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腺病毒介导的骨形态发生蛋白 9 过表达促进了非肥胖小鼠中蛋氨酸胆碱缺乏诱导的非酒精性脂肪性肝炎。

Adenovirus‑mediated overexpression of bone morphogenetic protein‑9 promotes methionine choline deficiency‑induced non‑alcoholic steatohepatitis in non‑obese mice.

机构信息

Department of Hepatology and Gastroenterology, Beijing You An Hospital, Capital Medical University, Beijing 100069, P.R. China.

Division of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.

出版信息

Mol Med Rep. 2019 Sep;20(3):2743-2753. doi: 10.3892/mmr.2019.10508. Epub 2019 Jul 19.

Abstract

Liver inflammation and macrophage infiltration are critical steps in the progression of non‑alcoholic fatty liver to the development of non‑alcoholic steatohepatitis. Bone morphogenetic protein‑9 is a cytokine involved in the regulation of chemokines and lipogenesis. However, the function of bone morphogenetic protein‑9 in non‑alcoholic steatohepatitis is still unknown. The present study hypothesized that bone morphogenetic protein‑9 may contribute to steatohepatitis in mice fed a methionine choline deficiency diet (MCD). C57BL/6 mice overexpressing bone morphogenetic protein‑9 and control mice were fed the MCD diet for 4 weeks. Liver tissue and serum samples were obtained for subsequent measurements. Bone morphogenetic protein‑9 overexpression exacerbated steatohepatitis in mice on the MCD diet, as indicated by liver histopathology, increased serum alanine aminotransferase activity, aspartate transaminase activity, hepatic inflammatory gene expression and M1 macrophage recruitment. Although bone morphogenetic protein‑9 overexpression did not affect the expression of pro‑fibrogenic genes, including Collagen I (α)1 or matrix metalloproteinase (MMP) 9, it did upregulate the expression of transforming growth factor‑β and plasminogen activator inhibitor 1, and downregulated the expression of MMP2. The above results indicate that bone morphogenetic protein‑9 exerts a pro‑inflammatory role in MCD diet‑induced non‑alcoholic steatohepatitis.

摘要

肝脏炎症和巨噬细胞浸润是非酒精性脂肪性肝病向非酒精性脂肪性肝炎发展的关键步骤。骨形态发生蛋白 9 是一种参与调节趋化因子和脂生成的细胞因子。然而,骨形态发生蛋白 9 在非酒精性脂肪性肝炎中的作用尚不清楚。本研究假设骨形态发生蛋白 9 可能参与了蛋氨酸胆碱缺乏饮食(MCD)喂养的小鼠的肝炎。过表达骨形态发生蛋白 9 的 C57BL/6 小鼠和对照小鼠分别用 MCD 饮食喂养 4 周。随后采集肝组织和血清样本进行后续测量。骨形态发生蛋白 9 的过表达加剧了 MCD 饮食喂养的小鼠的肝炎,肝组织病理学、血清丙氨酸氨基转移酶活性、天冬氨酸氨基转移酶活性、肝脏炎症基因表达和 M1 巨噬细胞募集均表明了这一点。尽管骨形态发生蛋白 9 的过表达并未影响包括 Collagen I (α)1 或基质金属蛋白酶 9 在内的促纤维化基因的表达,但它确实上调了转化生长因子-β和纤溶酶原激活物抑制剂 1 的表达,并下调了 MMP2 的表达。上述结果表明,骨形态发生蛋白 9 在 MCD 饮食诱导的非酒精性脂肪性肝炎中发挥促炎作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91fa/6691271/41b1a50ac22c/MMR-20-03-2743-g00.jpg

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