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Early diagnosis of acute rejection is of significance for the protection of renal allograft function. Pathological puncture biopsy is the gold standard for the diagnosis of acute rejection of renal allografts. Nevertheless, it may provoke multiple complications, such as bleeding, infection and renal parenchymal injury, which limit its widespread application. In recent years, the sensitivity of contrast-enhanced ultrasound in the diagnosis of acute rejection has been constantly improved. Ultrasound-targeted microbubble technique has further enhanced the diagnostic specificity of contrast-enhanced ultrasound, making it possible to replace pathological puncture biopsy. Besides, in the field of acute rejection treatment, microbubble ultrasonic cavitation may promote local delivery of immunosuppressants by inducing sonoporation and exhibit anti-rejection effect. In this article, the application of contrast-enhanced ultrasound in the diagnosis and treatment of acute rejection after kidney transplantation was reviewed, aiming to provide reference for widespread application of contrast-enhanced ultrasound in kidney transplantation.
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Objective To investigate the effect and mechanism of interleukin (IL)-17C in mice undergoing kidney transplantation. Methods The life-supporting kidney transplantation mice models were established using Balb/c (H-2Kd) mice as the donors, IL-17C gene knock out (IL-17CKO) mice (knockout group) and C57BL/6J(H-2Kb) mice (wild group) were chosen as the recipients. The postoperative body mass and survival time of mice were statistically compared between two groups. Pathological examination of the kidney graft was performed by using hematoxylin-eosin (HE) staining and periodic acid-Schiff (PAS) staining. The expression levels of granzyme B, interferon (IFN)-γ, tumor necrosis factor (TNF)-α, IL-6 and IL-1β messenger ribonucleic acid (mRNA) in the kidney graft tissue were quantitatively measured by reverse transcription polymerase chain reaction (RT-PCR). The proportion of inflammatory cell infiltration in the kidney graft tissue was detected by flow cytometry. Results In the knockout group, the survival time of mice after kidney transplantation was significantly shorter than that of the wild mice (P=0.031). The body mass was more evidently decreased in the knockout group with no statistical significance from that in the wild group. Pathological examination demonstrated that the kidney graft injury in the knockout group was significantly worse than that in the wild group. The mRNA expression levels of granzyme B, IFN-γ, TNF-α, IL-6 mRNA in the knockout group were significantly up-regulated compared with those in the wild group (all P < 0.01). The mRNA expression level of IL-1β showed a decreasing trend with no statistical significance (P=0.16). Flow cytometry analysis revealed that the infiltration of CD45+CD11b+Ly6G+ neutrophil and CD45+CD11b+Ly6Chi monocyte in the kidney graft of knockout mice was significantly higher compared with that of the wild mice (P < 0.05, P < 0.01), whereas the infiltration of CD45+Ly6ChiF4/80+ macrophage did not significantly differ between two groups (P > 0.05). Conclusions IL-17C participates in the regulation of inflammatory response after kidney transplantation. It can alleviate acute rejection and improve the survival of kidney graft by down-regulating the expression of pro-inflammatory cytokines and infiltration of inflammatory cells.
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Objective To detect the damage of hippocampal neurons and the changes in inflammatory cytokines in rats after cerebral ischemia-reperfusion(I/R)and compare the expressions of IL-1β,IL-6 and TNFαin hippocampal DG,CA1 and CA3 subregions.Methods The focal cerebral I/R model was induced by an intraluminal filament embolism.The SD rats were randomly divided into the sham-operated group(SHAM group)and the middle cerebral artery occlusion-reperfusion group(MCAO group).HE staining was employed to detect the damage to hippocampal DG, CA1 and CA3 subregions.The expression levels of IL-1β, IL-6 and TNFα were detected by immunofluorescence assay.Results Compared with SHAM group,hippocampal DG,CA1 and CA3 subregion neurons in MCAO group were severely damaged, with occurred inflammatory cell infiltration,and a large amount of neurons apoptosis, and the expressions of IL-1β, IL-6 and TNFαin each subregion increased significantly.At the same time, in MCAO group, the expression of inflammatory cytokines in CA1 subregion was more significant than that in DG and CA 3 subregions(P<0.05).Conclusion Cerebral I/R could cause neuronal damage, inflammatory cell infiltration, and neuronal apoptosis in the DG, CA1 and CA3 subregions of the hippocampus and increase the release of inflammatory cytokines.In MCAO group, the expression of inflammatory cytokines in CA1 subregion of hippocampus is significantly higher than that in DG and CA 3 subregions, suggesting that CA1 region is more sensitive to I/R injury.
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0.1), while in Yunnan Baiyao group, there were significant reductions in all scores (P