Kanai Shiho, Ishihara Keiichi, Kawashita Eri, Tomoo Toshiyuki, Nagahira Kazuhiro, Hayashi Yasuhiro, Akiba Satoshi
Department of Pathological Biochemistry, Kyoto Pharmaceutical University, Yamashina-ku, Kyoto, Japan (S.K., K.I., E.K., S.A.); and Asubio Pharma Co., Ltd., Chuo-ku, Kobe, Japan (T.T., K.N., Y.H.).
Department of Pathological Biochemistry, Kyoto Pharmaceutical University, Yamashina-ku, Kyoto, Japan (S.K., K.I., E.K., S.A.); and Asubio Pharma Co., Ltd., Chuo-ku, Kobe, Japan (T.T., K.N., Y.H.)
J Pharmacol Exp Ther. 2016 Mar;356(3):604-14. doi: 10.1124/jpet.115.229906. Epub 2015 Dec 23.
We have previously shown that high-fat cholesterol diet (HFCD)-induced fatty liver and carbon tetrachloride (CCl4)-induced hepatic fibrosis are reduced in mice deficient in group IVA phospholipase A2 (IVA-PLA2), which plays a role in inflammation. We herein demonstrate the beneficial effects of ASB14780 (3-[1-(4-phenoxyphenyl)-3-(2-phenylethyl)-1H-indol-5-yl]propanoic acid 2-amino-2-(hydroxymethyl)propane-1,3-diol salt), an orally active IVA-PLA2 inhibitor, on the development of fatty liver and hepatic fibrosis in mice. The daily coadministration of ASB14780 markedly ameliorated liver injury and hepatic fibrosis following 6 weeks of treatment with CCl4. ASB14780 markedly attenuated the CCl4-induced expression of smooth muscle α-actin (α-SMA) protein and the mRNA expression of collagen 1a2, α-SMA, and transforming growth factor-β1 in the liver, and inhibited the expression of monocyte/macrophage markers, CD11b and monocyte chemotactic protein-1, while preventing the recruitment of monocytes/macrophages to the liver. Importantly, ASB14780 also reduced the development of fibrosis even in matured hepatic fibrosis. Additionally, ASB14780 also reduced HFCD-induced lipid deposition not only in the liver, but also in already established fatty liver. Furthermore, treatment with ASB14780 suppressed the HFCD-induced expression of lipogenic mRNAs. The present findings suggest that an IVA-PLA2 inhibitor, such as ASB14780, could be useful for the treatment of nonalcoholic fatty liver diseases, including fatty liver and hepatic fibrosis.
我们之前已经表明,在缺乏IVA型磷脂酶A2(IVA-PLA2)的小鼠中,高脂胆固醇饮食(HFCD)诱导的脂肪肝和四氯化碳(CCl4)诱导的肝纤维化有所减轻,IVA-PLA2在炎症中起作用。我们在此证明了ASB14780(3-[1-(4-苯氧基苯基)-3-(2-苯乙基)-1H-吲哚-5-基]丙酸2-氨基-2-(羟甲基)丙烷-1,3-二醇盐),一种口服活性的IVA-PLA2抑制剂,对小鼠脂肪肝和肝纤维化发展的有益作用。在CCl4治疗6周后,每日联合给予ASB14780可显著改善肝损伤和肝纤维化。ASB14780显著减弱了CCl4诱导的肝脏中平滑肌α-肌动蛋白(α-SMA)蛋白表达以及胶原蛋白1a2、α-SMA和转化生长因子-β1的mRNA表达,并抑制单核细胞/巨噬细胞标志物CD11b和单核细胞趋化蛋白-1的表达,同时阻止单核细胞/巨噬细胞向肝脏募集。重要的是,即使在成熟的肝纤维化中,ASB14780也能减少纤维化的发展。此外,ASB14780不仅减少了HFCD诱导的肝脏脂质沉积,还减少了已形成的脂肪肝中的脂质沉积。此外,ASB14780治疗抑制了HFCD诱导的脂肪生成mRNA的表达。目前的研究结果表明,一种IVA-PLA2抑制剂,如ASB14780,可能对治疗非酒精性脂肪性肝病,包括脂肪肝和肝纤维化有用。