KD3010是一种具有口服活性的有效的选择性PPARδ激动剂。
KD3010 is a potent, orally active, and selective PPARδ agonist.
To determine whether PPARδ agonists are beneficial in experimental liver fibrosis, mice are treated orally with a PPARδ agonist, KD3010, or with the well-validated PPARδ agonist GW501516. KD3010, but not GW501516, shows hepatoprotective and antifibrotic effects in liver fibrosis induced by carbon tetrachloride (CCl4) or bile duct ligation (BDL). Liver injury is induced by repeated injections of CCl4, and mice are treated daily with vehicle, the widely used PPARδ agonist GW501516, or the PPARδ agonist KD3010 by oral gavage. Control oil-injected mice do not show any liver damage. Liver injury consisting of hepatocyte death and inflammation is seen in the vehicle- or GW501516-treated group injected with CCl4 on H&E-stained liver sections but is markedly reduced in the KD3010-treated group[1].
[1]. Iwaisako K, et al. Protection from liver fibrosis by a peroxisome proliferator-activated receptor δ agonist. Proc Natl Acad Sci U S A. 2012 May 22;109(21):E1369-76.
Animal experiment: | Mice[1]Male 11-wk-old C57/B6 mice are treated with CCl4 (2 μL/g body weight; 1:4 dilution with corn oil) or with corn oil as control (2 μL/g body weight) by i.p. injection every third day. Injections are repeated for a total of 12 times. Mice are injected i.p. 12 times with oil as control (n=4 in each group) or with CCl4 and are administered vehicle (n=14), GW501516 (2 mg/kg; n=12), or KD3010 (10 mg/kg; n=11) daily by oral gavage[1]. |
参考文献: [1]. Iwaisako K, et al. Protection from liver fibrosis by a peroxisome proliferator-activated receptor δ agonist. Proc Natl Acad Sci U S A. 2012 May 22;109(21):E1369-76. | |
动态评分
0.0