Screening for the protective effect target of deproteinized extract of calf blood and its mechanisms in mice with CCl4-induced acute liver injury

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.

Hepatoprotective Effects of Standardized Extracts from an Ancient Italian Apple Variety (Mela Rosa dei Monti Sibillini) against Carbon Tetrachloride (CCl4)-Induced Hepatotoxicity in Rats

“…Liver injury is characterized by cell degeneration, necrosis and apoptosis. Liver fibrosis and cirrhosis is the main cause of the incidence of liver cirrhosis and hepatocellular carcinoma [10]. Numerous halogenated chemicals like carbon tetrachloride (CCl 4 ) have potential hepatotoxic effects due to cellular damage via oxidative stress [11].…”

Identification of hepatitis B virus and liver cancer bridge molecules based on functional module network

“…The high expression of PIK3CD can promote the proliferation and migration of HCC cells, and also participates in acute liver injury model in mice. Long-term inflammation of liver injury is an important factor leading to liver fibrosis and even cirrhosis and HCC[34,35]. Later, interesting module pairs were observed and module 4 and module 6 showed significant crosstalk, including the most common DEGs of which most were related to chemokines and receptors.…”

<p>Carbon Dots from <em>Paeoniae Radix Alba</em> Carbonisata: Hepatoprotective Effect</p>

“…The acute liver injury model was established as previously reported. 13 Male mus musculus (n = 48) were randomized into the following six groups (n = 8 in each) and treated as indicated: the negative control group (normal saline [NS] intraperitoneal injection), the model group (intraperitoneal injection), the positive control group (2.25 mg/kg [Bifendate] subcutaneous injection) and the high-, medium-and low-dose PARC-CDs groups (6.16, 3.08 and 1.54 mg/kg, respectively, intraperitoneal injection). The normal group and the model group were given equal volumes of normal saline, and all the PARC-CDs groups underwent intragastric administration for 7 days.…”

“…Liver injury is defined as acute liver dysfunction caused by viral infection, liver toxicity, toxic substances or hepatic ischaemia-reperfusion. 13 The liver is the main organ involved in drug metabolism in the body, so chemical liver injury is very common. Commonly used drugs and laboratory chemicals such as paracetamol, amine sulfate and alcohol can damage the liver by producing reactive oxygen species.…”