Endogenous synthesis of n-3 polyunsaturated fatty acids in fat-1 transgenic mice ameliorates streptozocin-induced diabetic nephropathy
Endogenous synthesis of n-3 polyunsaturated fatty acids in fat-1 transgenic mice ameliorates streptozocin-induced diabetic nephropathy
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fat-1转基因小鼠内源合成n-3多不饱和脂肪酸可改善链佐星诱导的糖尿病肾病
DOI：
10.1016/j.jff.2018.04.010
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发表时间：
2018-06
影响因子：
5.6
通讯作者：
Bu Shi Zhong
中科院分区：
文献类型：
--
作者：
Zhang Yuan Ming;Zhang Xiao Hong;Zhu Pan;Tan Rong Hui;Zhao Jin Shun;Wang Feng;Zhang Jin Jie;Yan Wang;Xi Yang;Wan Jian Bo;Kang Jing Xuan;Zou Zu Quan;Bu Shi Zhong
虽然n-3多不饱和脂肪酸（PUFAs）在许多炎症性疾病中表现出生物活性，但其对糖尿病肾病（DN）的肾脏保护作用一直存在争议。在这里，使用fat-1转基因小鼠来研究n-3 PUFAs对链脲佐菌素（STZ）诱导的DN的影响。与野生型（WT）小鼠相比，Fat-1小鼠表现出肾脏n-3 PUFA和n-3 PUFA衍生的脂质介质增加。内源性n-3 PUFA保护STZ处理的fat-1小鼠免受高血糖诱导的肾功能障碍，如肾/体重比、尿蛋白、血尿素氮水平和肌酐清除率的显著降低所反映的。此外，内源性n-3 PUFAs通过调节E-钙粘蛋白表达显著改善高血糖诱导的肾损伤。还发现，在STZ处理的fat-1小鼠中，内源性n-3 PUFA减弱了DN诱导的NLRP 3炎性体活化。我们的研究结果表明，内源性n-3 PUFA可能通过以下方式改善DN：（i）形成n-3脂质介质，（ii）诱导E-钙粘蛋白表达和（iii）抑制NLRP 3炎性体。
Although n-3 polyunsaturated fatty acids (PUFAs) exhibit biological activity in many inflammatory diseases, their renoprotective effects against diabetic nephropathy (DN) have been controversial. Here, fat-1 transgenic mice were used to investigate the effects of n-3 PUFAs on streptozocin (STZ)-induced DN. Fat-1 mice exhibited increased renal n-3 PUFAs and n-3 PUFA-derived lipid mediators, compared to wild type (WT) mice. Endogenous n-3 PUFAs protected STZ-treated fat-1 mice against hyperglycemia-induced renal dysfunction, as reflected by significant decreases in kidney/body weight ratio, urinary protein, blood urea nitrogen levels and creatinine clearance. In addition, endogenous n-3 PUFAs significantly ameliorated hyperglycemia-induced renal damage by modulating E-cadhein expression. It was also found that DN-induced NLRP3 inflammasome activation was attenuated by endogenous n-3 PUFAs in STZ-treated fat-1 mice. Our findings suggest that endogenous n-3 PUFAs ameliorate DN potentially through the: (i) formation of n-3 lipid mediators, (ii) induction of E-cadherin expression and (iii) inhibition of NLRP3 inflammasome.
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影响因子：
3.7
作者：
Hsiao HM;Sapinoro RE;Thatcher TH;Croasdell A;Levy EP;Fulton RA;Olsen KC;Pollock SJ;Serhan CN;Phipps RP;Sime PJ
通讯作者：
Sime PJ
DOI：
10.3390/molecules19033247
发表时间：
2014-03-17
期刊：
Molecules (Basel, Switzerland)
影响因子：
--
作者：
Katakura M;Hashimoto M;Inoue T;Al Mamun A;Tanabe Y;Iwamoto R;Arita M;Tsuchikura S;Shido O
通讯作者：
Shido O
影响因子：
4.6
作者：
Bak DH;Zhang E;Yi MH;Kim DK;Lim K;Kim JJ;Kim DW
通讯作者：
Kim DW
Omega-3 脂肪酸通过抑制 NLRP3 炎症小体激活来预防炎症和代谢紊乱。
影响因子：
32.4
作者：
Yan, Yiqing;Jiang, Wei;Zhou, Rongbin
通讯作者：
Zhou, Rongbin
DOI：
10.1016/j.chroma.2014.07.006
发表时间：
2014-09-12
期刊：
Journal of chromatography. A
影响因子：
--
作者：
Wang Y;Armando AM;Quehenberger O;Yan C;Dennis EA
通讯作者：
Dennis EA