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文 丹.异甘草素通过 Smad3 / Arid2-IR/ NF-κB 轴改善顺铂诱导的急性肾损伤小鼠炎症反应[J].中国比较医学杂志,2020,30(6):25~30,46.
异甘草素通过 Smad3 / Arid2-IR/ NF-κB 轴改善顺铂诱导的急性肾损伤小鼠炎症反应
Effect of isoliquiritigenin on cisplatin-induced acute kidney injury in mice with inflammation through the Smad3 / Arid2-IR / NF-κB axis
投稿时间:2020-02-07  
DOI:10. 3969 / j.issn.1671-7856. 2020. 06. 004
中文关键词:  长链非编码 RNA(LncRNA)  Arid2-IR  异甘草素  急性肾损伤  炎症
英文关键词:long noncoding RNA (LncRNA)  Arid2-IR  isoliquiritigenin  acute kidney injury  inflammation
基金项目:
作者单位E-mail
文 丹 1.西南医科大学附属医院肾病内科,四川 泸州 646000
2.西南医科大学附属中医医院中西医结合研究中心, 四川 泸州 646000 
343991854@ qq.com 
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中文摘要:
      目的 研究异甘草素( ISO) 对顺铂诱导的急性肾损伤(AKI) 小鼠的作用并探讨潜在调控机制。 方法 30 只 C57BL/ 6 雄性小鼠随机分为空白对照组(NC 组),模型组(AKI 组),异甘草素药物低剂量(ISO-L)和高剂量(ISO-H)处理组,厄贝沙坦阳性对照组(Irb 组)。通过单次腹腔注射顺铂(20 mg / kg)建立 AKI 模型。在干预 过程中,NC 组和 AKI 组予以生理盐水,而 ISO-L 组和 ISO-H 组分别予以异甘草素 7. 5 mg / kg、30 mg / kg,Irb 组予以 20 mg / kg 厄贝沙坦,药物灌胃 3 d 后处死小鼠,收集血清检测肌酐、尿素氮,HE 和 PAS 染色检测肾病理改变,免疫 组化和免疫印迹法检测炎症关键因子(IL-6、IL-1β)和 Smad3、NF-κB 等关键蛋白活性,Real-time PCR 检测炎症因子和长链非编码 Arid2-IR 改变情况。 结果 与 AKI 组比,异甘草素干预能明显改善小鼠肌酐和尿素氮(P< 0. 05), 且呈浓度依赖性调节;病理染色结果显示药物干预后肾炎性细胞浸润减少,肾损伤明显改善;而炎症因子、Smad3、 NF-κB活性和长链非编码 Arid2-IR 等表达均出现显著下调(P< 0. 05),表明异甘草素可以抑制 Smad3 / Arid2-IR/ NF-κB轴的活化。结论 异甘草素可有效减轻 AKI 小鼠肾炎症反应,其机制可能与调节 Smad3 / Arid2-IR/ NF-κB 轴有关。
英文摘要:
      Objective To investigate the effects of isoliquiritigenin ( ISO) on cisplatin-induced acute kidney injury (AKI) in mice and explore the potential mechanism. Methods Thirty C57BL/ 6 male mice were randomly divided into a blank control group, model group, ISO-L and ISO-H groups and a positive control group. A single intraperitoneal injection of cisplatin (20 mg / kg) was applied to establish the AKI model. During the intervention, both blank control group and model group were treated with an equivalent volume of saline, while ISO-L group and ISO-H group were administered by gavage with 7. 5 mg / kg and 30 mg / kg ISO, respectively, while the positive control group was administered by gavage with 20 mg / kg irbesartan. After 3 days, serum was collected to determine the levels of serum creatinine ( SCr) and blood urea nitrogen (BUN). HE and PAS staining were used to detect pathological kidney changes, while immunohistochemical and western blot analyses were used to detect inflammatory cytokines’ ( IL-6 and IL-1β) expression and the activity of Smad3 and NF-κB. Real-time PCR was used to detect changes in inflammatory cytokines and long noncoding Arid2-IR. Results Compared with the model group, ISO intervention significantly reduced the SCr and BUN levels in AKI mice (P< 0. 05), in a concentration-dependent manner. Histopathological staining indicated that ISO intervention significantly reduced the infiltration of inflammatory cells and vacuolar degeneration of renal tubular epithelial cells. Furthermore, it significantly improved renal injury. Additionally, ISO significantly downregulated (P< 0. 05) inflammatory cytokines expression, the activity of Smad3 and NF-κB, and long noncoding Arid2-IR expression, suggesting that ISO inhibited the activation of the Smad3 / Arid2-IR/ NF-κB axis. Conclusions ISO effectively reduced kidney inflammation in AKI mice, possibly through regulation of the Smad3 / Arid2-IR/ NF-κB axis.
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