The effects of compound centella formula on OxInflammation and silent information regulator 1 in a high-fat diet/streptozotocin-induced diabetic kidney disease rat model.
The effects of compound centella formula on OxInflammation and silent information regulator 1 in a high-fat diet/streptozotocin-induced diabetic kidney disease rat model.
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DOI：
10.3892/etm.2021.10394
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发表时间：
2021-09
影响因子：
2.7
通讯作者：
Jin QY
中科院分区：
文献类型：
--
作者：
Zhu Q;Li XH;Chen HY;Jin QY
中药复方积雪草（CCF）治疗糖尿病肾病（DKD）临床有效，但确切机制尚不清楚。本研究旨在探讨CCF对链脲佐菌素（STZ）诱导的糖尿病大鼠氧化炎症和沉默信息调节因子1（SIRT 1）水平的影响。将SD大鼠分为CCF组、氯沙坦组、糖尿病对照组（DC）和正常对照组（NC），每组7只。除NC外，所有亚组大鼠均喂饲高脂饲料112天，并在第29天接受单次腹腔注射35 mg/kg STZ。在第112天处死所有大鼠。采用高效液相色谱法分析CCF中积雪苷、甘草苷和雷公藤内酯醇的含量（分别为0.3400、0.0640和0.0001 mg/ml）。测定空腹血糖、尿蛋白/肌酐比值、血清肌酐和血尿素氮。采用过碘酸希夫染色、H&E染色及透射电镜观察肾脏病理改变。采用逆转录-定量PCR、免疫印迹和免疫组织化学方法检测SIRT 1在肾组织中的mRNA和蛋白表达水平。通过测定肾组织中超氧化物歧化酶（SOD）、丙二醛（MDA）和烟酰胺腺嘌呤二核苷酸磷酸氧化酶4（NOX 4）的水平来评价氧化应激。检测肾组织中TNF-α和NF-κB p65亚单位的炎症反应。与NC组比较，DC组大鼠出现蛋白尿、SIRT 1和SOD表达降低（P<0.01），MDA、NOX 4、TNF-α和NF-κB p65表达升高（P<0.01）。CCF治疗组尿蛋白减少（P<0.01），肾损害减轻，MDA、NOX 4、TNF-α和NF-κB p65水平降低（P<0.01），SOD水平升高（P<0.05），SIRT 1 mRNA和蛋白表达水平升高（P<0.01）。目前的研究表明，CCF通过抑制OxInflammation和上调SIRT 1有效地保护肾脏免受糖尿病的影响。
The Chinese decoction compound centella formula (CCF) is clinically effective against diabetic kidney disease (DKD), but the exact mechanism remains unclear. The present study aimed to investigate the effects of CCF on OxInflammation and silent information regulator 1 (SIRT1) levels in rats with streptozotocin (STZ)-induced diabetes. Sprague-Dawley rats were divided into CCF, losartan, diabetic control (DC) and normal control (NC) groups (n=7). Except for the NC, all subgroups of rats were fed a high-fat diet for 112 days and received a single intraperitoneal injection of 35 mg/kg STZ on day 29. All rats were sacrificed on day 112. High-performance liquid chromatography was performed to analyse asiaticoside, astragaloside and triptolide levels in CCF (0.3400, 0.0640 and 0.0001 mg/ml, respectively). Fasting blood glucose, urine protein-to-creatinine ratio, serum creatinine and blood urea nitrogen were quantified. Periodic acid Schiff staining, H&E staining and transmission electron microscopy were used to examine kidney pathological changes. The mRNA and protein expression levels of SIRT1 in renal tissues were analysed by reverse transcription-quantitative PCR, western blotting and immunohistochemistry. Oxidative stress was evaluated by measuring the levels of superoxide dismutase (SOD), malondialdehyde (MDA) and nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) in renal tissues. TNF-α and NF-κB p65 subunit in renal tissues were assessed for inflammation. Compared with the rats in the NC group, the rats in the DC group exhibited renal injury with proteinuria, decreased expression levels of SIRT1 and SOD (P<0.01) and increased levels of MDA, NOX4, TNF-α and NF-κB p65 (P<0.01). CCF treatment reduced proteinuria (P<0.01), alleviated renal damage, decreased MDA, NOX4, TNF-α and NF-κB p65 levels (P<0.01), increased SOD levels (P<0.05) and increased SIRT1 mRNA and protein expression levels (P<0.01). The present study indicates that CCF effectively protects the kidney from diabetes by inhibiting OxInflammation and upregulating SIRT1.
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影响因子：
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作者：
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