保护肾脏免于纤维化，TRIB3 基因沉默的推测作用。
Protection from renal fibrosis, putative role of TRIB3 gene silencing.
机构信息
Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Department of Cardiology, Qilu Hospital of Shandong University, Ji'nan 250012, PR China; Department of Cardiology, Qilu Hospital of Shandong University, Ji'nan 250012, PR China.
Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Department of Cardiology, Qilu Hospital of Shandong University, Ji'nan 250012, PR China; Geriatrics, Qilu Hospital of Shandong University, Ji'nan 250012, PR China.
出版信息
Exp Mol Pathol. 2014 Feb;96(1):80-4. doi: 10.1016/j.yexmp.2013.12.003. Epub 2013 Dec 22.
BACKGROUND
Renal fibrosis is thought to be the common pathway in most cases of chronic kidney disease. Recently, TRIB3 was found to play an important role in progression of cardiac fibrosis in an insulin-resistant state. We investigated whether TRIB3 might participate in the pathogenesis of renal fibrosis in insulin-resistant rats.
METHODS
We randomly separated 40 male Sprague-Dawley into 4 groups for treatment (n = 10 each): control and high-fat diet (HFD) with TRIB3 siRNA adenovirus transfection, vehicle transfection or HFD alone. Insulin resistance markers were measured. Renal tissues were stained with hematoxylin and eosin, Masson's trichrome and periodic acid-Schiff.
RESULTS
Rats with HFD showed insulin resistance and TRIB3 overexpression. Upregulated TRIB3 expression could induce renal fibrosis accompanied by increased phosphorylation of extracellular signal-regulated kinase (ERK). Also, TRIB3 siRNA knockdown could ameliorate renal fibrosis, which was accompanied by decreased phosphorylation of ERK.
CONCLUSIONS
TRIB3 gene silencing can attenuate renal fibrosis for beneficial effect on the development of renal fibrosis in chronic kidney disease in rat.
背景
肾纤维化被认为是大多数慢性肾脏病的共同途径。最近，TRIB3 被发现在胰岛素抵抗状态下心脏纤维化的进展中发挥重要作用。我们研究了 TRIB3 是否可能参与胰岛素抵抗大鼠的肾纤维化发病机制。
方法
我们将 40 只雄性 Sprague-Dawley 大鼠随机分为 4 组进行治疗（每组 n = 10）：对照组和高脂肪饮食（HFD）+TRIB3 siRNA 腺病毒转染组、载体转染组或单独 HFD 组。测量胰岛素抵抗标志物。用苏木精和伊红、马松三色和过碘酸希夫染色肾组织。
结果
HFD 大鼠表现出胰岛素抵抗和 TRIB3 过表达。上调的 TRIB3 表达可诱导肾纤维化，同时细胞外信号调节激酶（ERK）磷酸化增加。此外，TRIB3 siRNA 敲低可改善肾纤维化，同时 ERK 磷酸化减少。
结论
TRIB3 基因沉默可减轻肾纤维化，对慢性肾脏病大鼠肾纤维化的发展有有益作用。
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