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Excretory Function of Intestinal Tract Enhanced in Kidney Impaired Rats Caused by Adenine

机译:腺嘌呤致肾脏损害大鼠肠道功能的排泄功能

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摘要

The main aim of the study was to prove the compensative effect of intestine for renal function. Rat kidney was impaired by intragastrically administrating adenine (400 mg per day for 5 days). Intestinal tract was harvested and equally divided into 20 segments except cecum. Kidneys were harvested and histologically examined with hematoxylin-eosin staining kits. Uric acid, urea (BUN), and creatinine in serum were determined with assay kits, and BUN and creatinine in every intestinal segment were also determined. The results showed that adenine was able to increase uric acid level in serum from 20.98 ± 6.98 μg/mL to 40.77 ± 7.52 μg/mL and cause renal function damage with BUN (from 3.87 ± 0.62 mM to 12.33 ± 3.27 mM) and creatinine (from 51.48 ± 6.98 μM to 118.25 ± 28.63 μM) increasing in serum and with abnormally micromorphological changes in kidney. The amount of BUN and creatinine distributed in intestinal tract was positively correlated with those in blood. In impaired renal function rats, the amount of BUN (from 4.26 ± 0.21 μMole to 10.72 ± 0.55 μMole) and creatinine (from 681.4 ± 23.3 nMole to 928.7 ± 21.3 nMole) distributed in intestinal tract significantly increased. All the results proved that intestinal tract had excretory function compensative for renal function.
机译:该研究的主要目的是证明肠对肾脏功能的补偿作用。胃内给予腺嘌呤(每天400mg,持续5天)会损害大鼠肾脏。收集肠道并将其除盲肠外平均分为20个部分。收获肾脏,并用苏木精-伊红染色试剂盒进行组织学检查。用检测试剂盒测定血清中的尿酸,尿素(BUN)和肌酐,还测定每个肠段中的BUN和肌酐。结果表明,腺嘌呤能够将血清中的尿酸水平从20.98±6.98μg/ mL增加到40.77±7.52μg/ mL,并导致BUN(从3.87±0.62 mM升高到12.33±3.27 mM)和肌酐(从51.48±6.98μM增至118.25±28.63μM),血清中肾组织形态异常改变。肠道中BUN和肌酐的分布与血液中的正相关。在肾功能受损的大鼠中,在肠道中分布的BUN(从4.26±0.21nMole至10.72±0.55μMole)和肌酐(从681.4±23.3 nMole至928.7±21.3 nMole)的量显着增加。所有结果证明肠道具有补偿肾脏功能的排泄功能。

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