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To screen the active fractions with lithagogue effects of Pyrrosia lingua from Guizhou province and preliminarily investigate its mechanism. The rats were fed with 1% ethylene glycol and 2% ammonium chloride to establish the nephrolithiasis models, which were used to evaluate thelithagogue effects of different polar fractions of P. lingua from Guizhou province. The level of urinary calcium and oxalic acid in urine, renal calcium, oxalic acid, superoxide dismutase (SOD), catalase(CAT) and malondialdehyde (MDA) in renal tissues,as well as crystalline deposit and lithogenesis in renal tissues and the levels of creatinine(Cr) and blood urea nitrogen (BUN) in the serum were detected. The effective compounds were inferred from the analysis of active fractions extract based on LC-MS technology. Petroleum ether fraction and dichloromethane fraction of P. lingua from Guizhou province can reduce renal oxalic acid and renal calcium concentration, increase urinary oxalic acid and urine calcium, with significant inhibitory effect on the formation of renal calculus in rats, significantly increase SOD and CAT activities in renal tissues, and significantly reduce MDA levels. LC-MS analysis showed that the caffeine, citric acid and tartaric acid among the compounds from petroleum ether fraction and dichloromethane fraction had lithagogue effects. Both the petroleum ether fraction and dichloromethane fraction of P. lingua from Guizhou province showed good effect on prevention and treatment of calculus in middle dose groups, and the mechanism may be associated with antioxidation, reducing calcium oxalate crystal deposition, and promoting calcium oxalatecrystal release, in addition, caffeine, citric acid and tartaric acid had lithagogue effects.
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OBJECTIVE: To establish a New Zealand rabbit model of acute kidney injury induced by cisplatin. METHODS: A total of 24 male New Zealand rabbits were randomly divided into control group,low-,medium-and high-dose cisplatin group according to the body mass. Rabbits were injected with cisplatin at 0. 0,1. 0,2. 0,4. 0 mg/kg body weight by auricular vein. Rabbits in low-dose group was continuously injected for 5 days,medium-dose group was continuously injected for 3 days,and the high-dose group was injected for once per day. Rabbits in the control group did not receive any treatment. Blood was collected from the middle ear artery and 24 h urine was taken before exposure and on day 1,day 3,day 5 and day 7 of injection. The serum creatinine( Scr) and urea nitrogen( BUN) were detected by colorimetric method,and 24 h urine kidney injury molecule 1( KIM-1) was measured by enzyme-linked immunosorbent assay. Plasma platinum,24 h urinary platinum and renal platinum level were detected by inductively coupled plasma mass spectrometry.At the end of the experiment,rabbits were sacrificed and the left kidney was taken for histopathological examination.RESULTS: The body mass of rabbits of the low-,medium-and high-dose groups on day 7 after cisplatin exposure was lower than that of the control group( P < 0. 05),and lower than that of the same group before exposure( P < 0. 05). After 3 days of exposure,the Scr level in each dose group was higher than that of the control group( P < 0. 05),the Scr level on day 3and day 5 in medium-and high-dose groups were higher than that of the low-dose group( P < 0. 05). The BUN levels on day 3 and day 5 in medium-and high-dose group were higher than that of the control group and low-dose group( P <0. 05),the BUN levels on day 7 in three dose groups were higher than that of the control group( P < 0. 05). The levels of plasma platinum and 24 h urinary platinum in the three doses groups of New Zealand rabbits on day 1,day 3,day 5 and day 7 after exposure were higher than that of the control group( P < 0. 05),and were higher than the pre-treatment levels of the same group( P < 0. 05). The level of 24 h urinary KIM-1 in the meclium-dose group of New Zealand rabbits was higher than that of the control group on day 3 of exposure( P < 0. 05). The level of 24 h urinary KIM-1 in the mediumdose group of New Zealand rabbits on the 5th day after exposure was higher than that of the control group( P < 0. 05). The renal platinum levels in the three groups of New Zealand rabbits were higher than that in the control group( P < 0. 05).The pathological changes of rabbit kidney caused by cisplatin are mainly tubular dilatation,protein cast,alkalophilic and interstitial nephritis. CONCLUSION: Cisplatin can induce acute kidney injury in rabbits,and the degree of injury is dosedependent. The dose of 1. 0 mg/kg body weight continuous injection for 5 days is closely related to clinical use of cisplatin,which is recommended for model establishment.
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Diffusion tensor imaging (DTI), which responds with the diffusion of water molecules in spinal cord white matter, may be used to detect the integrity of the spinal cord fiber bundles and the pathological changes after injury. It is sensitive in acute and chronic spi-nal cord injury, such as cervical spondylotic myelopathy, multiple sclerosis, brain damage secondary spinal cord injury, spinal nerve root damage, and so on. In basic studies, DTI can reveal the microstructure and pathological changes of the injured spinal, and be correlated with behavioral assessment, which involved mice, monkeys, calves, cats, swines, dogs, and so on.
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@#Diffusion tensor imaging (DTI), which responds with the diffusion of water molecules in spinal cord white matter, may be used to detect the integrity of the spinal cord fiber bundles and the pathological changes after injury. It is sensitive in acute and chronic spinal cord injury, such as cervical spondylotic myelopathy, multiple sclerosis, brain damage secondary spinal cord injury, spinal nerve root damage, and so on. In basic studies, DTI can reveal the microstructure and pathological changes of the injured spinal, and be correlated with behavioral assessment, which involved mice, monkeys, calves, cats, swines, dogs, and so on.
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An experimental model of cerebral concussion induced by blunt force stroke in 46 guinea pigs was established. 30 out of 46 animals were unconscious immediately after stroke followed by recovery Within few minutes without any seuqel in the posttraumatic period The animals were killed at 3,6,12,24,48 and 72 hours, 1,2,3,4 weeks after injury. Within 72 hours after injury, some of axons of both the afferent and the efferent nerve fibers of the corpus callosum and the brain stem were swelling like necklace or disrupted into segments macrophage infiltration, glosis, satellitosis, pyknosis of nuclioli of neuron, lysis of nissles bodies, vascular reaction as well as the retraction of the torn ends of axon as demonstrated by the silver stain were observed in animals killed 24 and 48 hours after injury. The reaction mentioned above became milder and milder 1～4 weeks after injury. Brain contusion were produced in other 16 experimental animals. In 7 animals of control group, no change was observed