Effects of Various Kinds of Edible Seaweeds in Diets on the Development of D-Galactosamine-Induced Hepatopathy in Rats

Abstract

SummaryIn the present study we investigated the effects of 11 kinds of edible seaweeds (6 brown and 5 red algae) which contain characteristic seaweed dietary fibers on the induction of D -GalN ( D -galactosamine)-hepatopathy in rats (Exps. 1 and 2). Then, the efficacy of various components prepared from Gelidium sp., which was found to alleviate the hepatopathy in Exps. 1 and 2, was examined (Exp. 3). The rats were fed the diets containing various kinds of seaweeds (Exps. 1 and 2), or several components of Gelidium sp. such as total dietary fiber (TDF), soluble dietary fiber (SDF), insoluble dietary fiber (IDF) and dietary fiber-free components (DFFC) (Exp. 3), for 8 d. The rats in all experiments were injected with D -GalN (800 mg/kg body weight) intraperitoneally at the 7th day to induce liver injury and were sacrificed 24 h after the injection of D -GalN. The serum transaminase activities (ALT and AST) and lactate dehydrogenase (LDH) were determined to evaluate the levels of hepatopathy. In Exp. 3, the total GSH concentration in the liver, plasma and cecal contents and organic acid concentration in cecal contents were also evaluated. In Exps. 1 and 2, repressive effects against D -GalN-hepatopathy were shown by four seaweeds Laminaria sp., Gelidium sp., Sargassum fulvellum and Eisenia bicyclis . In Exp. 3, it was found that protective activity in Gelidium sp. against D -GalN-hepatopathy existed not only in the SDF but also in the DFFC fraction. The results in Exp. 3 also indicated that the total GSH but not organic acid concentration in the cecal contents were significantly correlated with serum AST activity, suggesting that the protective effect of Gelidium sp. on D -GalN-hepatopathy in rats is related to GSH metabolism in the intestine. Key Words seaweed, D -galactosamine, Gelidium , agar, glutathione This research was conducted for investigation of the influence of seaweeds on the development of D -galactosamine-induced hepatopathy ( D -GalN-hepatopathy) in rats. Because D -GalN-hepatopathy resembles human acute viral hepatitis histologically, D -galactosamine ( DGalN) intoxication is used as an animal model of fulminant hepatic failure ( 1 , 2 ). D -GalN is converted to UDP-D -GalN by the enzymes in the galactose metabolic pathway in the liver ( 3 ). The exhaustion of UTP caused by the UDP-D -GalN formation process is accompanied by a decrease on hepatocellular UDP, UTP, and UDP-glucose levels ( 4 -6 ). Then, D -GalN prevents the synthesis of RNA and protein in the liver, which leads to a defect in some important cell membrane proteins. Besides the above-mentioned causes, the D -GalN-induced-hepatopathy is thought to be also induced by the increase of mesentery permeability of endotoxin which is a kind of natural hepatotoxin in the intestine ( 7 , 8 ). According to previous studies, bacterial translocation in D -GalNhepatopathy was reduced by intestinal excision or use of an antibiotic which reduces intestinal bacteria in the animals before D -GalN-treatment ( 9 , 10 ). In other reports, medication with g...

Fucoidan: Structure and Bioactivity

“…Fucoidan prevented concanavalin A-induced liver injury by mediating the endogenous interleukin (IL)-10 production and the inhibition of proinflammatory cytokine in mice [ 118 ]. The dietary fiber in edible brown seaweeds ( Laminaria sp ., Sargassum fulvellum and Eisenia bicyclis ) had the repressive effect against D-galactosamine (D-GalN)-induced hepatopathy and the protective effect was caused at least in part by fucoidan [ 119 , 120 ]. Hepatic fibrosis results from chronic damage to the liver in conjunction with the progressive accumulation of fibrillar extracellular matrix proteins.…”

Therapies from Fucoidan; Multifunctional Marine Polymers

“…Kawano had previously identified therapeutic potential of edible whole seaweeds in the diet of experimental rats with this type of liver damage [75]. In his 2007 study he identified the components of the seaweeds that gave rise to the inhibition of liver disease.…”

“…In his 2007 study he identified the components of the seaweeds that gave rise to the inhibition of liver disease. The elevated levels of aspartate and alanine aminotransferases were inhibited specifically by the fucoidan in the diet at levels equivalent to those in whole seaweed at 5% of the total diet [75,76]. Lastly, Hayakawa addressed the issue of hepatocarcinoma in ex vivo samples of chronic cirrhosis and hepatitis B and C from a clinical setting and found that Fucus vesiculosis fucoidan has a potentially therapeutic effect [77].…”

Pretreatment with Fucoidan from Fucus vesiculosus Protected against ConA-Induced Acute Liver Injury by Inhibiting Both Intrinsic and Extrinsic Apoptosis

“…In particular, Granert and colleagues in 1999 demonstrated that fucoidan inhibited inflammatory infiltration [ 21 ], and in 2012 Kang and Cui showed the protective effect of fucoidan on lipopolysaccharide (LPS)-induced rat neuronal damage [ 22 – 23 ]. In addition, with regard to liver damage, ConA and D-galactosamine (GalN)-induced hepatopathy was improved, as indicated by Kawanno and Saito [ 24 – 25 ]. Common findings in these studies were the downregulation of related pro-inflammatory factors, including TNF-α, IFN-γ, IL-6, IL-8 and IL-12, and established the foundation of anti-inflammatory treatment.…”