Camel milk and bee honey regulate profibrotic cytokine gene transcripts in liver cirrhosis induced by carbon tetrachloride

Abstract

The lack of studies regarding the mechanism of the protective effects of camel milk and bee honey against hepatotoxic compounds led us to perform this study. Thirty-six male rats were divided into two main groups. The first group (n = 9) comprised control non-cirrhotic rats. The rats of the second group (n = 27) were administered carbon tetrachloride (CCl) by intraperitoneal injection to induce liver cirrhosis. The cirrhotic rats were then divided into three equal subgroups, each comprising nine animals, as follows: (i) cirrhotic rats, (ii) cirrhotic rats treated with camel milk, and (iii) cirrhotic rats treated with camel milk and bee honey. The present findings revealed that CCl elevated the activities of liver enzymes, blood glucose levels, non-esterified fatty acids (NEFA) in the serum and glycogen content in the liver. On the other hand, CCl significantly decreased phosphorylase activity in the liver tissue and significantly increased carbohydrate intolerance and insulin resistance index (HOMA-IR). Moreover, CCl induced a significant increase in oxidative stress, along with increased expression of the profibrotic cytokine genes TNF-α and TGF-β. However, camel milk either alone or in combination with bee honey ameliorated these toxic actions. The antioxidant properties of these protective agents and their effects of downregulating certain procirrhotic cytokine gene transcripts underlie this protection.

Sidr honey abrogates the oxidative stress and downregulates the hyaluronic acid concentration and gene expression of TGF‐β1 and COL1a1 in rat model of thioacetamide‐induced hepatic fibrosis

“…This reduction may be due to regulation of the transcription of these pro-inflammatory cytokines by sidr honey via its antioxidant and anti-inflammatory properties. This result was in consistence with Sadek, Beltagy, Saleh, and Abouelkhair, (2016) who concluded that combinations of bee honey and camel milk downregulated the fibrotic genes in CCL4-induced liver damage.…”

Curcumin attenuates hepatic fibrosis and insulin resistance induced by bile duct ligation in rats

“…In hepatocytes, the IR refers to increased demand for insulin to maintain glucose homoeostasis, which leads to persistent stimulation of insulin production by pancreatic B-cells and subsequently, hyperinsulinaemia (18) , as well as failure of insulin to inhibit hepatic glucose production, which is responsible for development of hyperglycaemia (47) . Sadek et al (48) revealed that CCl4 significantly increases oxidative stress, expression of the profibrotic cytokine genes such as TNF-α and TGF-β, blood glucose and insulin levels and IR index (HOMA-IR). However, these effects were abolished by camel milk either alone or in combination with bee honey because of their antioxidant properties.…”

“…Sadek et al . ( 48 ) revealed that CCl4 significantly increases oxidative stress, expression of the profibrotic cytokine genes such as TNF-α and TGF-β , blood glucose and insulin levels and IR index (HOMA-IR). However, these effects were abolished by camel milk either alone or in combination with bee honey because of their antioxidant properties.…”

Protective effect of lyophilized sapodilla (Manilkara zapota) fruit extract against CCl4-induced liver damage in rats

“…In this study we used CCl 4 treated rat model of liver damage. Besides elevating the levels of liver enzymes, blood glucose, non-esterified fatty acids in the serum and glycogen in liver, CCl 4 also significantly decreases phosphorylase activity in liver and increases carbohydrate intolerance and insulin resistance ( Sadek et al, 2016 ). Administration of CCl 4 causes liver steatosis ( Cui et al, 2017 ) and therefor it has been used to develop experimental models of NAFLD ( Kanai et al, 2016 , Chheda et al, 2014 ) and NASH ( Tsuchida et al, 2018 , Owada et al, 2018 ); the latter condition is a type of NAFLD with inflammation and liver cell damage along with fat accumulation.…”