Objective To explore the effects of exogenous ubiquitin on lung injury and serum nitric oxide ( NO) level of mice in the early stage of sepsis induced by cecal ligation and perforation ( CLP) . Methods Seventy-seven mice were devided randomly into three groups, ie. CLP Group ( n =28) , SHAM Group ( n =28) and UB Group( n = 21) . Six hours after operation, seven mice of both Group CLP and SHAM were sacrificed for lung and blood sampling. Meanwhile all mice of Group UB were injected intravenously with exogenous ubiquitin of 10 mg/kg body weight. Seven mice of each group were sacrificed at seven, eight and nine hours after operation. Lung water content and serum level of nitrate /nitrite ( NO2 /NO3 , the stable end-products of NO) , were determined. Pathological changes of lung were compared among the groups. Results Lung water content of Group UB was lower than that of Group CLP at each observational time point. Futhermore, there was a significant differentce in lung water content between Group UB and CLP at 9 hours. Pathological examination revealed that inflammatory hyperemia and infiltration of pulmonary parenchyma reduced in Group UB, compared with Group CLP. Serum NO levels of Group CLP and UB were similar at each time point. Conclusions In the early stage of murine sepsis induced by CLP, a single introvenous bolus of exogenous ubiquitin significantly decreases lung capillary vascular permeability, and probably makes a temporal reduction of acute lung injury while it has no obvious effects on serumNO level.
In order to study effect of endothelin (ET-1) on hepatic blood flow in rats and effect of nitric oxide (NO) and prostacyclin (PGI2) on ET-1 biological function, 20 rats were randomized into control, ET-1, ET-1 plus nitric-Larginine, ET-1 plus prostacyclin and indomethen groups. The result showed that ET-1 decreased hepatic blood flow and lasted for longer time. NO and PGI2 may antagonize the biological action of ET-1 during endotoxemia. Therefore, the endothelium-derived vascular factors may regulate hepatic blood flow.
OBJECTIVE To study the protective effects of Schwann cell derived neurotrophic factor (SDNF) on motoneurons of spinal anterior horn from spinal root avulsion induced cell death. METHODS Twenty SD rats were made the animal model of C6.7 spinal root avulsion induced motoneuron degeneration, and SDNF was applied at the lesion site of spinal cord once a week. After three weeks, the C6.7 spinal region was dissected out for motoneuron count, morphological analysis and nitric oxide synthase (NOS) enzyme histochemistry. RESULTS 68.6% motoneurons of spinal anterior horn death were occurred after 3 weeks following surgery, the size of survivors was significantly atrophy and NOS positive neurons increased. However, in animals which received SDNF treatment, the death of motoneurons was significantly decreased, the atrophy of surviving motoneurons was prevented, and expression of NOS was inhibited. CONCLUSION SDNF can prevent the death of motoneurons following spinal root avulsion. Nitric oxide may play a role in these injury induced motoneuron death.
Objective To investigate the effects of nitric oxide precursor L-arginine on traumatic pulmonary contusion. Methods Sixty Sprague-Dawley rats were randomly divided into three groups, ie. a normal group, a model group, and a L-arginine group. The model of traumatic pulmonary contusion was established with self-made chest-impacter. Then the rats in the L-arginine group was injected intravenously with L-arginine in a dose of 250 mg/kg. All rats were sacrificed at 24 hours after these models established.Levels of TNF-α and nitric oxide ( NO2 - /NO3- ) in serum were measured by ELISA and diazo-reaction method. Lung wet/dry weight ratio, NF-κB, endothelin-1, apoptotic cell, and ICAM-1 ( intercellular adhesion molecule-1) mRNA expressions in the lung tissue were measured. Results Compared with the model group,TNF-αand lung wet/dry weight ratio decreased significantly in the L-arginine group( P lt; 0. 05) . After the L-arginine treatment, the concentration of nitric oxide, apoptotic index were significantly higher than the model group ( P lt; 0. 05) . The expressions of NF-κB, endothelin-1, and ICAM-1 mRNA in the L-arginine group were lower than those in the model group ( P lt;0. 05) . Conclusion L-arginine treatment can downregulate the expressions of NF-κB, ET-1, ICAM-1 mRNA and apoptosis obviously, and ameliorate the microcirculation of rats lung with traumatic pulmonary contusion.
【Abstract】ObjectiveTo investigate the protective effect of melatonin on renal injury induced by bile duct ligation in rats. MethodsSixtyfour rats were randomly divided into four experimental groups (n=16 rats per group): the control group (CN), sham operative group (SO), bile duct ligation group (BDL) and bile duct ligation melatonin treatment group (BDL+Mel). Obstructive jaundice was induced by common bile duct ligation. Plasma level of nitric oxide (NO), total bilirubin (TB), direct bilirubin (DB), alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea nitrogen (BUN) and creatinine (Cr) were measured 4 d and 8 d after operation. NO and inducible nitric oxide synthase (iNOS) in renal tissue were detected at the same time point, too. Histopathological changes of kidneys were examined by HE staining. ResultsIn BDL group, the plasma levels of NO, TB, DB, ALT, AST, BUN and Cr were higher than those of SO group (P＜0.01）, and the level of NO and activities of iNOS in renal tissue were significantly increased (P＜0.01）. However, in BDL+Mel group, the plasma levels of NO, ALT, AST, BUN and Cr were lower than those of the BDL group (P＜0.01）, and the level of NO and activities of iNOS in renal tissue were significantly suppressed (P＜0.01）; histopathological changes of kidneys were improved.ConclusionAugmentation of iNOS activities and increasing of NO production in local tissue contributed to renal injury induced by bile duct ligation, and the mode of melatonin’s protective actions, at least in part, relates to interference with no pathways.
The aim of this study is to assess ischemia/reperfusion injury in carbon tetrachloride induced cirrhotic liver as compared to normal liver in the rats. Results showed that in cirrhotic liver, instead of diminishing the hepatic vein nitric oxide level increased significantly after ischemia from 8.04 μmol/L to 11.52 μmol/L and remained high till 5 hrs after reperfusion. The hepatic adenosine triphosphate (ATP) contents decreased as that seen in normal rat but did not restore to normal till the end of 5 hrs after reperfusion. Based on these findings, it is postulated that in cirrhotic liver, ischemia/reperfusion injury is aggrvated as evidenced by of nitric oxide, and extended diminishing in ATP.
目的:研究呼吸操改善慢性阻塞性肺疾病(COPD)患者肺功能的机制。方法:对本院46例COPD 患者随机分成对照组和治疗组,按常规内科治疗并对其有计划地进行健康知识教育。治疗组在常规内科治疗加康复指导基础上,增加呼吸操训练。测定治疗前后6分钟步行距离、血清白三烯、呼出气中一氧化氮浓度(fractional exhaled nitric oxide, FENO)。结果:治疗组较对照组6分钟步行能力改善,血清白三烯水平下降(Plt;0.05)、呼气NO含量下降(Plt;0.05)。结论:加强COPD患者的健康指导及呼吸操训练可改善患者肺功能状况,明显提高生活质量
ObjectiveTo investigate the relationship between the changes of nerve cells in sphincter of Oddi and acute pancreatitis. MethodsThe rabbit models of acute pancreatitis were prepared by using sodium taurocholate perfusion. Immunohistochemical method was used to detect the expressions of nitric oxide synthase (NOS) and vasoactive intestinal peptide (VIP) in neurons of the sphincter of Oddi. ResultsIn the control group, (45.83±2.17)% of myenteric neurons were NOS-positive, (52.46±2.47)% of myenteric neurons were VIP positive, and (22.73±1.95)% of myenteric neurons were NOS and VIP double positive. In contrast, (11.26±0.93)% of myenteric neurons were NOS-positive and (28.62±2.83)% of myenteric neurons were VIP positive in SAP group, which were significantly less than those of control group (P < 0.01). ConclusionsThe sphincter of Oddi of normal rabbits is rich in VIP and NOS positive neurons. The significant reduction of NOS-positive and VIP-positive neurons when SAP, which may be the reason of decreased the activities of the sphincter of Oddi.