ABSTRACT
Objective To investigate the effects of sivelestat sodium on early inflammatory reaction in rats with smoke inhalation injury. Methods Forty SPF male SD rats were randomly divided into 5 groups:normal control group (A), injury group (B), smoke inhalation treated with 10 mg/kg sivelestat sodium group (C), smoke inhalation treated with 20 mg/kg sivelestat sodium group (D) and smoke inhalation treated with 30 mg/kg sivelestat sodium group (E), 8 rats for each group. After smoke inhalation injury model was established, the treatment groups were intraperitoneally injected sivelestat sodium 10 mg/kg, 20 mg/kg and 30 mg/kg separately. B group was treated with the same volume of physiological saline. After 24 hours,ELISA was used for detecting serum contents of neutrophil elastase (NE), myeloperoxidase (MPO), tumor necrosis factor-α(TNF-α) and interleukin-6 (IL-6) in five groups. Meanwhile the water content of lung tissue was measured, and the pathological changes were observed by HE staining. The thickness of alveolar septum was measured and compared between groups. Results Compared with control group, the serum levels of NE, MPO, IL-6, TNF-α, water content of the lung tissue and thickness of alveolar septum were significantly higher in other four groups (P<0.05). Compared with injury group, the serum levels of NE, MPO, IL-6, TNF-α, water content of the lung tissue and thickness of alveolar septum were significantly lower in treatment groups (P<0.05). Compared with 20 mg/kg treatment group and 30 mg/kg treatment group, the serum levels of NE, MPO, IL-6, TNF-α, water content of the lung tissue and thickness of alveolar septum were significantly lower in 10 mg/kg treatment group (P<0.05). Conclusion The result shows that sivelestat sodium can reduce the early inflammatory reaction of rats with smoke inhalation injury and attenuates the lung edema. In this experiment, the treatment effect of 10 mg/kg sivelestat sodium is better than other treatment doses.
ABSTRACT
BACKGROUND:It is unclear whether hydrogen-rich water can be used to protect skeletal muscle injury induced by eccentric exercise, as wel as the relative mechanism. OBJECTIVE:To observe the effect of hydrogen-rich water on the mitochondrial oxidative stress and inflammation in rat skeletal muscle after eccentric exercise, and to investigate the relative signaling pathway of hydrogen-rich water. METHODS:Forty Sprague Dawley rats were randomly divided into four groups: control group, eccentric exercise group, eccentric exercise+saline group, and eccentric exercise+hydrogen-rich water group. Rats in three eccentric exercise groups were exercised on a motor-driven rodent treadmil at a speed of 16-18 m/min and a slope of-16° for 90 minutes per day. Rats in the eccentric exercise+hydrogen-rich water group were subjected to intraperitoneal injection of hydrogen-rich water (10 mL/kg) immediately after exercise; and rats in the eccentric exercise+saline group were administrated with normal saline after exercise. Al the interventions lasted for 5 days. RESULTS AND CONCLUSION:Hydrogen-rich water intervention after eccentric exercise could markedly enhance the mitochondrial Sirtuin-3 expression, improve the mitochondrial membrane potential and activity of manganese superoxide dismutase, down-regulate the mitochondrial reactive oxygen species generation and mitochondrial DNA oxidative damage, thus inhibiting inflammatory cytokines expression, such as NLRP3 and interleukin-1β. The results indicated that hydrogen-rich saline could directly scavenge reactive oxygen species. In addition, hydrogen-rich water could improve mitochondrial energy metabolism and antioxidant capacity through up-regulation of Sirtuin-3, which in turn inhibits eccentric exercise-induced mitochondrial oxidative stress and secondary inflammation in the skeletal muscle.
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The level of the laboratory work is an important symbol for the levels of teaching,research and management in a college.The Logistics university of the chinese people's armed police force is in a institution of transitional restructuring and need to integrate existing research laboratories in order to form a comprehensive experimental center and to build collaborative research platform.On the basis of the current situation and the necessity of a college research laboratory analysis of the Armed Police,we produce the measures and methods and discuss the purpose and significance of the integration.Through these analysis,we both provide the leaders a reference for the development of the construction plan of the hospital research laboratories,but also provide a reference for the management of the research laboratories.At last we can build the scientific research system which the university need and improve the research quality.
ABSTRACT
BACKGROUND: Ischemic preconditioning (IPC) can induce endogenous protection mechanism, which effectively prevent ischemia/reperfusion injury following organ transplantation. Cold and warm ischemia may induce ischemia/reperfusion injury of pancreas transplantation, and apoptosis of pancreatic acinar cells is one of the important reasons of pancreas graft functional defect after transplantation. Mitochondrial DNA has repair system, and its balance with mitochondrial DNA injury influences disease occurrence and outcome.OBJECTIVE: To observe the effect of IPC on apoptosis of transplanted pancreatic acinar cells, and the possible role of reactive oxygen (ROS) and mitochondrial DNA repair enzyme.METHODS: A total of 50 health, male, Sprague-Dawley rats were randomly divided into three groups: sham operated (n = 10), donors (n = 20) and recipients (n = 20). The recipients were randomly divided into ischemia/reperfusion group (IR, n = 10) and IPC group (n = 10). The sham operated group was subjected to abdominal open and close operation. IR group and IPC group received establishment of diabetic model by streptozotocin injection. IR rats received whole pancreatic-duodenal transplantation alone. IPC rats received whole pancreatic-duodenal transplantation exposed ischemic preconditioning with 5 minutes ischemia and 5 minutes reperfusion twice. All grafts were keep with warm ischemia time 15 minutes and cold ischemia (in 4 ℃ UW preservation solution) time 180 minutes. Twelve hours after reperfusion, serum amylase, blood glucose, Caspase-3, -9 activity were detected. Pancreatic acinar cell apoptosis was measured by flow cytometry. Mitochondrial cross-membrane potential (Δψ) was measured by monitoring the fluorescence spectrum of rhodamine 123. Mitochondrial H2O2 generation was determined using dichlorofluorescein as a probe. 8-oxodG in mitochondrial DNA (mtDNA) was measured with HPLC system. Release of cytochrome C, phosphorylation of Akt and mitochondrial OGG1 protein expression were determined by Western-blotting. RESULTS AND CONCLUSION: The ischemia preconditioning can relieve the pancreatic acinar cell apoptosis in pancreas graft and relieve IR injury by decreasing mitochondrial oxidative stress, mtDNA injury, and increasing phosphorylation of Akt and mitochondrial OGG1 expression.