ABSTRACT
Sepsis is an important cause of acute kidney injury (AKI). About 60% of sepsis patients will develop AKI. At present, the standard of clinical diagnosis of AKI is still based on the changes in serum creatinine and urine volume. Because of its lag in time, it may lead to delay in treatment and increase the mortality. To find a new biomarker similar to "troponin" for the diagnosis of AKI, and to achieve the early diagnosis and prevention of AKI, is of great significance to reduce the mortality of AKI. In recent years, it has been found that tissue inhibitors of metalloproteinase-2 (TIMP-2) and insulin-like growth factor-binding protein 7 (IGFBP7) can be used for early diagnosis of sepsis associated-acute kidney injury (SA-AKI). They also have important values in risk stratification, prognosis judgment, intervention and other aspects of SA-AKI. In this paper, the research progress of the application of TIMP-2 and IGFBP7 in SA-AKI is reviewed.
ABSTRACT
Objective To investigate the expression of MMP-2 and TIMP-2 during the course of traumatic PVR treated with GM6001 and without GM6001,and to explore the potential role of MMP-2 and TIMP-2 during the course of traumatic PVR and to evaluate the effect of GM6001 on traumatic PVR prevention and treatment.Methods 360 SD rats were divided randomly into three groups: normal control group,the traumatic PVR group,the traumatic PVR treated with GM6001 group.The normal control group was intravitreous injected with normal saline.The traumatic PVR group was intravitreous injected with the PRP.The traumatic PVR treated with GM6001 group was intravitreous injected with the PRP and GM6001.The expression of MMP-2 and TIMP-2 were qualitativly and semiquantitativly analyzed with immunohistochemistry on day 1,3,7,14,21 and 28.Results 1.The results of immunohistochemistry showed that the expression of MMP-2,TIMP-2 was mainly located in the photoreceptor cells layer,out plexiform layer,inner plexiform layer and nerve fiber layer.2.The expression of MMP-2 in the normal group and the traumatic PVR treated with GM6001 group was weak at all time.The differences were statistical significance as compared with the normal group and the traumatic PVR treated with GM6001 group(P
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Objective To evaluate the effects of adenovirus mediated gene transfer of TIMP 2 and PTEN on invasion of human U87 glioma cells in vitro . Methods U87 cells were transinfected with AdTIMP 2 and AdPTEN in vitro . The mRNA and protein expressions of TIMP 2 and PTEN were detected with RT PCR and Western blotting, respectively. The relative activity of MMP 2 and MMP 9 was determined by gelatin zymogram, and invasion of U87 in vitro was observed using Boyden chamber. Results Gene and protein expressions of PTEN and TIMP 2 were shown to be up regulated when U87 was transinfected with AdPTEN and AdTIMP 2. The number of invasion cells of U87 infected with AdX gal, AdPTEN, AdTIMP 2 and PTEN+TIMP 2 was 55 64 13 27, 48 26 14 75, 35 27 10 94, 27 38 12 81, and 19 16 5 45, respectively. In vitro invasion of glioma cells was significantly inhibited after infected with AdTIMP 2 and/or AdPTEN, while the inhibition effect was more remarkable in the combined group than that in single group, and it was not consistent with the change in MMPs activity. Conclusion These results imply that combined TIMP 2 and PTEN gene therapy mediated by adenorirus may be useful for anti invasion therapy of malignant glioma
ABSTRACT
Objective To explore the effect and mechanism of fluvastatin preventing and curing restenosis. Methods 48 rabbits were randomly divided into 3 groups. In control group, rabbits were given basic food. In balloon injury group, rabbits were given basic food and balloon injury of general artery on right neck. In fluvastatin balloon group, rabbits were given basic food,ballon injury of general artery and 10mg?kg -1 ?d -1 fluvastatin. The expression of MMP-9 and TIMP-2 of mRNA was detected at 3, 7, 14 and 30 days after injury respectively by method of in site hybridization. Results There was little expression of MMP-9 and TIMP-2 mRNA in control group, and the expression of MMP-9 and TIMP-2 mRNA in middle membrane of blood vessels began at 3 days after blood injury, and reached maximum at 7 days after injury. There was a little expression of MMP-9 and TIMP mRNA in inner membrane of blood vessels at 14 and 30 days after injury, and MMP-9 expression significantly decreased after the fluvastatin interference(P