Xu Guangyu, Han Xiao, Yuan Guangxin, An Liping, Du Peige
College of Pharmacy, Beihua University, Jilin, Jilin, China.
PLoS One. 2017 Jul 10;12(7):e0180899. doi: 10.1371/journal.pone.0180899. eCollection 2017.
Liver injury is a common pathological basis of various liver diseases, and long-term liver injury is often an important initiation factor leading to liver fibrosis and even liver cirrhosis and hepatocellular carcinoma (HCC). It has been reported that deproteinized extract of calf blood (DECB) can inhibit the replication of hepatitis B virus and confers a protective effect on the liver after traumatic liver injury. However, few studies on the regulatory factors and mechanisms of DECB have been reported. In this current study, an acute mouse liver injury model was established with carbon tetrachloride (CCl4). The differentially expressed genes and related cell signal transduction pathways were screened using mRNA expression microarray. STEM software V1.3.6 was used for clustering gene functions, and the DAVID and KEGG databases were applied for the analysis. A total of 1355 differentially expressed genes were selected, among which nine were validated by RT-qPCR. The results showed that the Fas, IL1b, Pik3r1, Pik3r5, Traf2, Traf2, Csf2rb2, Map3k14, Pik3cd and Ppp3cc genes were involved in the regulation of DECB in an acute mouse liver injury model. Targets of the protective effects of DECB and its related mechanisms were found in mice with acute liver injury induced by carbon tetrachloride, which may provide an important theoretical basis for further DECB research.
肝损伤是各种肝脏疾病常见的病理基础，长期肝损伤往往是导致肝纤维化甚至肝硬化及肝细胞癌（HCC）的重要起始因素。据报道，小牛血去蛋白提取物（DECB）可抑制乙型肝炎病毒复制，并对外伤性肝损伤后的肝脏具有保护作用。然而，关于DECB调控因子及机制的研究报道较少。在本研究中，用四氯化碳（CCl4）建立急性小鼠肝损伤模型。使用mRNA表达微阵列筛选差异表达基因及相关细胞信号转导通路。用STEM软件V1.3.6对基因功能进行聚类，并应用DAVID和KEGG数据库进行分析。共筛选出1355个差异表达基因，其中9个通过RT-qPCR验证。结果表明，Fas、IL1b、Pik3r1、Pik3r5、Traf2、Traf2、Csf2rb2、Map3k14、Pik3cd和Ppp3cc基因参与急性小鼠肝损伤模型中DECB的调控。在四氯化碳诱导的急性肝损伤小鼠中发现了DECB保护作用的靶点及其相关机制，这可能为进一步研究DECB提供重要的理论依据。
