Song Tuzz-Ying, Yen Gow-Chin
Department of Food Science, National Chung Hsing University, 250 Kuokuang Road, Taichung 40227, Taiwan, Republic of China.
J Agric Food Chem. 2003 Mar 12;51(6):1571-7. doi: 10.1021/jf0209701.
The protective effects and the possible mechanisms of dry matter of fermented filtrate (DMF) from Antrodia camphorata in submerged culture (ACSC) on H(2)O(2)-induced cytotoxicity in HepG2 and carbon tetrachloride (CCl(4))-induced hepatotoxicity in Sprague-Dawley rats were investigated. The results showed that the inhibitory effect of DMF and its crude triterpenoids on lipid peroxidation occurred in a dose-response manner in an AAPH/linoleic acid system. When HepG2 cells were pretreated with DMF at the concentration of 0.10 mg/mL for 4 h and then induced by 1 h of treatment with H(2)O(2) (100 microM), lipid peroxidation was significantly (p < 0.05) decreased, as measured by the formation of malondialdehyde. The oral pretreatment with DMF [0.25 and 0.50 mg/kg of body weight (bw)] for 5 consecutive days prior to the administration of a single dose of 40% CCl(4) (0.10 mL/100 g of bw, ip) significantly prevented the increase in serum levels of hepatic enzyme markers (alanine and aspartate aminotransferase) and liver lipid peroxidation (p < 0.05). Histopathological evaluation of the rat liver revealed that DMF reduced the incidence of liver lesions, including neutrophil infiltration, hydropic swelling, and necrosis induced by CCl(4) in rats. Moreover, reduced glutathione (GSH)-dependent enzymes (glutathione peroxidase, glutathione reductase, and glutathione S-transferase) and the GSH/GSSG ratio were significantly improved in the oral pretreatment DMF of rats (p < 0.01). The results suggest that DMF may play a role in preventing oxidative damage in living systems by up-regulating hepatic GSH-dependent enzymes to preserve the normal GSH/GSSH ratio and scavenging free radicals formed during CCl(4) metabolism.
研究了樟芝深层发酵液干物质（DMF）对H2O2诱导的HepG2细胞毒性及四氯化碳（CCl4）诱导的Sprague-Dawley大鼠肝毒性的保护作用及其可能机制。结果表明，在AAPH/亚油酸体系中，DMF及其粗三萜类化合物对脂质过氧化的抑制作用呈剂量反应关系。当HepG2细胞用0.10 mg/mL浓度的DMF预处理4 h，然后用100 μM H2O2处理1 h诱导时，丙二醛的形成表明脂质过氧化显著（p < 0.05）降低。在单次腹腔注射40% CCl4（0.10 mL/100 g体重，ip）前连续5天口服预处理DMF [0.25和0.50 mg/kg体重（bw）]，可显著预防肝酶标志物（丙氨酸和天冬氨酸转氨酶）血清水平的升高及肝脏脂质过氧化（p < 0.05）。大鼠肝脏的组织病理学评估显示，DMF降低了肝脏病变的发生率，包括中性粒细胞浸润、水样肿胀和CCl4诱导的大鼠坏死。此外，大鼠口服预处理DMF后，谷胱甘肽（GSH）依赖性酶（谷胱甘肽过氧化物酶、谷胱甘肽还原酶和谷胱甘肽S-转移酶）及GSH/GSSG比值显著改善（p < 0.01）。结果表明，DMF可能通过上调肝脏GSH依赖性酶以维持正常的GSH/GSSH比值并清除CCl4代谢过程中形成的自由基，从而在预防生物系统中的氧化损伤方面发挥作用。
