体内
增殖细胞核抗原
细胞凋亡
基因敲除
癌症研究
KLF4公司
下调和上调
化学
标记法
肝损伤
细胞生长
分子生物学
生物
药理学
生物化学
转录因子
SOX2
生物技术
基因
作者
Bing‐Shen Huang,Shih‐Chiang Huang,Fang-Hsin Chen,Yu Han Chang,Hsiu-Fu Mei,Hsuan-Li Huang,Wan‐Yu Chen,Jong‐Hwei S. Pang
出处
期刊:Life Sciences
[Elsevier]
日期:2022-12-01
卷期号:310: 121072-121072
被引量:12
标识
DOI:10.1016/j.lfs.2022.121072
摘要
Radiation-induced liver disease (RILD) is the major complication for cancer patients after radiation therapy. We investigated the protective effects of BPC 157 peptide in reducing RILD.Mice were irradiated with a single dose of 12 Gy to induce acute liver injury with or without oral BPC 157. Plasma levels of AST and ALT were determined. In vitro rat liver clone 9 cells and in vivo liver tissues were harvested for MTT assay, TUNEL assay, lipid staining, polypoid cell counts, Western blotting of caspase-3, PCNA, KLF-4 and HIF-2α, and immunocytochemistry for PCNA, KLF-4 and HIF-2α. SiRNAs were used to knockdown KLF-4.BPC 157 was firstly demonstrated to reduce RILD by decreasing plasma levels of AST and ALT, and inhibiting hydropic degeneration of liver. BPC 157 significantly decreased radiation-induced cell apoptosis, increased PCNA expression, promoted the expression of KLF4, decreased the radiation-induced hepatic lipid accumulation and HIF-2α expression both in mice liver and in clone 9 liver cells. The knockdown of KLF4 abolished the protective effect of BPC 157 on radiation-induced apoptosis and lipid accumulation in clone 9 liver cells, indicating that the protective effect of BPC 157 was mediated by KLF4 in liver cells.The present study provided a good model for molecular mechanism underlying the acute RILD. BPC 157, as a stable pentadecapeptide that can be chemically synthesized and purified easily for research, together with its in vivo markedly protective effect made it worth of being investigated for future clinical application for RILD.
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