Abstract
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.
Highlights
Liver injury is defined as acute liver dysfunction caused by viral infection, liver toxicity, toxic substances or hepatic ischemia reperfusion, and the common pathological basis of various liver diseases is generally characterized by pathological characteristics such as liver cell degeneration, necrosis, and apoptosis [1]
The results showed that the Fas, IL1b, PIK3R1, and Pik3r5 genes played a significant role in the CCl4-induced mice liver injury model (p-values = 0.00510, 0.00048, 0.00572, and 0.00006, respectively), their expressions were down-regulated, and deproteinized extract of calf blood (DECB)
The results showed that SOD activity and GSH level were significantly increased, while MDA content was significantly decreased in the DECB group, indicating that DECB can enhance the antioxidant capacity of the liver and reduce the formation of lipid
Summary
Liver injury is defined as acute liver dysfunction caused by viral infection, liver toxicity, toxic substances or hepatic ischemia reperfusion, and the common pathological basis of various liver diseases is generally characterized by pathological characteristics such as liver cell degeneration, necrosis, and apoptosis [1]. Long-term liver injury can often lead to liver fibrosis and is an important initiating factor in the occurrence of liver cirrhosis and hepatocellular carcinoma (HCC) [2]. The prevention and treatment of liver injury is a major step in the clinical treatment of liver diseases, and controlling liver injury occurrence and development hold great clinical significance for the treatment of liver diseases [3]. Screening for protective effect target of deproteinized extract of calf blood in mice.
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