■研究的目的是研究纳米细菌在肾结石形成中的作用及其潜在机制。
■将90只清洁Wistar雄性大鼠随机分为阴性对照组,一个实验组,和一个干扰组。从建模的第一周结束,每周连续10次,每组随机抽取3只年夜鼠测定生化血液标志物和尿代谢。牺牲之后,通过电子显微镜和病理组织学观察肾脏的超微结构来评估肾结石的形成。最后,通过蛋白质印迹法检测肾组织中钙敏感受体(CaSR)和claudin-14蛋白的表达。
■与对照组相比,模型组大鼠肾脏总体结构发生改变。在建模的第四周,纳米细菌组的大鼠肾脏明显增大,肾体比增加,差异有统计学意义(p<0.05)。肾脏轮廓的颜色是深色的,皮肤纸浆的结构不太清楚,在皮质髓的交界处观察到淡黄色颗粒的积累。肌酐,尿酸,尿素氮,纳米细菌组大鼠的尿钙在第三周开始增加,第3周和第8周差异有统计学意义(p<0.05)。然而,第8周后,3组间差异无统计学意义。在第四个星期,我们观察到结石的形成,主要分布在肾小管及周围组织中。纳米细菌组肾结石形成率为52.4%,干扰组为27.8%,差异有统计学意义(p<0.05)。超微结构观察显示,从第四周开始,纳米细菌组的肾组织显示肾小管扩张,肾小管上皮肿胀,颗粒变性,肾小管上皮细胞的脱落和淋巴细胞浸润,和少量的钙盐晶体在肾小管。第三周,CaSR和Claudin-14蛋白在纳米细菌组中的表达增加,差异有统计学意义(p<0.05)。CaSR和Claudin-14的表达与尿钙呈正相关(p<0.05)。
■肾结石的形成始于模型建立后的第4周,晶体主要位于肾小管中。在肾结石的形成过程中,肾小管上皮细胞受损,显示颗粒状变性和少量的钙盐晶体,伴有一些肾小管开始扩张和上皮肿胀,颗粒变性,肾小管上皮细胞坏死和脱落,肾间质中的淋巴细胞浸润,和少量的钙盐晶体在肾小管中,随着时间的推移而恶化。血清肌酐,血清尿酸,尿素氮,尿钙水平从第三周开始随时间增加而增加,第八周后恢复正常。CaSR和Claudin-14蛋白的表达上调,并与24h尿钙排泄值呈正相关。
UNASSIGNED: The aim of the study was to study the role of
nanobacteria in the formation of renal calculi and the underlying mechanism.
UNASSIGNED: A total of 90 clean Wistar male rats were randomly divided into a negative control group, an experimental group, and an interference group. From the end of the first week of modelling, 10 consecutive times once a week, 3 rats in each group were randomly selected to measure the biochemical blood markers and urine metabolism. After sacrifice, the formation of kidney stones was assessed by observing the ultrastructure of the kidney by electron microscopy and pathohistology. Finally, the expression of calcium-sensitive receptor (CaSR) and claudin-14 protein in the kidney tissue was examined by western blotting.
UNASSIGNED: Compared with the control group, the gross structure of the kidney was changed in the model group. At the fourth week of modelling, the rats in the
nanobacteria group had significantly enlarged kidneys and increased kidney-to-body ratio, and the difference had statistical significance (p < 0.05). The colour of the kidney profile was dark, the structure of the skin pulp was less clear, and the accumulation of yellowish particles was observed at the junction of the cortical pulp. The creatinine, uric acid, urea nitrogen, and urinary calcium of the rats in the nanobacteria group began to increase at the third week, and the difference between the third and eighth week had statistical significance (p < 0.05). However, the difference between the 3 groups had no statistical significance after the eighth week. At the fourth week, we observed the formation of calculi, which were mainly distributed in the renal tubules and surrounding tissues. The kidney stone formation rate was 52.4% in the
nanobacteria group and 27.8% in the interference group, and the difference had statistical significance (p < 0.05). Ultrastructure observations revealed that from the fourth week, the renal tissues in the
nanobacteria group showed expanded renal tubules, swollen renal tubular epithelium, granular degeneration, shedding and lymphocyte infiltration of renal tubular epithelial cells, and a small amount of calcium salt crystals in renal tubules. At the third week, the expression of CaSR and Claudin-14 protein in the
nanobacteria group increased, and the difference had statistical significance (p < 0.05). The expression of CaSR and Claudin-14 was positively correlated with urinary calcium (p < 0.05).
UNASSIGNED: The formation of renal calculi began in the fourth week after the model was established, and the crystals were mostly located in the renal tubules. During the formation of renal calculi, the renal tubular epithelial cells were damaged, showing granular degeneration and small amounts of calcium salt crystals, accompanied by a few renal tubules beginning to expand and epithelial swelling, granular degeneration, necrosis and shedding of renal tubular epithelial cells, lymphocyte infiltration in the renal interstitium, and small amounts of calcium salt crystals in the renal tubules, which aggravated with time. The serum creatinine, serum uric acid, urea nitrogen, and urinary calcium levels increased with time from the third week and returned to normal after the eighth week. The expression of CaSR and Claudin-14 protein was upregulated and positively correlated with the 24-h urinary calcium excretion value.