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The interaction between Lymphocyte function-associated antigen 1 (LFA-1) and intercellular-adhesion molecule-1 (ICAM-1) plays important roles in the cell-mediated immune response and inflammation associated with dry eye disease. LFA-1/ICAM-1 antagonists can be used for the treatment of dry eye disease, such as Lifitegrast which has been approved by the FDA in 2016 as a new drug for the treatment of dry eye disease. In this study, we designed and synthesized some new structure compounds that are analogues to Lifitegrast, and their biological activities were evaluated by in vitro cell-based assay and also by in vivo mouse dry eye model. Our results demonstrated that one of these analogues of Lifitegrast (compound 1b) showed good LFA-1/ICAM-1 antagonist activity in in vitro assay; meanwhile, it also significantly reduced ocular surface epithelial cells damage, increased goblet cell density in dry eye mouse and highly improved the symptoms of dry eye mouse. Graphical abstract.
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Public trust in the criminal justice system, including the jury system, is important for maintaining a democracy that is fair for all citizens. However, there is little research on trust in the jury system generally and even less cross-country comparison research specifically. Trust in the jury system might relate to other legal attitude measures (e.g., authoritarianism). This study identified the degree to which trust in the jury system relates to legal attitudes and compared perceptions of trust between the U.S. and Australia. Community members completed a survey that included measures of trust in the jury system and legal attitudes. The U.S. sample had higher levels of trust in juries than the Australian sample. In both samples, just world beliefs and legal authoritarianism were positively related to trust. Results have both theoretical and practical implications regarding legal attitudes, trust in the jury system, and public opinions of juries in each country.
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Objective To evaluate the effect of electroacupuncture ( EA) preconditioning on hipp-ocampal I-kappa B-α ( IκB-α)∕nuclear factor κB ( NF-κB)∕intercellular adhesion molecule-1 ( ICAM-1) signaling pathway during cerebral ischemia-reperfusion ( I∕R) in mice. Methods A total of 120 healthy male C57BL∕6 mice, aged 10-12 weeks, weighing 20-25 g, were divided into 4 groups ( n=30 each) u-sing a random number table method: control group ( group C) , cerebral I∕R group ( group I∕R) , precondi-tioning with EA at non-acupoint+cerebral I∕R group ( group S+I∕R) and preconditioning with EA at Baihui acupoint + cerebral I∕R group ( group E+I∕R) . The cerebral I∕R injury model was established by occlusion of bilateral common carotid arteries followed by reperfusion for 72 h in mice anesthetized with halothane or chloral hydrate in group I∕R. Group S+I∕R received EA at the points 2 mm lateral to the acupoints of Baihui for 5 consecutive days, and then the cerebral I∕R injury model was established. Group E+I∕R received EA at Baihui acupoints with a sparse-dense wave at an intensity of 1 mA and a frequency of 2 Hz∕15 Hz for 30 min once a day for 5 consecutive days, and then the cerebral I∕R injury model was established. Neurobe-havioral score was assessed at 24 and 48 h of reperfusion. Then 5 mice in each group were sacrificed, and the hippocampal tissues were obtained and stained with haematoxylin and eosin for examination of the patho-logical changes in hippocampal CA1 region and for determination of the expression of IκB-α, NF-κB, ICAM-1, interleukin-6 ( IL-6) , IL-1β protein and mRNA by Western blot and real-time polymerase chain reaction, respectively. Results Compared with group C, neurobehavioral score was significantly in-creased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1βprotein and mRNA was up-regulated in I∕R, S+I∕R and E+I∕R groups ( P<0. 05) . Compared with group I∕R, neurobehavioral score was significantly decreased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1β protein and mRNA was down-regulated in group E+I∕R (P<0. 05), and no significant change was found in the parameters mentioned above in group S+I∕R (P>0. 05). Compared with group S+I∕R, neu-robehavioral score was significantly decreased, and the expression of hippocampal IκB-α, NF-κB, ICAM-1, IL-6 and IL-1β protein and mRNA was down-regulated in group E+I∕R ( P<0. 05) . Conclusion The mechanism by which EA preconditioning attenuates cerebral I∕R injury may be related to inhibiting activation of hippocampal IκB-α∕NF-κB∕ICAM-1 signaling pathway in mice.
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Objective To evaluate the role of classⅠhistone deacetylase (HDAC) in myocardial ischemia-reperfusion (I∕R) injury in diabetic rats and the relationship with adenosine monophosphate-acti- vated protein kinase (AMPK)∕mammalian target of rapamycin (mTOR) signaling pathway. Methods SPF healthy adult male Sprague-Dawley rats, weighing 210-220 g, were used in this study. Type I diabetes mellitus was induced by single intraperitoneal injection of streptozotocin dissolved in citrate buffer 60 mg∕kg, and 8 weeks later the rats with type I diabetes mellitus were used for experiment. Forty-eight diabetic rats were divided into 4 groups (n＝12 each) by using a random number table method: sham operation group (group S), myocardial I∕R group (group I∕R), myocardial I∕R plus class I HDAC inhibitor MS-275 group (group I∕R+MS) and myocardial I∕R plus MS-275 plus AMPK inhibitor Compound C group ( group I∕R+MS+CC). Myocardial I∕R was induced by ligation of the left anterior descending branch of the coronary ar-tery for 45 min followed by 180 min of reperfusion in anesthetized rats. In group I∕R+MS, MS-275 10 mg∕kg was intraperitoneally injected once a day for 7 consecutive days, and myocardial I∕R was produced after the end of administration. AMPK inhibitor Compound C 0. 5 mg∕kg was intravenously injected at 30 min before ischemia in group I∕R+MS+CC. Six rats were sacrificed at the end of reperfusion for determina-tion of myocardial infarct size. Another 6 rats were selected at the end of reperfusion and sacrificed for deter-mination of the level of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) in serum (by en-zyme-linked immunosorbent assay), expression of AMPK, phosphorylated AMPK ( p-AMPK), mTOR, phosphorylated mTOR (p-mTOR), ubiquitin-binding protein P62 (P62), microtubule-associated protein 1 light chain 3 Ⅰ(LC3 Ⅰ) and LC3Ⅱ in myocardial tissues (by Western blot). The ratios of p-AMPK∕AMPK, p-mTOR∕mTOR and LC3Ⅱ∕Ⅰwere calculated. Results Compared with group S, the myocardial infarct size and levels of serum CK-MB and LDH were significantly increased in I∕R, I∕R+MS and I∕R+M+CC groups, the ratios of p-AMPK∕AMPK and LC3Ⅱ∕Ⅰwere significantly increased, p-mTOR∕mTOR ratio was decreased, and P62 expression was down-regulated in group I∕R+MS (P＜0. 05), and no significant change was found in p-AMPK∕AMPK ratio, p-mTOR∕mTOR ratio, LC3Ⅱ∕Ⅰ ratio or P62 expression in I∕R and I∕R+M+CC groups (P＞0. 05). Compared with group I∕R, the myocardial infarct size and levels of serum CK-MB and LDH were significantly decreased, the ratios of p-AMPK∕AMPK and LC3Ⅱ∕Ⅰwere in-creased, p-mTOR∕mTOR ratio was decreased, and P62 expression was down-regulated in group I∕R+MS (P＜0. 05), and no significant change was found in the parameters mentioned above in group I∕R+M+CC (P＞0. 05). Compared with group I∕R+MS, the myocardial infarct size and levels of serum CK-MB and LDH were significantly increased, the ratios of p-AMPK∕AMPK and LC3Ⅱ∕Ⅰ were decreased, p-mTOR∕mTOR ratio was increased, and P62 expression was up-regulated in group I∕R+M+CC ( P＜0. 05). Con-clusion Class Ⅰ HDAC is involved in myocardial I∕R injury through enhancing AMPK∕mTOR signaling pathway-regulated level of autophagy in diabetic rats.
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Aim To investigate the protective effect of immunomodulating peptide(PGPIPN) on the acute al-coholic liver injury in mice. Methods Kunming mice were randomly divided into control group, model group,glutataione(GSH) group, PGPIPN low dose group, PGPIPN moderate and high dose groups. The mice were treated with different doses of PGPIPN or GSH for two weeks except control group and model group. The acute alcoholic liver injury model was in-duced by gavage with 56° alcohol for three days. The indices including the activities of AST,ALT in serum, and the contents of TNF-α, MDA, SOD and GSH-Px in liver were examined. Liver histopathological changes were examined by HE staining. Results Compared with control group,the levels of serum ALT,AST and the contents of TNF-α, MDA significantly increased, while the contents of SOD and GSH-Px significantly de-creased in model group. There was hepatocyte apopto-sis and inflammatory cell infiltration in liver tissues. Compared with model group, the activities of serum ALT, AST and the contents of TNF-α, MDA were re-markably reduced in PGPIPN high dose group. The contents of SOD and GSH-Px significantly increased in PGPIPN high dose group. PGPIPN could alleviate the injury of liver. Conclusion PGPIPN has certain pro-tective effect on acute alcoholic liver injury of mice, providing a theoretical guidance.
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Objective To investigate the diagnostic value of combined detection of NGAL,L-FABP and KIM-1 in urine for early acute kidney injury in children.Methods 128 cases sepsis patients in our hospital during ICU from September 2015 to September 2016 were enrolled in the study,according to the occurrence of acute renal injury(AIK)were divided into observation group and control group,the incidence of AKI in 26 ca-ses as the observation group,102 cases without AKI as control group;the content of urine collected from two groups of children,NGAL L-FABP,KIM-1.Results In AKI group 6 h NGAL,L-FABP,Kim-1 in urine in-creased significantly higher than that of the other time points and non AKI group level,significant difference was statistically significant;6h NGAL,L-FABP,Kim-1 in urine combined detection efficiency is highest,sen-sitivity,specificity and positive pre detection value and negative predictive value were measured 86.7%,97. 8%,78.3% a,98.7% a,was significantly higher than the diagnostic efficacy of urinary NGAL,L-FABP,Kim-1;6h,L-FABP,NGAL in the urine level of KIM-1 and 48h in patients with creatinine and GFR levels of correla-tion analysis found that in children with early urinary NGAL,L-FABP,KIM-1 and 48h in children with creati-nine and GFR levels were positive related.Conclusion The detection of NGAL,L-FABP and KIM-1 in urine is of great significance in the diagnosis of AKI in children,which is worthy of clinical application.
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Objective To investigate the significance of urine neutrophil gelatinase associated lipocalin (NGAL ) and renal injury molecule-1 (KIM-1) in predicting the acute kidney injury (AKI) in children with congenital heart disease after operation .Methods From April 2014 to December 2015 ,67 cases of cardiopulmonary bypass in children with congenital heart disease were studied in our hospital ,all patients were divided into AKI group (n=24) and non AKI group (n=43) by pRIFLE standard .Serum creatinine , urine NGAL and urine KIM-1 levels were compared between the two groups before and after the operation ,the receiver operating characteristic curve (ROC curve) and the area under the curve (AUC) were used to evaluate the value of NGAL and KIM-1 in pre-dicting the postoperative AKI in children with congenital heart disease .Results There was no significant difference between the two groups in preoperative and postoperative 2 h and 4 h creatinine (P>0 .05) ,but the levels of postoperative 12 ,24 ,48 h creati-nine in the non AKI group were significantly lower than those in the AKI group (P<0 .05) .The NGAL level of postoperative 2 ,4 , 6 ,12 h in non AKI group was significantly lower than that in AKI group (P<0 .05) ,but there was no significant difference in the level of postoperative 24 h urine NGAL between the two groups (P>0 .05) .There was no significant difference between the two groups of patients with postoperative 2 h urinary KIM-1 (P>0 .05) ,postoperative 4 ,6 ,12 ,24 h urinary KIM-1 levels in the non AKI group were significantly lower than those in the AKI group (P<0 .05) .The optimal time point separate detection of urinary NGAL levels to assist in diagnosis of AKI after 12 h ,AUC was 0 .834 (95% CI:0 .631-0 .912);the best time point separately to detect the level of KIM-1 AKI to assist in the diagnosis of AKI after 24 h ,AUC was 0 .871 (95% CI:0 .665-0 .933);combined de-tection of urinary NGAL and KIM-1 levels to assist the best time for the diagnosis of AKI after 24 h ,AUC was 0 .913(95% CI:0 .745-0 .968) .Conclusion Urine NGAL and urine KIM-1 in children with congenital heart disease after operation have important clinical significance in predicting the occurrence of AKI .
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Objective To investigate the significance of urine neutrophil gelatinase associated lipocalin (NGAL ) and renal injury molecule-1 (KIM-1) in predicting the acute kidney injury (AKI) in children with congenital heart disease after operation .Methods From April 2014 to December 2015 ,67 cases of cardiopulmonary bypass in children with congenital heart disease were studied in our hospital ,all patients were divided into AKI group (n=24) and non AKI group (n=43) by pRIFLE standard .Serum creatinine , urine NGAL and urine KIM-1 levels were compared between the two groups before and after the operation ,the receiver operating characteristic curve (ROC curve) and the area under the curve (AUC) were used to evaluate the value of NGAL and KIM-1 in pre-dicting the postoperative AKI in children with congenital heart disease .Results There was no significant difference between the two groups in preoperative and postoperative 2 h and 4 h creatinine (P>0 .05) ,but the levels of postoperative 12 ,24 ,48 h creati-nine in the non AKI group were significantly lower than those in the AKI group (P<0 .05) .The NGAL level of postoperative 2 ,4 , 6 ,12 h in non AKI group was significantly lower than that in AKI group (P<0 .05) ,but there was no significant difference in the level of postoperative 24 h urine NGAL between the two groups (P>0 .05) .There was no significant difference between the two groups of patients with postoperative 2 h urinary KIM-1 (P>0 .05) ,postoperative 4 ,6 ,12 ,24 h urinary KIM-1 levels in the non AKI group were significantly lower than those in the AKI group (P<0 .05) .The optimal time point separate detection of urinary NGAL levels to assist in diagnosis of AKI after 12 h ,AUC was 0 .834 (95% CI:0 .631-0 .912);the best time point separately to detect the level of KIM-1 AKI to assist in the diagnosis of AKI after 24 h ,AUC was 0 .871 (95% CI:0 .665-0 .933);combined de-tection of urinary NGAL and KIM-1 levels to assist the best time for the diagnosis of AKI after 24 h ,AUC was 0 .913(95% CI:0 .745-0 .968) .Conclusion Urine NGAL and urine KIM-1 in children with congenital heart disease after operation have important clinical significance in predicting the occurrence of AKI .
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Aim To study the development of acute lung inflammation in mice induced by activation of the complement alternative pathway and the changes of the related indicators, and to provide an ideal pathological model of acute lung inflammation in mice for drug screening and intervention. Methods Cobra venom factor( CVF) was used to activate complement alterna-tive pathway of SPF Kunming mice by intravenous injection. According to different sampling time, the mice were divided into 15 min, 30 min, 1 h, 2 h, 6 h group, and the parallel PBS control groups were set at the same time. Lung coefficient, lung water content, myeloperoxidase ( MPO ) activity, BALF cell number and protein content were tested. The pathological changes of lung tissue were observed by HE staining. The concentration of IL-6 , TNF-α, P-selectin and ICAM-1 in bronchoalveolar lavage fluid ( BALF ) and serum were determined by ELISA. Results CVF caused pulmonary inflammatory cell infiltration in mice obviously. Compared with PBS groups, MPO activity of lung tissue, BALF cell and the protein concentration were significantly increased. The contents of IL-6, TNF-α, P-selectin in BALF and serum were in-creased, and the content of ICAM-1 in serum was also increased. The content of P-selectin in BALF reached the first peak at 30 min point, the content of IL-6 and TNF-α in BALF reached the first peak at 1 h point, but the indicators had no further changes at 2 h point, and all the indicators rose again at 6 h point. The lev-els of IL-6 and TNF-α in serum reached peak at 1 h point,then the content showed lower levels at the sub-sequent time points. The levels of P-selectin and ICAM-1 in serum increased along the time. Lung coef-ficient, lung water content and ICAM-1 of the BALF showed no significant alteration. Conclusion The ac-tivation of the complement alternative pathway can lead to acute lung inflammation in mice and the inflammato-ry response is the most obvious at 30 min to 1 h. The study could provide an ideal pathological model of a-cute lung inflammation in mice for drug screening and intervention.
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Aim To investigate the role of the interac-tion between necroptosis ( Nec ) and p38 mitogen-acti-vated protein kinase ( MAPK) pathway in the high glu-cose (HG)-induced H9c2 cardiac cells injury.Meth-ods The cell viability was measured by cell counter kit-8 assay .The intracellular level of reactive oxygen species ( ROS ) was tested by DCFH-DA stating fol-lowed by photofluorography .Mitochondrial membrane potential ( MMP) was detected by Rhodamine 123 stai-ning followed by photofluorography . The expression levels of receptor interaction protein 3 ( RIP3, an indi-cator of Nec ) and p38 MAPK protein were tested by Western blot assay .Results The treatment of H9c2 cardiac cells with 35 mmol? L-1 glucose ( high glu-cose, HG) for 24 h induced considerable injuries , in-cluding a decrease in cell viability , increases in ROS generation as well as MMP loss .The co-treatment of the cells with 100 μmol? L-1 necrostatin-1(Nec-1,a specific inhibitor of Nec ) and HG for 24 h or the pre-treatment of the cells with 3 μmol? L-1 SB 2 0 3 5 8 0 ( an inhibitor of p38MAPK) for 60 min before HG exposure attenuated the above injuries induced by HG .Moreo-ver, the treatment of the cells with HG for 1,3,6,9, 12 ,24 ,36 and 48 h significantly increased the expres-sion levels of RIP3, peaking at 24 h.The co-treatment of the cells with 100 μmol? L-1 Nec-1 or the pre-treatment of the cells with 3 μmol? L-1 SB203580 considerably blocked the up-regulation of RIP3 expres-sion induced by HG .On the other hand , the co-treat-ment of the cells with 100 μmol? L-1 Nec-1 alleviated the HG-induced up-regulation of the expression of p-p38MAPK.Conclusion The interaction between Nec and p38 MAPK pathway mediates the HG-induced inju-ry in H9c2 cardiac cells.
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mTOR signaling pathway is a highly conserved intracellular signaling pathway,which partici-pates in several signaling pathways, such as PI3K/AKT/mTOR, AKT/TSC1-TSC2/Rheb/mTOR, LKB1-AMPK-TSC-mTOR and FGF-10-Spry2-mTORC1-STAT3/HIF-1α-VEGF-A. mTOR signaling implicate in the regulation of the development of lung and many pulmonary diseases in many aspects,may be connected to bron-chopulmonary dysplasia. Bronchopulmonary dysplasia is one of the very common chronic lung diseases in pre-term,physical and chemical factors have been shown to induce acute lung injury, aberrant wound healing and lung fibrosis in the immature lung. This review summarizes relationship of mTOR signaling among lung develop-ment,acute lung injury and lung fibrosis,to explore the role of mTOR signaling in the development of bronchop-ulmonary dysplasia,in hope of providing novel method in the prevention and treatment of bronchopulmonary dysplasia.
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Objective To detect the protective role of high mobility group box-1 protein (HMGB1 )antibody in concanavalin A(ConA)-induced liver injury in mice.Methods The healthy male Balb/c mice were grouped into con-trol group (saline injection),model group(ConA injection)and experimental group(ConA+HMGB1 antibody injec-tion).After 6 hours of injection,mice blood was collected for detecting alanine transaminase (ALT)and HMGB1 , liver tissue was used to do HE stain,Tunel,and immunofluorescence detection.Results Pathological inflammation in experimental group was slighter than model group.The levels of ALT and HMGB1 in mice serum were (52.00± 8.34)U/L and (7.54 ±0.53)ng/mL in control group,(5 551 .50 ±1 445.74)U/L and (18.06 ±1 .65 )ng/mL in model group,(1 977.40±654.89)U/L and (10.77±0.71)ng/mL in experimental group,respectively;the expres-sion levels of HMGB1 mRNA and HMGB1 (relative value)in liver tissue were 1 .886±0.253 and 0.086±0.028 in control group,4.718±0.341 and 0.268±0.043 in model group,3.005 ±0.331 and 0.116±0.008 in experimental group,respectively;the expression levels of ALT and HMGB1 in serum,as well as HMGB1 mRNA and HMGB1 in liver tissue of experimental group were all lower than model group(all P <0.001).Apoptosis and HMGB1 migra-tion in the liver cell (normalized)were 1 ±0 and 1 ±0 in control group,4.67 ±0.33 and 4.50 ±0.22 in model group,2.67±0.21 and 2.33 ±0.21 in experimental group,respectively;apoptosis and HMGB1 migration in liver tissue of experimental group were both lower than model group(both P <0.001).Conclusion HMGB1 antibody can improve the pathological injury of liver tissue,and protect mice liver against the injury induced by ConA.
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BACKGROUND: A number of medicinal plants and there compounds played a major role in the treatment of hepatic disorders. They were widely used for the treatment of these disorders, and oxidant stress injury was one of the liver injury mechanisms. The present study evaluated the antioxidant activity and the hepatoprotective effect of each extracts of Phlomis maximowiczii. MATERIALS AND METHODS: The antioxidant activity was assayed by the methods of ABTS, FRAP and DPPH in vitro. Hepatoprotective effect of P. maximowiczii extracts was examined using carbon tetrachloride-induced acute liver injury in mice. RESULTS: P. maximowiczii n-butanol (PMBU) extract, ABTS (IC50=18.96 µg/mL), DPPH (IC50=25.15 µg/mL), and FRAP (RACT50=2775.6±144.18 µmol/g), showed higher scavenging capacity than that of P. maximowiczii ethyl acetate (PMEA). The n-butanol extract could significantly reduce the level of GPT, GOT and MDA (P<0.05, P<0.001 and P<0.001, respectively) and increase the level of SOD (P<0.001), respectively. CONCLUSION: The antioxidant activity of n-butanol extract in vitro was related with the level of MDA and SOD in vivo, and hepatoprotective effect of n-butanol extract also had relationship with its antioxidant activity in vivo.
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Antioxidantes/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Phlomis/química , Extratos Vegetais/administração & dosagem , Substâncias Protetoras/administração & dosagem , Alanina Transaminase/metabolismo , Aldeídos/metabolismo , Animais , Aspartato Aminotransferases/metabolismo , Tetracloreto de Carbono/efeitos adversos , Doença Hepática Induzida por Substâncias e Drogas/tratamento farmacológico , Doença Hepática Induzida por Substâncias e Drogas/enzimologia , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Humanos , Fígado/efeitos dos fármacos , Fígado/enzimologia , Fígado/metabolismo , Camundongos , Extratos Vegetais/análise , Substâncias Protetoras/análise , Superóxido Dismutase/metabolismoRESUMO
Objective Paeoniflorin ( PAE) is a potential neuroprotective agent.In this study, we investigated the protective effect of PAE on cerebral ischemia/reperfusion ( CI/R) injury in gerbils and its underlying mechanisms. Methods The model of CI/R was established in 50 gerbils by bilateral common carotid occlusion for 10 min followed by 6-hour reperfusion.Then the animals were equally randomized into five groups:sham, model, 5 mg/kg PAE, 10 mg/kg PAE, and 20 mg/kg PAE.The latter three groups were treated with intraperitoneal injection of PAE once daily for 3 days before carotid occlusion, while the former two groups with saline only, all at 10 ml/kg.Stroke indexes were calculated during the reperfusion.The contents of endogenous neuropeptides, endothelin and calcitonin gene-related peptide ( CGRP) in the plasma were measured by radioimmunoassay.The levels of superoxide dismutase ( SOD) and malondialdehyde ( MDA) in the brain tissue homogenate were determined by the method of xanthine oxidase. Results The 5, 10, and 20 mg/kg PAE groups showed significantly decreased stroke index (14.8 ±3.6, 12.3 ±2.0, and 12.7 ±1.4) as compared with the model group (18.4 ±2.9) (P<0.05), but remarkably increased SOD activity ([99.30 ±9.71], [106.85 ± 15.13] , and [110.25 ±14.90] vs [86.54 ±10.22] nU/mgPro, P<0.05) .The MDA content was significantly lower in the 10 and 20 mg/kg PAE groups than in the model group ([69.23 ±8.42] and [65.91 ±7.64] vs [94.76 ±10.30] μmol/mgPro, P<0.01). The plasma endothelin level was markedly decreased in all the PAE groups in comparison with the model group ([24.06 ±5.37], [19.62 ±5.60] and [21.08 ±4.64] vs [30.52 ±7.13] ng/L, P<0.05). Conclusion The protective effect of PAE pretreatment in CI/R injury appears to be associated with the inhibition of the brain free radicals, lipid peroxidation and endothelin production.
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Objective To investigate whether intensive atorvastatin treatment in patients after percutaneous coro-nary intervention ( PCI) could decrease the effect of contrast medium on kidney function and the incidence of con-trast-induced acute kidney injury( CI-AKI) . Methods A total of 128 patients with PCI were randomly divided into two groups:the enhanced treatment group (n=64) and the control group(n=64). The enhanced treatment group received 80 mg atorvastatin at 12~24 h before PCI and 24,48 h after PCI. The control group was given 20 mg ator-vastatin respectively before and after PCI. The primary end point was the incidence of CI-AKI. Serum creatinine (Scr), cystatin C, glomerular filtration rate(eGFR), urinary albumin and urinary β-2 microglobulin levels were observed at 24 h before PCI and 24, 48, 72 h after PCI. Results In the enhanced treatment group 3. 1 % (n=2) of patients developed CI-AKI versus 4. 7 % (n=3) in the control group, without statistical difference (P=1.00). There was no significant difference between two groups in postoperative Scr, cystatin C, eGFR, urinary al-bumin, urinary β-2 microglobulin and creatine kinase(CK). Three days after the operation, alanine aminotrans-ferase ( ALT) elevated in two groups, and aspartate aminotransferase ( AST) increased in the enhanced treatment group (P<0. 05), but they were all in the normal range. Conclusion There has been no significant difference in decreasing the incidence of CI-AKI and the damage of contrast medium on renal function between the enhanced treatment group and the control group before PCI.
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Acute myocardial ischemia and reperfusion led to arrhythmias and increase of glutamic oxalacetic transaminase (GOT),lactate dehydrogenase (LDH),non-csterified fatty acid (FFA) and malondialdehyde (MDA) content, and decrease of superoxide dismutase (SOD) activity in rats. 3, 6-di-methylamino-dibenzopyri-odonium edetate (IHC-72) 5 mg?kg-1 iv significantly reduced the incidence of ventricular tachy-cardia (VT) and ventricular fibrillation(VF) ,shortened the duration of arrhythmias induced by reperfusion, decreased the release of GOT, LDH and FFA, obviously reduced the MDA content,and effectively protected SOD activity in ischemia-reperfused rat hearts. Our experimental results suggested that IHC-72 had protective effects on ischemia-reperfusion injury rat hearts in vivo. The mechanism of the protection might be associated with the inhibition of cellular lipid peroxidation.
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AIM To study the effects of nalox-one on plasma endothelin-1 and nitric oxide during myocardiac ischemia-reperfusion ( I/R ) injury. METHODS Using myocardiac ischemia models and myocardiac ischemia -reperfusion injury models that was made by means of ligating sinistra corona-ria arteria,to investigate the change of plasma ET-1 and NO during I/R injury, and after the protection and treatment with naloxone,an antagonist of opoid receptor. 40 New Zealand rabbits were randomly assigned to 4 groupsCischemia group, nalox-one protection group, naloxone treatment group and ischemia-reperfusion group, 10 in each group). The blood was phlebotomized at different time in each group. The concentration of ET-1 was detected with radioimmunology method and NO with nitrate reductase method. RESULTS The levels of ET-1 had the trend of improvement after ischemia and were at its peak at the end of 4 h, but the levels of NO were significantly decreased. The ET-1 levels were significantly improved after 0. 5-1 h of injury compared with that before ischemia (P 0. 05). The levels of NO decreased after injury , whereas its levels in naloxone protection group increased significantly compared with that before ischemia ( P 0.05). CONCLUSION Naloxone may effectively reduce the level of ET-1 and enhance the level of NO after myocardiac ischemia and during I/R injury; whereby it decreases the injury to vascular and myocardium.
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Acute lung injury(ALI)/acute respiratory distress syndrome(ARDS),the complicated and devastating illness,resulted from various processes of systemic inflammatory response syndrome(SIRS),injure directly or indirectly the lung.With the advance of investigations in SIRS and multiple organs disfunction syndrome(MODS),inflammation development and control have been considered to be the important mechanism of ALI/ARDS.The research hotspot is also focused on the inflammatory cells and cytokines.Dachengqi decoction can influence on the functions of inflammatory cells and cytokines,so the strategies of anti-inflammatory treatment on immunoregulation became the key point for prevention and treatment of ALI/ARDS with traditional Chinese medicine.
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The dynamic changes of the maximal platelet aggregation rate (PARm) and serum fibrin derived products (FDP) after smoke inhalation injury in rabbits were observed. The pathological changes of the lung tissues and lung water content were also studied after the animals were killed. It was found that PARm increased in the 6th and 22nd postburn hours(PBH), the platelet count decreased progressively right after injury, and FDP increased in the 6th and 24th PBH. In addition, there were alveolar edema and hemorrhage with deposition of fibrin in the lung parenchyma. In the lumen of some small pulmonary vessels, platelet aggregation with evacuation of their granules was demonstrated, which implies there is release of certain chemical mediators. The lung water content increased apparently. Clinical symptoms such as difficulty in bretahing. rales over the chest, etc developed along with the changes of platelets and FDP.On the basis of the analysis of the results listed above, it is proposed that the changes of platelets and FDP may play an important role in the development of pulmonary damage after smoke inhalation.
