Sparassis crispa Attenuates Carbon Tetrachloride-Induced Hepatic Injury in Rats.
10.11637/kjpa.2014.27.3.113
- Author:
Guang Hai YAN
1
;
Yun Ho CHOI
Author Information
1. Department of Anatomy and Histology and Embryology, Yanbian University School of Basic Medical Sciences, China.
- Publication Type:Original Article
- Keywords:
Sparassis crispa;
Carbon tetrachloride;
Hepatotoxicity
- MeSH:
Agaricales;
Animals;
Carbon Tetrachloride;
Carbon*;
Catalase;
Cyclooxygenase 2;
Cytochrome P-450 CYP2E1;
Ethanol;
Humans;
Lipid Peroxidation;
Liver;
Male;
Methylcellulose;
Nitric Oxide Synthase Type II;
Olea;
Oxidative Stress;
Rats*;
Rats, Sprague-Dawley;
Silymarin;
Superoxide Dismutase;
Transaminases;
Tumor Necrosis Factor-alpha;
Olive Oil
- From:Korean Journal of Physical Anthropology
2014;27(3):113-122
- CountryRepublic of Korea
- Language:English
-
Abstract:
Sparassis crispa is an edible mushroom with various medicinal properties. Here we demonstrate the effect 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-Dawley rats 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 and CCl4 treatment. At 16 h after the CCl4 treatment, the levels of serum aminotransferases, TNF-alpha, and lipid peroxidation were substantially increased, whereas the activity of hepatic antioxidative enzymes, such as superoxide dismutase and catalase, was decreased. These changes were attenuated by SCE. The histological studies also showed that SCE inhibited 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 over-expression of iNOS and COX-2 proteins, but restored the liver CYP2E1 content compared with the CCl4-treated model group. The present data elucidate that SCE protects the liver against CCl4-induced acute hepatotoxicity, which might be due to its ability to restore the CYP2E1 function and suppress the inflammatory responses, in combination with its capacity to reduce oxidative stress.
