Sparassis crispa Attenuates Carbon Tetrachloride-Induced Hepatic Injury in Rats
2
조회
0
다운로드
2
인용
0
참고문헌
키워드
초록
Sparassis crispa is an edible mushroom with various medicinal properties. Here we demonstrate theeffect of Sparassis crispa on carbon tetrachloride (CCl4)-induced hepatotoxicity and the underlying mechanism. To evaluate the hepatoprotective effects of Sparassis crispa ethanol extract (SCE), 50 male Sprague-Dawleyrats were equally divided into 5 groups. Group I is the normal control rats with an intraperitoneal (i.p.) 0.5%carboxy methyl cellulose (CMC) pretreatment and olive oil treatment. Group II is the model group with an i.p. 0.5% CMC and 0.5 mL/kg CCl4 treatment. Group III and IV is the CCl4-administered rats pretreated with an i.p. 100 and 200 mg/kg SCE, respectively. Group V includes the silymarin group with an i.p. 50 mg/kg silymarin andCCl4 treatment. At 16 h after the CCl4 treatment, the levels of serum aminotransferases, TNF-α, and lipid peroxidation weresubstantially increased, whereas the activity of hepatic antioxidative enzymes, such as superoxide dismutase andcatalase, was decreased. These changes were attenuated by SCE. The histological studies also showed that SCEinhibited the CCl4-induced liver injury. Furthermore, the contents of hepatic nitrite, inducible nitric oxide synthase(iNOS), and cyclooxygenase-2 (COX-2) were elevated after CCl4 treatment, while the cytochrome P450 2E1(CYP2E1) expression was suppressed. SCE treatment inhibited the formation of liver nitrite, reduced the overexpressionof iNOS and COX-2 proteins, but restored the liver CYP2E1 content compared with the CCl4-treatedmodel group. The present data elucidate that SCE protects the liver against CCl4-induced acute hepatotoxicity, which mightbe due to its ability to restore the CYP2E1 function and suppress the inflammatory responses, in combination withits capacity to reduce oxidative stress.
Abstract
Sparassis crispa is an edible mushroom with various medicinal properties. Here we demonstrate theeffect of Sparassis crispa on carbon tetrachloride (CCl4)-induced hepatotoxicity and the underlying mechanism. To evaluate the hepatoprotective effects of Sparassis crispa ethanol extract (SCE), 50 male Sprague-Dawleyrats were equally divided into 5 groups. Group I is the normal control rats with an intraperitoneal (i.p.) 0.5%carboxy methyl cellulose (CMC) pretreatment and olive oil treatment. Group II is the model group with an i.p. 0.5% CMC and 0.5 mL/kg CCl4 treatment. Group III and IV is the CCl4-administered rats pretreated with an i.p. 100 and 200 mg/kg SCE, respectively. Group V includes the silymarin group with an i.p. 50 mg/kg silymarin andCCl4 treatment. At 16 h after the CCl4 treatment, the levels of serum aminotransferases, TNF-α, and lipid peroxidation weresubstantially increased, whereas the activity of hepatic antioxidative enzymes, such as superoxide dismutase andcatalase, was decreased. These changes were attenuated by SCE. The histological studies also showed that SCEinhibited the CCl4-induced liver injury. Furthermore, the contents of hepatic nitrite, inducible nitric oxide synthase(iNOS), and cyclooxygenase-2 (COX-2) were elevated after CCl4 treatment, while the cytochrome P450 2E1(CYP2E1) expression was suppressed. SCE treatment inhibited the formation of liver nitrite, reduced the overexpressionof iNOS and COX-2 proteins, but restored the liver CYP2E1 content compared with the CCl4-treatedmodel group. The present data elucidate that SCE protects the liver against CCl4-induced acute hepatotoxicity, which mightbe due to its ability to restore the CYP2E1 function and suppress the inflammatory responses, in combination withits capacity to reduce oxidative stress.
참고문헌 (28)
- Basu S., "Carbon tetrachloride-induced lipid peroxidation:eicosanoid formation and their regulation by antioxidant nutrients", Toxicology, 189, pp.113~127 (2003)
- Manibusan MK, "Postulated carbon tetrachloride mode of action: a review", J Environ Sci Health C Environ Carcinog Ecotoxicol Rev, 25, pp.185~209 (2007)
- Planaguma A, "The selective cyclooxygenase-2 inhibitor SC-236 reduces liver fibrosis by mechanisms involving nonparenchymal cell apoptosis and PPARgamma activation", FASEB J, 19, pp.1120~1122 (2005)
- Weber LW, "Hepatotoxicity and mechanism of action of haloalkanes: carbon tetrachloride as a toxicological model", Crit Rev Toxicol, 33, pp.105~136 (2003)
- Hierholzer C, "Essential role of induced nitric oxide in the initiation of the inflammatory response after hemorrhagic shock", J Exp Med, 187, pp.917~928 (1998)
- Zhu W, "The roles played by crucial free radicals like lipid free radicals, nitric oxide, and enzymes NOS and NADPH in CCl4-induced acute liver injury of mice", Free Radic Biol Med, 29, pp.870~880 (2000)
- Al-Shabanah OA, "Protective effect of aminoguanidine, a nitric oxide synthase inhibitor, against carbon tetrachloride induced hepatotoxicity in mice", Life Sci, 66, pp.265~270 (2000)
- Gardner CR, "Role of nitric oxide in acetaminopheninduced hepatotoxicity in the rat", Hepatology, 27, pp.748~754 (1998)
- Kimura T, "Sparassis crispa (Hanabiratake) ameliorates skin conditions in rats and humans", Biosci Biotechnol Biochem, 77, pp.1961~1963 (2013)
- Kimura T., "Natural products and biological activity of the pharmacologically active cauliflower mushroom Sparassis crispa", Biomed Res Int, 2013, pp.982317~ (2013)
- Kim HH, "Sparassis crispa suppresses mast cell-mediated allergic inflammation: Role of calcium, mitogen-activated protein kinase and nuclear factor-kappaB", Int J Mol Med, 30, pp.344~350 (2012)
- Hida TH, "Kawaminami H, Ishibashi K, Miura NN, Adachi Y, Ohno N. Oral administration of soluble beta-glucan preparation from the cauliflower mushroom, Sparassis crispa (Higher Basidiomycetes) modulated cytokine production in mice", Int J Med Mushrooms, 15, pp.525~538 (2013)
- Batey RG, "Complementary and alternative medicine in the treatment of chronic liver disease", Curr Gastroenterol Rep, 7, pp.63~70 (2005)
- Recknagel RO, "Mechanisms of carbon tetrachloride toxicity", Pharmacol Ther, 43, pp.139~154 (1989)
- Bruccoleri A, "Induction of early-immediate genes by tumor necrosis factor alpha contribute to liver repair following chemical-induced hepatotoxicity", Hepatology, 25, pp.133~141 (1997)
- DeCicco LA, "Serum and liver concentrations of tumor necrosis factor alpha and interleukin-1beta following administration of carbon tetrachloride to male rats", Toxicol Lett, 98, pp.115~121 (1998)
- Lowenstein CJ, "a novel biologic messenger", Cell, 70, pp.705~707 (1992)
- Morio LA, "Distinct roles of tumor necrosis factor-alpha and nitric oxide in acute liver injury induced by carbon tetrachloride in mice", Toxicol Appl Pharmacol, 172, pp.44~51 (2001)
- Bohlinger I, "Interleukin-1 and nitric oxide protect against tumor necrosis factor alpha-induced liver injury through distinct pathways", Hepatology, 22, pp.1829~1837 (1995)
- Nadler EP, "Scavenging nitric oxide reduces hepatocellular injury after endotoxin challenge", Am J Physiol Gastrointest Liver Physiol, 281, pp.G173~G181 (2001)
- Inoue T, "Hypoxia and heat inhibit inducible nitric oxide synthase gene expression by different mechanisms in rat hepatocytes", Hepatology, 32, pp.1037~1044 (2000)
- Griswold DE, "Constitutive cyclooxygenase(COX-1) and inducible cyclooxygenase (COX-2): rationale for selective inhibition and progress to date", Med Res Rev, 16, pp.181~206 (1996)
- Chun KS, "Signal transduction pathways regulating cyclooxygenase-2 expression: potential molecular targets for chemoprevention", Biochem Pharmacol, 68, pp.1089~1100 (2004)
- Edwards MJ, "The involvement of Kupffer cells in carbon tetrachloride toxicity", Toxicol Appl Pharmacol, 119, pp.275~279 (1993)
- Fernandez G, "Covalent binding of carbon tetrachloride metabolites to the heme moiety of cytochrome P-450 and its degradation products", Res Commun Chem Pathol Pharmacol, 35, pp.283~290 (1982)
- Papa S, "Mechanisms of liver disease: cross-talk between the NF-kappaB and JNK pathways", Biol Chem, 390, pp.965~976 (2009)
- Dambach DM, "Distinct roles of NF-kappaB p50 in the regulation of acetaminopheninduced inflammatory mediator production and hepatotoxicity", Toxicol Appl Pharmacol, 211, pp.157~165 (2006)
- Nakahira K, "Protective role of heme oxygenase-1 induction in carbon tetrachloride-induced hepatotoxicity", Biochem Pharmacol, 66, pp.1091~1105 (2003)