樟芝发酵菌丝体滤液可减轻四氯化碳诱导的大鼠肝纤维化。
Filtrate of fermented mycelia from Antrodia camphorata reduces liver fibrosis induced by carbon tetrachloride in rats.
作者信息
Lin Wen-Chuan, Kuo Shu-Ching, Lin Wei-Lii, Fang Hsun-Lang, Wang Bor-Chen
机构信息
Department of Pharmacology, China Medical University, Taichung 404, Taiwan, China.
出版信息
World J Gastroenterol. 2006 Apr 21;12(15):2369-74. doi: 10.3748/wjg.v12.i15.2369.
AIM
To investigate the effects of filtrate of fermented mycelia from Antrodia camphorata (FMAC) on liver fibrosis induced by carbon tetrachloride (CCl(4)) in rats.
METHODS
Forty Wistar rats were divided randomly into control group and model group. All model rats were given 200 mL/L CCl(4) (2 mL/Kg, po) twice a week for 8 wk. Four weeks after CCl(4) treatment, thirty model rats were further divided randomly into 3 subgroups: CCl(4) and two FMAC subgroups. Rats in CCl(4) and 2 FMAC subgroups were treated with FMAC 0, 0.5 and 1.0 g/kg, daily via gastrogavage beginning at the fifth week and the end of the eighth week. Spleen weight, blood synthetic markers (albumin and prothrombin time) and hepatic malondialdehyde (MDA) and hydroxyproline (HP) concentrations were determined. Expression of collagen I, tissue inhibitor of metalloproteinases (TIMP)-1 and transforming growth factor beta1 (TGF-beta1) mRNA were detected by RT-PCR. Histochemical staining of Masson's trichrome was performed.
RESULTS
CCl(4) caused liver fibrosis, featuring increased prothrombin time, hepatic MDA and HP contents, and spleen weight and decreased plasma albumin level. Compared with CCl(4) subgroup, FMAC subgroup (1 g/kg) significantly decreased the prothrombin time (36.7+/-7.2 and 25.1+/-10.2 in CCl(4) and FMAC groups, respectively, P<0.05) and increased plasma albumin concentration (22.7+/-1.0 and 30.7+/-2.5 in CCl(4) and FMAC groups, respectively, P<0.05). Spleen weight was significantly lower in rats treated with CCl(4) and FMAC (1 g/kg) compared to CCl(4) treated rats only (2.7+/-0.1 and 2.4+/-0.2 in CCl(4) and FMAC groups, respectively, P<0.05). The amounts of hepatic MDA and HP in CCl(4)+FAMC (1 g/kg) subgroup were also lower than those in CCl(4) subgroup (MDA: 3.9+/-0.1 and 2.4+/-0.6 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01; HP: 1730.7+/-258.0 and 1311.5+/-238.8 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01). Histologic examinations showed that CCl(4)+FMAC subgroups had thinner or less fibrotic septa than CCl(4) group. RT-PCR analysis indicated that FMAC (1 g/kg) reduced mRNA levels of collagen I, TIMP-1 and TGF-beta1 (collagen I: 5.63+/-2.08 and 1.78+/-0.48 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01; TIMP-1: 1.70+/-0.82 and 0.34+/-0.02 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01; TGF-beta1:38.03+/-11.9 and 4.26+/-2.17 in CCl(4) and CCl(4)+FMAC groups, respectively, P<0.01) in the CCl(4)-treated liver.
CONCLUSION
It demonstrates that FMAC can retard the progression of liver fibrosis induced by CCl(4) in rats.
目的
研究樟芝发酵菌丝体滤液（FMAC）对四氯化碳（CCl₄）诱导的大鼠肝纤维化的影响。
方法
40只Wistar大鼠随机分为对照组和模型组。所有模型大鼠每周经口给予200 mL/L CCl₄（2 mL/kg）2次，共8周。CCl₄处理4周后，将30只模型大鼠进一步随机分为3个亚组：CCl₄组和两个FMAC亚组。CCl₄组和两个FMAC亚组的大鼠从第5周开始至第8周结束，每天经胃管给予0、0.5和1.0 g/kg的FMAC。测定脾脏重量、血液合成指标（白蛋白和凝血酶原时间）以及肝脏丙二醛（MDA）和羟脯氨酸（HP）浓度。通过RT-PCR检测I型胶原蛋白、金属蛋白酶组织抑制剂（TIMP）-1和转化生长因子β1（TGF-β1）mRNA的表达。进行Masson三色法组织化学染色。
结果
CCl₄导致肝纤维化，表现为凝血酶原时间延长、肝脏MDA和HP含量增加、脾脏重量增加以及血浆白蛋白水平降低。与CCl₄亚组相比，FMAC亚组（1 g/kg）显著缩短了凝血酶原时间（CCl₄组和FMAC组分别为36.7±7.2和25.1±10.2，P<0.05），并提高了血浆白蛋白浓度（CCl₄组和FMAC组分别为22.7±1.0和30.7±2.5，P<0.05）。与仅用CCl₄处理的大鼠相比，用CCl₄和FMAC（1 g/kg）处理的大鼠脾脏重量显著降低（CCl₄组和FMAC组分别为2.7±0.1和2.4±0.2，P<0.05）。CCl₄+FAMC（1 g/kg）亚组肝脏的MDA和HP含量也低于CCl₄亚组（MDA：CCl₄组和CCl₄+FMAC组分别为3.9±0.1和2.4±0.6，P<0.01；HP：CCl₄组和CCl₄+FMAC组分别为1730.7±258.0和1311.5±238.8，P<0.01）。组织学检查显示，CCl₄+FMAC亚组的纤维化间隔比CCl₄组更薄或更少。RT-PCR分析表明，FMAC（1 g/kg）降低了CCl₄处理肝脏中I型胶原蛋白、TIMP-1和TGF-β1的mRNA水平（I型胶原蛋白：CCl₄组和CCl₄+FMAC组分别为5.63±2.08和1.78±0.48，P<0.01；TIMP-1：CCl₄组和CCl₄+FMAC组分别为1.70±0.82和0.34±0.02，P<0.01；TGF-β1：CCl₄组和CCl₄+FMAC组分别为38.03±11.9和4.26±2.17，P<0.01）。
结论
表明FMAC可延缓CCl₄诱导的大鼠肝纤维化进程。
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