Abstract
Herbal medicines containing emodin, widely used for the treatment of hepatitis in clinic, have been reported with hepatotoxicity in individuals. A modest inflammatory stress potentiating liver injury has been linked to the idiosyncratic drug-induced liver injury (IDILI). In this study, we investigated the hypothesis that lipopolysaccharide (LPS) interacts with emodin could synergize to cause liver injury in rats. Emodin (ranging from 20, 40, to 80 mg/kg), which is in the range of liver protection, was administered to rats, before LPS (2.8 mg/kg) or saline vehicle treatment. The biochemical tests showed that non-toxic dosage of LPS coupled with emodin caused significant increases of plasma ALT and AST activities as compared to emodin alone treated groups (P < 0.05). In addition, with LPS or emodin alone could not induce any changes in ALT and AST activity, as compared with the control group (0.5% CMC-Na treatment). Meanwhile, the plasma proinflammatory cytokines, TNF-α, IL-1β, and IL-6 increased significantly in the emodin/LPS groups compared to either emodin groups or the LPS (P < 0.05). Histological analysis showed that liver damage was only found in emodin/LPS cotreatmented rat livers samples. These results indicate that non-toxic dosage of LPS potentiates the hepatotoxicity of emodin. This discovery raises the possibility that emodin and herbal medicines containing it may induce liver injury in the inflammatory stress even in their therapeutic dosages.
Highlights
Liver injury is a fundamental pathological process in most hepatic diseases
Treatment of rats with emodin or LPS alone did not cause an increase in plasma Alanine transaminase (ALT), AST activity and total bile acid (TBA) content, (Figure 1)
The phenomenon indicates that emodin or LPS alone did not induce liver injury in rats at any of the doses given, while rats had significant liver injury after co-treatment
Summary
Liver injury is a fundamental pathological process in most hepatic diseases. Chronic liver injury leads to hepatic fibrosis, liver cirrhosis, and even liver cancer (Beyoğlu and Idle, 2013; Huang et al, 2013). Many studies have been focused on the protective effects of natural compounds or plant extracts upon various liver injury in vivo (Harnack et al, 2001; Bent and Ko, 2004). As penetration and usage increase, consecutive reports of hepatotoxic effects have appeared gradually, such as Shou-Wu Pian, Capsule Shengjing, and some herbs containing anthraquinones including Polygonum multiflorum, Sennae fructus angustifoliae, and Rheum palmatum L. Emodin (1,3,8-trihydroxy-6-methyl anthraquinone) is an anthraquinone derivative from Chinese herbs Rheum palmatum (rhubarb), Polygonum multiflorum, Cassia obtusifolia, etc. As penetration and usage increase, consecutive reports of hepatotoxic effects have appeared gradually, such as Shou-Wu Pian, Capsule Shengjing, and some herbs containing anthraquinones including Polygonum multiflorum, Sennae fructus angustifoliae, and Rheum palmatum L. (Panis et al, 2005; Stickel et al, 2005; Wang et al, 2011; Ma et al, 2015).
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