| 摘要: |
| 目的 探讨慢性肾功能衰竭（CRF）胃肠道症状的发生机制，明确结肠是否参与CRF氧化应激的激活。方法 将30只雄性SD大鼠随机分为对照组（10只）和CRF组（20只），CRF组大鼠予以5/6肾切除建立CRF模型，对照组仅打开肾包膜后缝合。成模后10周处死大鼠，收集2组大鼠的血清及回盲瓣附近结肠组织。检测大鼠肾功能指标血尿素氮（BUN）和血清肌酐（SCr）以评估造模是否成功，检测大鼠血清及结肠组织中丙二醛（MDA）、超氧化物歧化酶（SOD）、总抗氧化能力（TAC）和8-羟脱氧鸟苷（8-OHdG）以评估氧化应激水平，检测泛素细胞色素C诱导核心蛋白酶Ⅰ（UQCRC1）mRNA和蛋白水平以评估线粒体功能。结果 与对照组相比，CRF组血清BUN及SCr水平升高，提示造模成功；CRF组血清及结肠组织中MDA水平升高（P<0.05），但2组间8-OHdG和抗氧化指标SOD、TAC差异无统计学意义（P >0.05）；CRF组结肠组织中UQCRC1蛋白水平较对照组低（P<0.05），但UQCRC1 mRNA水平与对照组相比差异无统计学意义（P >0.05）。结论 CRF大鼠的结肠组织中存在氧化与抗氧化反应失衡现象，其机制可能涉及线粒体的功能障碍。 |
| 关键词: 慢性肾功能衰竭 胃肠道功能障碍 氧化性应激 线粒体 |
| DOI：10.16781/j.0258-879x.2019.01.0043 |
| 投稿时间：2018-08-28修订日期：2018-11-22 |
| 基金项目:国家自然科学基金（81300613）. |
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| Colon participates in activation of oxidative stress in rats with chronic renal failure |
| GUO Zhi-yun1,LI He-wen2,XIA Zhen-na3,XU Jing1,DONG Rui1* |
(1. Department of Nephrology, Changhai Hospital, Naval Medical University(Second Military Medical University), Shanghai 200433, China;
2. Department of Cardiology and Nephrology, No.5 Hospital of PLA, Yinchuan 750000, Ningxia Hui Autonomous Region, China;
3. Center for Evaluation of Drug Safety, Naval Medical University(Second Military Medical University), Shanghai 200433, China
*Corresponding author) |
| Abstract: |
| Objective To explore the mechanism of gastrointestinal dysfunction caused by chronic renal failure (CRF), and to determine whether colon is involved in the activation of oxidative stress (OS) in CRF.Methods Thirty male SD rats were randomly divided into control group (n=10) and CRF group (n=20). The rats in the CRF group were treated with 5/6 nephrectomy to establish CRF model, and the rats in the control group were only sutured after opening renal capsule. The rats were sacrificed at 10 weeks after model administration, and the serums and colon tissues near ileocecal valve were collected. Blood urea nitrogen (BUN) and serum creatinine (SCr) were measured to evaluate the success of the model. Malonodialdehyde (MDA), superoxide dismutase (SOD), total antioxidant capacity (TAC) and 8-hydroxy deoxyguanosine (8-OHdG) in the serum and colon tissues were detected to evaluate the level of OS. The ubiquinol cytochrome C reductase core proteinⅠ(UQCRC1) was tested for the evaluation of mitochondrial function.Results Compared with the control group, the levels of BUN and SCr in serum of the rats in the CRF group were increased, suggesting that the model was successfully established. Compared with the control group, serum and colonic MDA levels were significantly increased in the CRF group (P<0.05); however, there were no significant differences in 8-OHdG or anti-oxidative markers (SOD, TAC) in serum or colon tissues between the two groups (P >0.05). The protein level of UQCRC1 in colon tissues was significantly reduced in the CRF group compared with the control group (P<0.05). However, there was no significant difference in the mRNA level of UQCRC1 in colon tissues between the control and CRF groups (P >0.05).Conclusion There is an imbalance between oxidation and antioxidation in the colonic tissues of CRF rats, which may be related to mitochondrial dysfunction. |
| Key words: chronic kidney failure gastrointestinal dysfunction oxidative stress mitochondria |
