| Serious endotoxicemia can cause infectious shock and multiple organ dysfunctions, and among which kidney is the most common to be involved. The mechanism of organ dysfunction caused by endotoxicemia is complicated. Presently , it is concerned more and more on cytokines and inflammatory factor. It' known that many cytokines play a role in the inflammatory reaction in endotoxicemia. NF -κB, as a transtranscript modifier of cytokines, work significantly in endotoxic shock. The anti - inflammatory system must be startup and participate in tissue repair while the body undergoes inflammatory injury. TGF - β1 is paid more and more attention as anti - inflammatory factor. In this study this two factor are detected to manifest the mechanism of renal injury in endotoxicemia.Materials and Methods1.Establishment of animal model: 80 healthy big rats while 7 - day old was randomly redistributed to control group and endotoxin group. The rats were injected 0. 9% Natrichloridii for 0. 1 ml into abdominal cavity and LPS for 5mg/kg in endotoxin group.2. Ten rats from each group were killed after 1,4,8,12 hours, kidneys were fixed in situ with 4% formaldehyde/PBS. Three renal tissues about 1mm3 were got from each animal and fixed with glutaraldehyde and osmic acid.3. The varieties of NF - κB and TGF - β1 were detected by immunohisto-chemistry.4. The changes of renal ultrastructure were observed by electron microscopy.5. Statistical analysis: Data were expressed as mean SD values. Results were compared with Dunnett t test. P < 0.05 was statistical significance.Result1. The changes of renal ultrastructure by electron microscopy: in electron microscopy, the fuse of foot process was reduced in epithelia, but the change of endodermis cells were not obvious. In the chondriosome of renal tubule cells, the vacuole formed. The brush border was not changed evidently. On 12 hour, the fuse of foot process was clearly. The ridge of chondriosome in endodermis cells ruptured, the vacuole denaturalization. The chondriosome in renal tubule cells was dilation to form large vacuole.2. the varieties of NF - κB in kidney: the NF - κB in kidney mainly lies in renal tubule cells, the values in LPS group was higher than that in controlled group in each spot. The difference had statistical significance.3. the varieties of TGF - β1 in kidney: the TGF - β1 in kidney mainly lies in renal tubule cells, the value in LPS group was higher than that in controlled group in 12 - hour spot. The difference had statistical significance.DiscussionSerious endotoxicemia can cause multiple organ dysfunctions or failure. Kidney is the most common organ to be involved. Present study showed the mass release of inflammatory factors and the succedent waterfall reactions were one of the important mechanisms among the complicated pathological processes caused by endotoxin. It caused the obstacle of microcirculation,anoxic condition of tissue and cell,loss control of inflammatory reaction and lead to MODS/MOF. It' s been known that TNF - a,IL - 1,IL -6 ,IL -8 ,ICAM ,iNOS were all involved in the multiple organ failure caused by endotoxicemia. And the transcription of all the factors needed the modulation of NF - KB. In the study we found NF -KB was mainly expressed more in renal tubule when the renal injury occurred by endotoxicemia,suggesting when endotoxicemia caused renal failure, it involvedthe renal tubule. The sevious the renal injury, the more expression of NF -saying NF -κB might modify the transcription of several inflammatory factors. TGF - β1 is a kind of anti - inflammatory factor, taking part in the repair of inju-ryd tissue. In this study we also found that at the same time of renal injury, the expression of TGF -β1 in renal tubule was also increased. That meant TGF - β1 worked in renal repair. The increase of TGF-β1 lagged the increase of NF -κB. That was because the activation of anti - inflammatory factor was behind the action of inflammatory factor. This study provides the theory base an... |
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