatic I/R injury.NAC inhibited the activation of TLR2/4 and the induction of TNF-α resulting from I/R injury via modulating the redox state, thus it may mitigate liver and lung injury following partial hepatic I/R in mice. | Jin, Xin Wang, Lin Wu, He-Shui Zhang, Lei Wang, Chun-You Tian, Yuan Zhang, Jing-Hui | 2007 | Hepatobiliary & Pancreatic Diseases International2007，6，3： | 15 |
| 11 | Sangxingtang inhibits the inflammation of LPS-induced acute lung injury in mice by down-regulating the MAPK/NF-κB pathway显示文摘In the present study, we investigated anti-inflammatory effects of Sangxingtang(SXT) on acute lung injury using a lipopolysaccharide(LPS)-induced acute lung injury(ALI) mouse model. The cell counting in the bronchoalveolar lavage fluid(BALF) was performed. The degree of lung edema was evaluated by measuring the wet/dry weight(W/D) ratio. The superoxidase dismutase(SOD) and myeloperoxidase(MPO) activities were assayed by SOD and MPO kits, respectively. The levels of inflammatory mediators, including tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6), were assayed by the enzyme-linked immunosorbent assay methods. Pathological changes of lung tissues were observed by Hematoxylin and eosin(HE) staining. The inflammatory signaling pathway-related proteins nuclear factor mitogen activated protein kinases(P38MAPK), extracellular regulated protein kinases(Erk), c-Jun N-terminal kinase(Jnk) and nuclear transcription factor(NF-κB) p65 expressions were measured by Western blotting. Our results showed that the treatment with the SXT markedly attenuated the inflammatory cell numbers in the BALF, decreased the levels of P-P38 MAPK, P-Erk, P-Jnk and P-NF-κB p65 and the total protein levels in lungs, improved the SOD activity and inhibited the MPO activity. Histological studies demonstrated that SXT substantially reduced the LPS-induced neutrophils in lung tissues, compared with the untreated LPS group. In conclusion, our results indicated that SXT had protective effects on LPS-induced ALI in mice. | ZHANG Tian-Zhu YANG Shi-Hai YAO Jin-Fu DU Juan YAN Tian-hua | 2015 | Chinese Journal of Natural Medicines2015，13，12： | 14 |
| 12 | A pulmonary source of infection in patients with sepsis-associated acute kidney injury leads to a worse outcome and poor recovery of kidney function显示文摘BACKGROUND:Hospital mortality rates are higher among patients with sepsis-associated acute kidney injury(SA-AKI)than among patients with sepsis.However,the pathogenesis underlying SA-AKI remains unclear.We hypothesized that the source of infection affects development of SA-AKI.We aim to explore the relationship between the anatomical source of infection and outcome in patients with SA-AKI.METHODS:Between January 2013 and January 2018,113 patients with SA-AKI admitted to our Emergency Center were identifi ed and divided into two groups:those with pulmonary infections and those with other sources of infection.For each patient,we collected data from admission until either discharge or death.We also recorded the clinical outcome after 90 days for the discharged patients.RESULTS:The most common source of infection was the lung(52/113 cases,46%),followed by gastrointestinal(GI)(25/113 cases,22.1%)and urinary(22/113,19.5%)sources.Our analysis showed that patients with SA-AKI had a significantly worse outcome(30/52 cases,P<0.001)and poorer kidney recovery(P=0.015)with pulmonary sources of infection than those infected by another source.Data also showed that patients not infected by a pulmonary source more likely experienced shock(28/61 cases,P=0.037).CONCLUSION:This study demonstrated that the source of infection infl uenced the outcome of SA-AKI patients in an independent manner.Lung injury may influence renal function in an asyet undetermined manner as the recovery of kidney function was poorer in SA-AKI patients with a pulmonary source of infection. | Yi-wen Fan Shao-wei Jiang Jia-meng Chen Hui-qi Wang Dan Liu Shu-ming Pan Cheng-jin Gao | 2020 | World Journal of Emergency Medicine2020，11，1： | 14 |
| 13 | Interleukin-22 ameliorates acute severe pancreatitisassociated lung injury in mice显示文摘AIM: To investigate the potential protective effect of exogenous recombinant interleukin-22(r IL-22) on L-arginine-induced acute severe pancreatitis(SAP)-associated lung injury and the possible signaling pathway involved.METHODS: Balb/c mice were injected intraperitoneally with L-arginine to induce SAP. Recombinant mouse IL-22 was then administered subcutaneously to mice. Serum amylase levels and myeloperoxidase(MPO) activity in the lung tissue were measured after the L-arginine administration. Histopathology of the pancreas and lung was evaluated by hematoxylin and eosin(HE) staining. Expression of B cell lymphoma/leukemia-2(Bcl-2), Bcl-x L and IL-22RA1 m RNAs in the lung tissue was detected by real-time PCR. Expression and phosphorylation of STAT3 were analyzed by Western blot. RESULTS: Serum amylase levels and MPO activity in the lung tissue in the SAP group were significantly higher than those in the normal control group(P < 0.05). In addition, the animals in the SAP group showed significant pancreatic and lung injuries. The expression of Bcl-2 and Bcl-x L m RNAs in the SAP group was decreased markedly, while the IL-22RA1 m RNA expression was increased significantly relative to the normal control group(P < 0.05). Pretreatment with PBS did not significantly affect the serum amylase levels, MPO activity or expression of Bcl-2, Bcl-x L or IL-22RA1 m RNA(P > 0.05). Moreover, no significant differences in the degrees of pancreatic and lung injuries were observed between the PBS and SAP groups. However, the serum amylase levels and lung tissue MPO activity in the r IL-22 group were significantly lower than those in the SAP group(P < 0.05), and the injuries in the pancreas and lung were also improved. Compared with the PBS group, r IL-22 stimulated the expression of Bcl-2, Bcl-x L and IL-22RA1 m RNAs in the lung(P < 0.05). In addition, the ratio of p-STAT3 to STAT3 protein in the r IL-22 group was significantly higher than that in the PBS group(P < 0.05).CONCLUSION: Exogenous recombinant IL-22 protects mice against L-arginine-induced SAP-associated lung injury by enhancing the expression of anti-apoptosis genes through the STAT3 signaling pathway. | Ying-Ying Qiao Xiao-Qin Liu Chang-Qin Xu Zheng Zhang Hong-Wei Xu | 2016 | World Journal of Gastroenterology2016，22，21： | 13 |
| 14 | Cyclooxygenase-2 plays a central role in the genesis of pancreatitis and associated lung injury显示文摘BACKGROUND: The exact mechanism by which cyclooxy- genase-2 (COX-2) promotes inflammation in pancreatitis in obscure. This study was undertaken to investigate the role of COX-2 inhibition in an animal model of pancreati- tis , a disease process characterized by a systemic inflamma- tory response and ensuing neutrophil-mediated lung injury. METHODS: Pancreatitis was induced in 24 Sprague-Daw- ley rats by intraperitoneal injection of 20% L-arginine (500 mg/100 g body weight). The animals were randomized into 3 groups (8 rats in each group); controls and rats with pancreatitis intravenously resuscitated with either normal saline (0.9% NaCl 3 ml/kg) at 24 and 48 hours or COX-2 inhibitor (parecoxib 1 mg/kg). Pancreatic and lung inju- ries were assessed histologically. Lung injury was assessed utilizing wet;dry ratio and myeloperoxidase activity to in- dicate pulmonary neutrophil infiltration. A Western blot was used to determine COX-2 protein expression in pancrea- tic tissue. RESULTS: The animals treated with COX-2 inhibitors dis- played significantly less pancreatic and lung injuries than their normal saline counterparts. Histological pancreatic and lung injury scores were significantly reduced (P <0.05) in the COX-2 treated group. Lung wet: dry ratios were sig- nificantly improved and pulmonary neutrophil infiltration was attenuated in the COX-2 group (P<0.05). Western blot analysis confirmed attenuated COX-2 protein expression. CONCLUSION: This study shows, for the first time in a rat model, that adjuvant COX-2 inhibition significandy attenu- ates the severity of both pancreatitis and its associated sys- temic inflammatory response and end-organ injury. | Gavin O'Brien Conor J Shields Desmond C Winter John P Dillon | 2005 | Hepatobiliary & Pancreatic Diseases International2005，4，1： | 12 |
| 15 | 线粒体与急性肺损伤显示文摘 | 尚涛 李立萍 张建新 | 2007 | 河北医药2007，29，4： | 12 |
| 16 | Acute respiratory distress syndrome and lung injury: Pathogenetic mechanism and therapeutic implication显示文摘To review possible mechanisms and therapeutics for acute lung injury(ALI) and acute respiratory distress syndrome(ARDS). ALI/ARDS causes high mortality. The risk factors include head injury, intracranial disorders, sepsis, infections and others. Investigations have indicated the detrimental role of nitric oxide(NO) through the inducible NO synthase(i NOS). The possible therapeutic regimen includes extracorporeal membrane oxygenation, prone position, fluid and hemodynamic management and permissive hypercapnic acidosis etc. Other pharmacological treatments are anti-inflammatory and/or antimicrobial agents, inhalation of NO, glucocorticoids, surfactant therapy and agents facilitating lung water resolution and ion transports. β-adrenergic agonists are able to accelerate lung fluid and ion removal and to stimulate surfactant secretion. In con-scious rats, regular exercise training alleviates the endotoxin-induced ALI. Propofol and N-acetylcysteine exert protective effect on the ALI induced by endotoxin. Insulin possesses anti-inflammatory effect. Pentobarbital is capable of reducing the endotoxin-induced ALI. In addition, nicotinamide or niacinamide abrogates the ALI caused by ischemia/reperfusion or endotoxemia. This review includes historical retrospective of ALI/ARDS, the neurogenic pulmonary edema due to head injury, the detrimental role of NO, the risk factors, and the possible pathogenetic mechanisms as well as therapeutic regimen for ALI/ARDS. | Chain-Fa Su Shang Jyh Kao Hsing I Chen | 2012 | World Journal of Critical Care Medicine2012，1，2： | 12 |
| 17 | Establishment of the critical period of severe acute pancreatitis-associated lung injury显示文摘BACKGROUND:Since respiratory dysfunction is the main cause of death in patients with severe acute pancreatitis (SAP),elucidating the critical period of acute pancreatitis-associated lung injury(APALI)is of important clinical value. This study aimed to define the risk period of APALI by a series of studies including a dynamic analysis of total water content,ultrastructure and number of typeⅡalveolar epithelial cells,and reactive oxygen metabolites(ROMs)of lung tissue in a mouse model of SAP,and a clinical analysis of APALI patients. METHODS:ICR mice were selected to establish a SAP model.They were given 7 intraperitoneal injections of cerulein(50μg/kg body weight)at hourly intervals,followed by an intraperitoneal injection of lipopolysaccharide(15 mg/kg body weight).The total water content,ultrastructure, and number of typeⅡalveolar epithelial cells,and ROMs of lung tissue were assessed before(0 hour)and after the establishment of SAP model(6 hours,12 hours,1 day,4 days,and 7 days).In addition,we analyzed the data from 215 patients with APALI(PaO2<60 mmHg)treated at our hospital between January 1998 and December 2006. Statistical analyses were made using the F test.P values less than 0.05 were regarded as statistically significant. RESULTS:The total water content and ultrastructure of typeⅡalveolar epithelial cells(mitochondria and lamellar bodies)of the lung in the SAP mice were significantly altered at 12 hours after the establishment of SAP model,and reached a maximum at 1 to 4 days.The number of typeⅡalveolar epithelial cells and ROMs increased maximally at 1 day after the establishment of the model.Furthermore,clinical results showed that lung injury occurred at a mean of 3.1435±1.0199 days in patients with SAP.These clinical data were almost consistent with the results of the SAP model.CONCLUSION:The risk period for APALI is between the first and fourth day during the course of SAP. | Chen, Yi-Peng Ning, Jian-Wen Ji, Feng | 2009 | Hepatobiliary & Pancreatic Diseases International2009，8，5： | 10 |
| 18 | Erucic acid from Isatis indigotica Fort. suppresses influenza A virus replication and inflammation in vitro and in vivo through modulation of NF-kB and p38 MAPK pathway显示文摘Isatis indigotica Fort.(Ban-Lan-Gen)is an herbal medicine prescribed for influenza treatment.However,its active components and mode of action remain mostly unknown.In the present study,erucic acid was isolated from Isatis indigotica Fort.,and subsequently its underlying mechanism against influenza A virus(IAV)infection was investigated in vitro and in vivo.Our results demonstrated that erucic acid exhibited broad-spectrum antiviral activity against IAV resulting from reduction of viral polymerase transcription activity.Erucic acid was found to exert inhibitory effects on IAV or viral(v)RNA-induced pro-inflam-matory mediators as well as interferons(IFNs).The molecular mechanism by which erucic acid with antiviral and anti-inflammatory properties was attributed to inactivation of NF-kB and p38 MAPK signaling.Furthermore,the NF-kB and p38 MAPK inhibitory effect of erucic acid led to diminishing the transcriptional activity of interferon-stimulated gene factor 3(ISGF-3),and thereby reducing IAV-triggered pro-inflammatory response amplification in IFN-β-sensitized cells.Additionally,IAV-or vRNA-triggered apoptosis of alveolar epithelial A549 cells was prevented by erucic acid.In vivo,erucic acid administration consistently displayed decreased lung viral load and viral antigens expression.Meanwhile,erucic acid markedly reduced CD8+cytotoxic T lymphocyte(CTL)recruitment,pro-apoptotic signaling,hyperactivity of multiple signaling pathways,and exacerbated immune inflammation in the lung,which resulted in decreased lung injury and mortality in mice with a mouse-adapted A/FM/1/47-MA(H1N1)strain infection.Our findings provided a mechanistic basis for the action of erucic acid against IAV-mediated inflammation and injury,suggesting that erucic acid may have a therapeutic potential in the treatment of influenza. | Xiaoli Liang Yuan Huang Xiping Pan Yanbing Hao Xiaowei Chen Haiming Jiang Jing Li Beixian Zhou Zifeng Yang | 2020 | Journal of Pharmaceutical Analysis2020，10，2： | 10 |
| 19 | Ligustrazine alleviates acute lung injury in a rat model of acute necrotizing pancreatitis显示文摘BACKGROUND: Acute necrotizing pancreatitis leads to a systemic inflammatory response characterized by widespread leukocyte activation and, as a consequence, distant lung injury. The aim of this study was to evaluate the effect of ligustrazine, extracted from Ligusticum wallichii a traditional Chinese medicine, on lung injury in a rat model of acute necrotizing pancreatitis (ANP). METHODS: A total of 192 rats were randomly divided into three groups: control (C group); ANP without treatment (P group); and ANP treated with ligustrazine (T group). Each group was further divided into 0.5, 2, 6 and 12 hours subgroups. All rats were anesthetized with an intraperitoneal injection of sodium pentobarbital. Sodium taurocholate was infused through the pancreatic membrane to induce ANP. For the T group, sodium taurocholate was infused as above, then 0.6% ligustrazine was administered via the femoral vein. The effects of ligustrazine on the severity of lung injury were assessed by lung wet/dry weight ratio, myeloperoxidase (MPO) activity and histopathological changes. Pulmonary blood flow was determined by the radioactive microsphere technique (RMT). RESULTS: The blood flow in the P group was significantly lower than that of the C group, while the blood flow in the T group was significantly higher than that of the P group but showed no significant difference from the C group. Compared with C group, the lung wet/dry ratios in both the P and T groups were significantly increased, but there was no significant difference between them. The MPO activity in the P group was greatly increased over that of the C group. In the T group, although the MPO activity was also higher than in the C group, it much less increased than in the P group. Moreover, the difference between P and T groups was significant after 0.5 to 12 hours. After induction of the ANP model, the pancreas showed mild edema and congestion; the longer the time, the more severe this became. The pulmonary pathological changes wereaggravated significantly in the P group. Histopathological scores were higher in the P group than in the C group throughout the experimental course. Histopathological scores in the T group were lower than those in the P group at 6 and 12 hours. CONCLUSIONS: Microcirculatory disorder is an important factor of lung injury in ANP. Ligustrazine can ameliorate microcirculatory disorder and alleviate the damage to the lung. | Jian-Xin Zhang and Sheng-Chun Dang Department of General Surgery, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, China | 2006 | Hepatobiliary & Pancreatic Diseases International2006，5，4： | 10 |
| 20 | 清热燥湿方对急性肺损伤大鼠肺组织核转录因子-κB蛋白及mRNA表达的影响显示文摘目的 探讨清热燥湿方对脂多糖(LPS)诱导的急性肺损伤(ALI)大鼠肺组织核转录因子-κB(NF-κB)蛋白及mRNA表达的影响.方法 40只雄性Wistar大鼠按随机数字表法均分为对照组、模型组、地塞米松组、清热燥湿方组4组.地塞米松和清热燥湿方在LPS诱导ALI模型前预处理3 d.分别于制模后4 h和8 h采用免疫组化法和逆转录-聚合酶链反应(RT-PCR)检测NF-κB的蛋白及mRNA表达,并进行肺组织病理观察.结果 与模型组相比,地塞米松组和清热燥湿方组4 h、8 h NF-κB蛋白染色阳性面积率[4 h:(3.40±0.39)%、(2.59±0.62)%比(4.28±0.55)%;8 h:(3.04±0.74)%、(2.60±0.11)%比(4.20±0.62)%]及mRNA表达[4 h:(12.88±2.28)×10-4、(3.07±2.63)×10-4比(44.82±9.27)×10-4;8 h:(3.30±2.64)×10-4、(1.53±1.51)×10-4比(26.07±3.81)×10-4]均明显降低(P<0.05或P<0.01).光镜下观察,模型组大鼠肺组织出现大片出血及坏死;清热燥湿方组大鼠肺组织病理损伤程度较模型组减轻.结论 清热燥湿方能减轻内毒素致ALI大鼠肺组织损伤,对肺损伤有保护作用,其机制可能与其能降低损伤肺组织NF-κB蛋白及mRNA表达有关. | 阮琼 汪东颖 杨爱东 李文雯 吴中华 郭永洁 王利霞 | 2010 | 中国中西医结合急救杂志2010，17，2： | 10 |
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