Background: To uncover the diagnostic potential of periph-eral blood microRNA-200b (miRNA-200b) in renal intersti-tial injury in diabetic nephropathy (DN) patients.Methods: A total of 50 diabetes subjects, 50 mild DN sub-jects, 50 moderate-severe DN subjects and 50 healthy sub-jects were included. Peripheral blood level of miRNA-200b in every subject was detected by reverse transcriptase-poly-merase chain reaction (RT-PCR). Serum levels of renal function indicators were determined by enzyme-linked immunosorbent assay (ELISA). Meanwhile, relative levels of fibrosis damage indicators were examined by chemilumi-nescent immunoassay. Diagnostic potentials of miRNA-200b in diabetes, mild DN and moderate-severe DN were assessed by depicting receiver operating characteristic (ROC) curves.Results: Peripheral blood level of miRNA-200b was higher in DN subjects than diabetes subjects without vascular complications, especially moderate-severe DN patients. Peripheral blood level of miRNA-200b in DN subjects was negatively correlated to relative levels of serum creatinine, urinary nitrogen, cystatin, TGF-B, CIV and PCIII. ROC curves demonstrated diagnostic potentials of miRNA-200b in mild and moderate-severe DN.Conclusions: Peripheral blood level of miRNA-200b is closely linked to the degree of renal interstitial injury in DN patients. MiRNA-200b may be a vital indicator in predict-ing the development of DN.

慢性肾脏病(chronic kidney diseases,CKD)进展到终末期,往往需要肾脏替代治疗.血液透析(hemodialysis,HD)是目前主要的肾脏替代方式之一.我国的血液透析主要在医疗机构进行,患者每周需要到医院接受2～3次血液透析.这就意味着患者及其家庭需要承担非常大的人力、物力及财力负担.然而,多数患者经济收入不高,导致其常常因担忧花费而处于焦虑的状态;同时,患者刚进入血液透析状态时,因自身的血透知识、经验相对匮乏,加上需要应对血液透析所造成的自己及家庭生活改变,很多患者在透析过程中普遍表现出不同程度的焦虑,甚至抑郁状态[1].掌握患者在血液透析过程中焦虑情绪和抑郁状态变化规律,发现其影响因素,为更好的照顾患者有重要的现实意义.本文就新入血透患者展开心理状态调查,观察提前血管通路准备对其透析起始阶段的心理状态影响,总结出目前社会状态下患者心理状态变化的普遍规律,增加医患沟通,为更好的服务终末期血液透析患者提供指导.

In order to explore the mechanism of Extract Gingko biloba (EGb761) inhibiting vascular calcification in rats with chronic kidney disease (CKD) through ROS-NF-kappa B signaling pathway, adult male healthy SD (Sprague Dawley) rats were selected as the research objects. Animal models were constructed and randomly divided into control group, high phosphorus-induced residual renal vascular calcification model group (HPIAC group), and EGb761 intervention calcification group. Samples were collected from each group of rats, and the renal function, aortic calcification, and the expression of related proteins were detected by Western blot. The results showed that the contents of urea nitrogen, creatinine, and phosphorus in calcification model group increased significantly, with significant statistical difference (P < 0.05), but did not decrease significantly after intervention with EGb761. In the comparative analysis of calcium content in aorta of rats in each group, it was found that the calcium content of abdominal aorta in model group was significantly higher than that in control group. After the intervention of EGb761, the calcium content of abdominal aorta was significantly decreased, with significant statistical difference (P < 0.05). Western blot was used to detect the expression levels of NF-kappa B (nuclear factor-kappa B) P65, cbf alpha 1 (core binding factor-alpha 1), and alpha-SM (a-smooth muscle) actin in thoracic aorta of rats in each group. It was found that the expression levels of NF-kappa B p65 and cbf alpha 1 in thoracic aorta of rats in HPIAC group increased significantly, while the expression of alpha-SM actin decreased significantly, with significant statistical difference (P < 0.05). After the intervention of EGb761, the change of the protein was alleviated obviously, with significant statistical difference (P < 0.05). Therefore, through this study, it was found that EGb761 can partially alleviate the calcification of chronic renal failure (CRF) caused by high phosphorus by interfering with the expression of NF-kappa B p65 protein in rat thoracic artery. Although there are some shortcomings in the experiment, it still provides experimental basis for the treatment of CRF in the later clinical stage. (C) 2019 The Author(s). Published by Elsevier B.V. on behalf of King Saud University.

Objective: We sought to investigate the effect of variations in pH on vascular calcification (VC) in rats with chronic kidney disease (CKD) and the expression of Runt-related transcription factor 2. Methods: A total of healthy male Sprague-Dawley rats of a clean grade were randomly stratified into a control group, CKD group, CKD with VC (CKD+VC) group, acid intervention (CKD+VC+AC) group, and alkaline intervention (CKD+VC+AC) group. Rat models with CKD, chronic metabolic acidosis, and chronic metabolic alkalosis were established. Rat arterial pH values and HCO3- concentrations were detected by blood gas analysis. Serum creatinine (SCR) and urea nitrogen (BUN) content were detected by automatic biochemical analysis. Calcium content was determined by o-cresol oxime complex ketone colourimetry. The calcification condition of rat thoracic aorta and Runt-related transcription factor 2 expression were detected by Von Kossa staining and immunohistochemistry, respectively. Results: The levels of SCR and BUN were much higher in the CKD group, CKD+VC group, CKD+VC+AC group, and CKD+VC+BC group than in the control group (P<0.05). Separately, pH level and HCO3- concentration results were much lower in the CKD+VC+AC group than in the CKD+VC group (P<0.05) but were much higher in the CKD+VC+BC group than in the CKD+VC group (P<0.05). Also, the calcium contents of the thoracic aorta were significantly higher in the CKD+VC and CKD+VC+BC groups than in the control group, much lower in the CKD+VC+AC group than in the control group, and much higher in the CKD+VC+BC group than in the control group. (P<0.05). There were many brown-black calcium deposits noted in the media layer of the thoracic aorta of rats in the CKD+VC group and CKD+VC+BC group (P<0.05), while no such findings were observed in the control group, CKD group, or CKD+VC+AC group (P<0.05); further, the level of brown-black calcium deposition in the media layer of the thoracic aorta was much higher in the CKD+VC+BC group than in the CKD+VC group (P<0.05). Finally, the CKD+VC group and CKD+VC+BC group had significantly higher RUNX2 immunohistochemical scores than did the control group or CKD group (P<0.05), while the RUNX2 immunohistochemical scores were much lower in the CKD+VC+BC but much higher in the CKD+VC+BC group than in the CKDD+VC group (P<0.05). Conclusions: An acidic pH environment inhibits the occurrence of VC in rats with CHD and an alkaline environment promotes VC in rats with the same, which may be achieved by regulating RUNX2 expression.

Acute kidney injury (AKI) is a clinical syndrome associated with high rates of morbidity and mortality. It has previously been reported that stem cells may be considered a potential therapeutic strategy for the treatment of AKI. The present study aimed to determine whether administration of urine‑derived stem cells (USCs) to rats with ischemia/reperfusion (I/R)‑induced AKI could improve renal function. USCs were isolated and cultured from 8 healthy men. Subsequently, USCs transduced with green fluorescent protein were mixed with hydrogel and were injected into rats with renal I/R injury. Renal tubular injury, proliferation and apoptosis were detected in the I/R model. Hematoxylin and eosin staining was used to detect the morphological of kidney injury. Immunohistochemistry and TUNEL kits used to evaluate the proliferation and apoptosis of the I/R model. The results demonstrated that USCs could be detected in the tubular epithelial lining of the rats and administration of USCs was able to improve renal function in the I/R model. The USCs‑treated group exhibited significantly reduced serum creatinine and blood urea nitrogen levels, decreased tubular injury score, an increased number of proliferating cells and a decreased number of apoptotic cells. Compared with the control group, the mRNA expression levels of the anti‑inflammatory factors interleukin (IL)‑10 and transforming growth factor‑β1 were significantly upregulated, whereas the expression levels of the proinflammatory factors interferon‑γ and IL‑1β were significantly reduced in the USCs‑treated group. These findings suggested that USCs may promote kidney repair and improve function following ischemic AKI, which may be useful in treating human kidney disease.

Background Diabetic nephropathy is one of the most serious complications in patients with diabetes. At present, there are no satisfactory treatments available for diabetic nephropathy. Stem cells are currently the main candidates for the development of new treatments for diabetic nephropathy, as they may exert their therapeutic effects mainly through paracrine mechanisms. Exosomes derived from stem cells have been reported to play an important role in kidney injury. In this article, we try to investigate whether exosomes retrieved from urine stem cells could itself prevent diabetic nephropathy at an early stage in vivo and in vitro. Methods Exosomes from conditioned medium of urine-derived stem cells (USCs-Exo) were isolated using ultrafiltration-combined purification methods. USCs-Exo were then verified by morphology, size, and specific biomarkers using transmission electron microscopy, tunable resistive pulse sensing analysis, and western blotting. After establishment of the streptozotocin-induced Sprague–Dawley rat model, the effects of USCs-Exo on kidney injury and angiogenesis were observed via weekly tail intravenous injection of USCs-Exo or control until 12 weeks. In vitro, podocytes cultured in high-glucose medium were treated with USCs-Exo to test the protective effect of USCs-Exo on podocytic apoptosis. Meanwhile, the potential factors in promoting vascular regeneration in USCs-Exo and urine-derived stem cell conditioned medium were investigated by enzyme-linked immunosorbent assay. Results Urine-derived stem cells were cultured and were verified by positive markers for CD29, CD73, CD90 and CD44 antigens, and negative markers for CD34, CD45 and HLA-DR. USCs-Exo were approximately 50–100 nm spherical vesicles, and the specific markers included CD9, CD63 and CD81. Intravenous injections of USCs-Exo could potentially reduce the urine volume and urinary microalbumin excretion, prevent podocyte and tubular epithelial cell apoptosis, suppress the caspase-3 overexpression and increase glomerular endothelial cell proliferation in diabetic rats. In addition, USCs-Exo could reduce podocytic apoptosis induced by high glucose in vitro. USCs-Exo contained the potential factors, including growth factor, transforming growth factor-β1, angiogenin and bone morphogenetic protein-7, which may be related with vascular regeneration and cell survival. Conclusion USCs-Exo may have the potential to prevent kidney injury from diabetes by inhibiting podocyte apoptosis and promoting vascular regeneration and cell survival.

Chronic kidney disease is associated with higher risk of cardiovascular complication and this interaction can lead to accelerated dysfunction in both organs. Renalase, a kidney-derived cytokine, not only protects against various renal diseases but also exerts cardio-protective effects. Here, we investigated the role of renalase in the progression of cardiorenal syndrome (CRS) after subtotal nephrectomy. Sprague-Dawley rats were randomly subjected to sham operation or subtotal (5/6) nephrectomy (STNx). Two weeks after surgery, sham rats were intravenously injected with Hanks' balanced salt solution (sham), and STNx rats were randomly intravenously injected with adenovirus-β-gal (STNx+Ad-β-gal) or adenovirus-renalase (STNx+Ad-renalase) respectively. After 4 weeks of therapy, Ad-renalase administration significantly restored plasma, kidney and heart renalase expression levels in STNx rats. We noticed that STNx rats receiving Ad-renalase exhibited reduced proteinuria, glomerular hypertrophy and interstitial fibrosis after renal ablation compared with STNx rats receiving Ad-β-gal; these changes were associated with significant decreased expression of genes for fibrosis markers, proinflammatory cytokines and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase components. At the same time, systemic delivery of renalase attenuated hypertension, cardiomyocytes hypertrophy and cardiac interstitial fibrosis; prevented cardiac remodelling through inhibition of pro-fibrotic genes expression and phosphorylation of extracellular signal-regulated kinase (ERK)-1/2. In summary, these results indicate that renalase protects against renal injury and cardiac remodelling after subtotal nephrectomy via inhibiting inflammation, oxidative stress and phosphorylation of ERK-1/2. Renalase shows potential as a therapeutic target for the prevention and treatment of CRS in patients with chronic kidney disease.

OBJECTIVE:To determine the incidence, causes and prognosis of pregnancy-related acute kidney injury (PR-AKI) in Chinese women.METHODS:From July 2004 to February 2013, 18,589 women of Han ethnicity who attended the Obstetrics and Nephrology Department of our tertiary hospital were investigated, and individuals meeting the PR-AKI criteria were included in the analysis. The WanFang, Chinese Science Journal, Chinese Knowledge, MEDLINE, EMBASE and Cochrane library databases were searched, and literature describing PR-AKI diagnoses with Chinese women as study subjects and a sample size of ≥5 were included.RESULTS:The incidence of PR-AKI was 0.1183% (22/18,589). Hemorrhagic shock (31.8%) and pre-eclampsia (severe, 18.2%) were the two most common causes of PR-AKI. Twelve women recovered completely, six women displayed persistent proteinuria and four women had an increased serum creatinine level at discharge. There were no cases of death. Twenty women demonstrated adverse pregnancy outcomes (90.9%), including eight cases of stillbirth (36.4%). In our literature review, 29 of 4,076 articles were included, and the incidence of PR-AKI in China was found to range from 0.02% to 1.84%. Pregnancy hypertension (49.2%) and postpartum hemorrhage (13.8%) were found to be the most common causes of PR-AKI in China. The prognosis improved in 81.9% of the patients, the renal function deteriorated in 4.5% of the patients and 13.6% of the patients died. The rate of stillbirth was 27.0%.CONCLUSION:The maternal condition after active treatment was good, whereas the pregnancy outcomes were generally poor. Although the incidence of PR-AKI was relatively low, this finding is noteworthy. Further studies are thus warranted to improve maternal-fetal outcomes.

Glomerular mesangial cell (MC) hypertrophy is regarded as one of the earliest pathological characteristics of diabetic nephropathy (DN), which plays a critical role in the pathogenesis of glomerulosclerosis. This study investigated the role of microRNAs (miRNAs) in MC hypertrophy due to exposure to high glucose. With a microarray, we screened the differential profiles of miRNAs in the renal cortex of DN mice, as verified by reverse transcription PCR with subsequent analysis of bioinformatics. We found miR-196a was downregulated remarkably in DN mice and increased the hypertrophy-related gene of p27kip1 in high-enrichment gene ontologies. Furthermore, transfection of the miR-196a mimic greatly inhibited the expression of p27kip1 with recovery of MC hypertrophic morphology. With flow cytometry, we also found that overexpression of miR-196a significantly reduced the percentage of G1 phase arrest in the cell cycle. Cotransfection of the miR-196a mimic with a wild type of 3′ UTR of the p27kip1 vector reduced the activity of the luciferase reporter significantly in contrast to the miR-196a mimic with a mutant of the counterpart in HEK293 cell lines, suggesting that miR-196a directly targets p27kip1. Finally, knockdown of p27kip1 with specific small interfering RNA in MCs substantially reversed MC hypertrophy induced by transfection of the miR-196a inhibitor. This study revealed that miR-196a acts as an important molecular regulator in high glucose-induced MC hypertrophy by targeting p27kip1.

Objective To know the status of work engagement and specialty identity of medical students. Methods Based on Utrecht work engagement scale (UWES) and vocational identity scale, 195 medical students and 99 non-medical students from Shanghai Jiao Tong University were investigated. Results Scores of work engagement and specialty identity of students from clinical medicine and stomatology were higher than that of students from preventive and laboratory medicine and nursing, with statistical significance. Students from clinical medicine had the highest score of specialty identity, while students from preventive and medicine had the lowest. Undergraduate students from clinical medicine had higher scores of work engagement and specialty identity than graduate students. There was a positive correlation between work engagement and specialty identity. There was no statistical significance in work engagement and specialty identity between medical and non-medical students. But medical students had higher sense of dedication, certainty, significance, self-efficacy and self-decision, with statistical significance. Conclusions The more specialty identity, the more work engagement. Work engagement and specialty identity of students in our study is not very much, but medical students had higher sense than non-medical students.

Objective:To extract stem cells through normal urine and to investigate the effects of conditioned medium(CM) from human urine derived stem cells(hUSCs)on podocyte lesion induced by high glucose. Methods:hUSCs were isolated from void-ed urine of healthy men. After identification and proliferation,hUSCs - CM was prepared. According to the different culture condi-tions,human podocytes were divided into normal glucose group,high permeability group,high glucose group(HG),and HG +hUSCs - CM(1 × ,5 × ,10 × )group. Real - time PCR was applied to detect the expression levels of synaptopodin,and human podocytes apoptosis in each group were examined by flow cytometry after cultured for 24 hours. Results:Compared with incubated in NG,the expression of synaptopodin mRNA in HG was found to decrease(vs. NG,P < 0. 05). HUSCs - CM increased the expression of podocytic synaptopodin mRNA(vs. HG,P < 0. 05). Early Podocytes apoptosis rate was mildly higher in HG group than in NG group(P < 0. 05),hUSCs - CM reduced the early podocytes apoptosis in a dose - dependent manner(vs. HG,P < 0. 05). Conclu-sion:hUSCs - CM prevents podocytic apoptosis and injury induced by HG,and may be a new therapeutic method to ameliorate the progress of DKD.

目的 探讨我国妊娠相关急性肾损伤(PR-AKI)的发病率、病因及预后.方法 回顾性分析上海交通大学附属第六人民医院自2004年7月至2013年2月在产科和肾脏科住院的18 589例汉族妊娠女性,记录符合PR-AKI定义患者的临床表现和实验室检查,应用方差分析和Friedman M检验对其基线、产前和产后临床及实验室结果进行分析比较,同时统计分析PR-AKI的发病情况、病因及妊娠结局.检索中、英文数据库,纳入符合PR-AKI诊断、研究对象为中国妊娠女性且研究样本量≥10例的文献,进行相应的统计分析.结果 上海交通大学附属第六人民医院有18例患者符合PR-AKI诊断;PR-AKI患者终止妊娠前相关指标与基线水平比较,平均动脉压、血清肌酐、尿素氮、尿蛋白明显增加,血小板明显减少,差异有统计学意义(P＜0.05);患者终止妊娠7d时尿蛋白明显减少,血小板明显增加,差异有统计学意义(P＜0.05);平均动脉压、血清肌酐、尿素氮呈下降趋势,血清白蛋白呈上升趋势.PR-AKI的发生率为0.97‰,最常见的原因为重度子痫前期;13例产后7d好转,2例肾功能恶化,无死亡病例;15例妊娠结局不良(15/19,1例为双胎妊娠),6例为死胎或新生儿死亡(6/19).共检索到15 966篇文献,纳入30篇符合标准的文献进行分析:我国各地区PR-AKI的发生率为0.30％～6.82％;引起我国PR-AKI常见的病因为妊娠高血压病(48.9％)和产后出血(13.9％);PR-AKI的好转率为81.4％,病死率为13.5％,肾功能恶化率为5.1％;死胎率为26.9％.结论 关于PR-AKI研究的证据级别较低,PR-AKI值得引起重视,经积极诊治,母体预后情况较好,但妊娠结局较差.

干细胞(stem cell)是一类具有自我更新、多系分化和高度增殖功能的细胞.随着对干细胞研究的逐渐深入,人们利用SC可塑性大、体外扩增能力强、易于转染外源基因等优点,开始将干细胞应用于治疗急性及慢性肾病的研究.目前相关研究涉及到的干细胞大致可以分为胚胎干细胞、成体肾干细胞和非肾脏来源的成体干细胞,其中包含了研究最多最广泛的间充质干细胞(mesenchymal stem cell,MSC),例如骨髓间充质干细胞(bone mesenchymal stem cell,BMSC)、脐带血间充质干细胞(umbilical cord blood mesenchymal stem cells,UMSC)、脂肪源(adipose-derived mesenchymal stem cells,AMSC)等多种类型干细胞.干细胞疗法及其机制的深入研究,为干细胞再生医学应用于肾脏疾病治疗提供了具有良好前景的治疗策略.

干细胞(stem cell)是一类具有自我更新、多系分化和高度增殖功能的细胞.随着对干细胞研究的逐渐深入,人们利用SC可塑性大、体外扩增能力强、易于转染外源基因等优点,开始将干细胞应用于治疗急性及慢性肾病的研究.目前相关研究涉及到的干细胞大致可以分为胚胎干细胞、成体肾干细胞和非肾脏来源的成体干细胞,其中包含了研究最多最广泛的间充质干细胞(mesenchymal stem cell,MSC),例如骨髓间充质干细胞(bone mesenchymal stem cell,BMSC)、脐带血间充质干细胞(umbilical cord blood mesenchymal stem cells,UMSC)、脂肪源(adipose-derived mesenchymal stem cells,AMSC)等多种类型干细胞.干细胞疗法及其机制的深入研究,为干细胞再生医学应用于肾脏疾病治疗提供了具有良好前景的治疗策略.

Objective:To investigate mechanism by which miR-26b regulates high glucose-induced mesangial cells(MCs) hypertrophy,providing a novel clue for the insight into diabetic nephropathy(DN) at early stage.Methods:Applying bioinformatics to predict the candidates of miRNAs potentially targeting glycogen synthase kinase-3β(GSK3β).To verify the expressions of all of miRNAs candidates in renal cortex of db / db mice and perform pearson relavant analysis between miRNAs and GSK3βrespectively as well.The selected miRNA and GSK3β were detected in MCs exposure to high glucose condition by using real time PCR.Furthermore,GSK3β,hypertrophic gene α-SMA and Collagen IV were detected in MCs cultured in high glucose 72 hours after transfection of selected miRNA inhibitor by real-time PCR and western blot.Results:A total of 9 miRNAs candidates potentially targeting GSK3βwere screened by bioinformatics,which were miR-199a-5p,miR-128,miR-23b,miR-23a,miR 29a,miR-29c,29b,miR-26b,miR-26a.Among these candidates,miR-128,miR-23b,miR-26b,miR-29a upregulated remarkably in renal cortex in db / db mice compare with db / m controls(P < 0.05).One of these four miRNAs,namely miR-26b showing significantly negative relevance with GSK3βby person analysis(r =-0.470 29).The similar results were found in high glucose-induced MCs.The levels of GSK3β were restored partly by transfection of miR-26b inhibitor,meanwhile α-SMA and Collagen IV ameliorated accordingly in cultured MCs in high glucose conditions.Conclusion:Taken together,miR-26b might involve in the regulation of high glucose-induced MCs hypertrophy via targeting GSK3β.The current study provides a novel insight into the pathogenesis of DN at early stage.

糖尿病肾病(diabetic nephropathy,DN)是导致终末期肾衰竭(end-stage renal disease,ESRD)的主要原因,也是糖尿病患者的主要死亡原因之一.DN一旦出现临床蛋白尿(尿蛋白＞0.5 g/24 h),就会不断进展,肾小球功能将呈进行性不可逆转地下降.美国Joslin临床研究显示糖尿病患者发生蛋白尿的平均病程为17年,出现蛋白尿后平均生存期为10年左右,最终都将进入ESRD[1].DN的治疗已经成为全世界糖尿病和DN界的关注热点,但目前临床尚无有效的治疗手段能够阻止DN的发生和进展.干细胞是在动物胚胎和成体组织中具有自我更新、高度增殖和多向分化潜能的干细胞.它在一定条件下可以分化为多种功能的细胞.目前试验研究中和肾脏相关的干细胞主要有胚胎干细胞(embryonic stem cells,ESC)、成体干细胞,后者又泛指包含了间充质干细胞(mesenchymal stem cells,MSC)、内皮祖细胞(endothelial progenitor cells,EPC)、诱导多能干细胞(induced pluripotent stem cells,IPS)等多种类型干细胞.随着干细胞医学、再生医学等学科的发展,DN的治疗也有了一个全新的思路.目前有关干细胞治疗DN的报道较少,本文将对干细胞治疗DN的相关研究进展作如下综述.

Objective:To investigate mechanism by which miR-153 regulates high glucose-induced the epithelial-mesenchymal transition(EMT) in human renal proximal tubule cell(HK2),providing a novel insight into interstitial fibrosis in the process of DN.Methods:We used bioinformatics to predict the candidates of miRNAs potentially targeting Snail,followed by confirming the expressions of all of miRNA candidates in renal cortex of db/db mice;Pearson relavant analysis was performed between miRNAs and Snail respectively.We further focus on miRNA showing the most significantly negative relevance with Snail.The selected miRNA and Snail mRNA were detected in HK2 cells exposure to high glucose condition by using real-time PCR.The protein levels of Snail,E-cadherin in HK2 cells were measured 72 hours after transfection of selected miRNA mimics.Results:A total of 7 miRNA candidates potentially targeting Snail were screened by bioinformatics,which were miR-153,miR-30e,miR-30d,miR-30b,miR-384-5p,miR-30a,miR-30c.Among these candidates,miR-153、miR-30d and miR-30e down-regulated remarkably in renal cortex in db/db mice compare with db/m controls(P0.05).Pearson analysis indicated only miR-153 showing the most significantly negative relevance with Snail(r=-0.501 56).The similar results were found in high glucose-induced HK2 cells.Overexpression of miR-153 decreased the levels of Snail,whereas E-cadherin increased in cultured HK2 cells instead.Conclusion:The current study reveals that miR-153 might involve in the regulation of high glucose-mediated tubule epithelial cell EMT via targeting Snail.

炎症泛指任何组织对创伤、感染、缺血、毒素以及自身免疫等损伤因素反应而产生的各种分子与细胞的一系列相互作用过程,而胶原的沉积和组织的纤维化是炎症导致的永久性损伤的病理过程[1].邢昌赢[2]提出肾脏疾病的发生有众多炎症因子的参与,局部的炎症因子或/全身的炎症因子可以导致或加重肾脏发生和进展,同时全身性的炎症因子可以导致全身的炎症状态或者动脉粥样硬化,甚至于导致患者死亡.而老年人因为衰老引起机体各脏器技能、应激能力和维持内环境能力均低下、免疫功能减低和动脉硬化,对于炎症的抵抗能力更加低下,所以了解老年肾脏疾病的特点、研究炎症在其发病中的机制对于老年肾脏疾病非常必要.