Objeetive To discuss the correlation of creatinine reduction ratio(CRR2)from posttransplant day 1 to day 2 and early graft function recovery status after kidney transplantation. Methods Clinical data of 80 patients after renal transplantation from Jan 2005 to Mar 2007 were retrospectively analyzed.Patients were divided into three groups according to the post-operative serum creatinine level:53 patients within IGF group[cereatinine＜265.2 μmol/L by post-operative day(POD)no.5],14 patients within SGF group(creatinine＞265.2 μmol/L on POD no.5,but no need for dialysis),and 13 patients within DGF group(need for dialysis in the first week post-transplant).Then the value and 99%CI of CRRz of these three groups were calculated. Results The value of CRR2 of IGF,SGF and DGF was(46.8±14.6)%,(25.6±13.5)%and(0.7±17.7)%respectively.And CRR2 99%CI of IGF,SGF and DGF was 41%-52%,15%-36%and-14%-16 0A respectively.There was significant difference in the value of CRR2 among IGF,SGF and DGF group.So a criteria for early diagnosis of IGF,SGF and DGF by CRR2 99%C1 was established:IGF(CRR2≥40%),SGF (15%＜CRR2＜40%)and DGF(CRR2≤15%). Conclusion CRR2 has a good correlation with early graft function recovery after kidney transplantation,and can be used to predict the occurrence of SGF and DGF.

ObjectiveTo examine the protective mechanism of wogonin in SH-SY5Y cells cultured in the conditioned media with lipopolysaccharide （LPS）-induced BV-2 microglia. MethodBV-2 microglia were divided into the blank group， LPS group， low concentration group of wogonin （4 μmol∙L^-1）， medium concentration group of wogonin （8 μmol∙L^-1）， and high concentration group of wogonin （16 μmol∙L^-1）. The LPS group was given 1 mg·L^-1 LPS， and the other three groups were treated with the corresponding concentration of wogonin for 4 h and then given 1 mg·L^-1 LPS. The conditioned media from these groups were used to cultivate SH-SY5Y cells. Cell counting kit-8 （CCK-8） was used to assess the vitality of BV-2 cells in the above groups. The contents of interleukin-6 （IL-6） and tumor necrosis factor-alpha （TNF-α） in the supernatant of BV-2 cells were determined by enzyme-linked immunosorbent assay （ELISA）. The expression of tyrosine hydroxylase （TH） and α-Synuclein （α-Syn） in SH-SY5Y cells was detected by immunohistochemical staining （IHC）. The nuclear transfer and fluorescence expression intensity of nuclear transcription factor-κB p65 （NF-κB p65） protein in SH-SY5Y cells were detected by immunofluorescence staining （IF）. Western blot was used to detect the expression of Toll-like receptor 4 （TLR4）/myeloid differentiation factor 88 （MyD88）/NF-κB pathway-related proteins in SH-SY5Y cells. ResultThe levels of IL-6 and TNF-α in the supernatant of BV-2 cells in the LPS group were significantly higher than those in the blank group （P<0.01）. Compared with those in the LPS group， the IL-6 content of BV-2 cells in the low concentration group of wogonin was statistically significantly lower （P<0.05）， whereas the IL-6 and TNF-α contents of the medium and high concentration groups of wogonin were statistically lower （P<0.05，P<0.01）. The IL-6 and TNF-α contents in the high concentration group of wogonin decreased most significantly （P<0.01）， and the intervention effect was the best. Compared with that in the blank group， the expression of α-Syn protein in SH-SY5Y cells cultured with conditioned media in the LPS group was significantly increased， and the expression of TH protein was significantly decreased （P<0.05）. Compared with that in the LPS group， α-Syn protein expression in the medium and high concentration groups of wogonin showed a decreasing trend （P<0.05， P<0.01）. TH protein expression was increased in the low， medium， and high concentration groups of wogonin （P<0.05， P<0.01）. Compared with the blank group， NF-κB p65 protein gradually accumulated into the nucleus， and the fluorescence expression intensity was significantly enhanced （P<0.01）. Compared with the LPS group， the NF-κB p65 protein was gradually dispersed outside the nucleus， and the fluorescence expression intensity was gradually weakened in all concentration groups of wogonin. The fluorescence intensity in the high concentration group of wogonin was significantly reduced （P<0.01）. Compared with those in the blank group， the expression levels of TLR4 protein， phosphorylated（p）-NF-κB p65 protein， and MyD88 protein in the LPS group were significantly increased （P<0.05， P<0.01）. Compared with those in the LPS group， the expressions of TLR4 protein， p-NF-κB p65 protein， and MyD88 protein in the medium concentration group of wogonin were all significantly decreased （P<0.05， P<0.01）. The expressions of TLR4 protein， and MyD88 protein in the high concentration group of wogonin were significantly decreased （P<0.05， P<0.01）. ConclusionWogonin may regulate the TLR4/MyD88/NF-κB signaling pathway to inhibit the release of LPS-induced inflammatory factors in BV-2 microglia and protect SH-SY5Y cells， thereby reducing inflammation and achieving neuroprotective effects.

ObjectiveTo investigate the effect of baicalein （BAI） on SH-SY5Y cell injury in lipopolysaccharide （LPS）-activated BV-2 cells conditioned medium and its mechanism. MethodThe BV-2 cells were activated with 1 mg∙L^-1 of LPS to establish the conditioned medium of the LPS group， and a blank group and groups of BAI with low， medium， and high concentrations （4， 8， 16 μmol∙L^-1） were established. SH-SY5Y cells were cultured with the conditioned medium of each group. The cell viability of BV-2 cells in each group after the intervention was determined by cell counting kit-8 （CCK-8）. The content of tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6）， and interleukin-1β （IL-1β） in the supernatant of BV-2 cells in each group was determined by enzyme-linked immunosorbent assay （ELISA）. The protein expression of α-synuclein （α-syn） and tyrosine hydroxylase （TH） in SH-SY5Y cells was observed by immunohistochemical （IHC） staining， and the nuclear transfer of nuclear factor kappa-B p65 protein （NF-κB p65， p65） in SH-SY5Y cells was observed by immunofluorescence （IF）. The protein expression of Toll-like receptor 4（TLR4）， p65， phosphorylated p65 （p-p65）， and Myeloid differentiation factor 88 （MyD88） in SH-SY5Y cells was observed by Western blot. ResultAs compared with the blank group， the viability of BV-2 cells in the LPS group was significantly decreased （P<0.01）， and the content of TNF-α， IL-6， and IL-1β in the cell supernatant was significantly increased （P<0.01）. As compared with the LPS group， the cell viability was significantly increased in groups of BAI with low， medium， and high concentrations （P<0.01）， and TNF-α in the cell supernatant was significantly decreased （P<0.01）. The content of IL-6 in the cell supernatant was decreased in the BAI group with high concentration （P<0.05）， and the content of IL-1β in the cell supernatant was significantly decreased in the BAI groups with medium and high concentrations （P<0.01）. The results of conditioned medium cultured SH-SY5Y cells showed that as compared with the blank group， the protein expression of p65 in the LPS group entered into the nucleus and accumulated， and the protein expression of TH was significantly decreased （P<0.01）， while that of α-syn， TLR4， MyD88， and p-p65 was increased （P<0.05， P<0.01）. Compared with the LPS group， the protein expression of p65 in SH-SY5Y cells in BAI groups with low， medium， and high concentrations gradually dispersed into the cytoplasm and had the enhanced protein expression of TH （P<0.01） but the lowered protein expression of α-syn （P<0.01）. The protein expression of TLR4， MyD88， and p-p65 was decreased in the BAI group with high concentration （P<0.05， P<0.01）， the protein expression of p-p65 and MyD88 was decreased in the BAI group with medium concentration， and the protein expression of MyD88 was decreased in the BAI group with low concentration （P<0.05）. There was no significant difference in the protein expression of p65 among groups. ConclusionBAI can inhibit the activation of BV-2 cells， thereby inhibiting the inflammatory response caused by LPS and further inhibiting the damage of inflammation to SH-SY5Y cells. The mechanism may be related to the regulation of the TLR4/MyD88/NF-κB signaling pathway and reduction of the inflammatory response， thus playing a neuroprotective role.