Siegers C P, Pauli V, Korb G, Younes M
Agents Actions. 1986 Aug;18(5-6):600-3. doi: 10.1007/BF01964970.
Subchronic treatment of male rats with carbon tetrachloride (CCl4, twice weekly 0.2 ml/kg p.o.) and feeding a 5% alcohol solution instead of drinking water led to a nearly complete liver cirrhosis in all animals within 4 weeks. This was also documented by a three fold increase in hepatic total hydroxyproline content. Steatosis was quantified by enhanced liver triglyceride concentrations and acute necroses by increments of serum enzyme activities (GPT, SDH). Daily oral treatment with malotilate (100 mg/kg) totally prevented the development of liver cirrhosis, hepatic hydroxyproline accumulation and increases in serum enzyme activities induced by CCl4-alcohol. In cianidanol-treated rats (100 mg/kg p.o.) only portoseptal fibrosis was seen, however hydroxyproline and triglyceride accumulation as well as enhanced serum enzyme activities were not suppressed. D-penicillamine (300 mg/kg p.o.) and colchicine (50 micrograms/kg i.p.) failed to protect rats against CCl4-alcohol induced fibrosis, necrosis and steatosis in this model.
用四氯化碳（CCl4，每周两次，口服0.2 ml/kg）对雄性大鼠进行亚慢性治疗，并喂食5%的酒精溶液而非饮用水，4周内所有动物均出现了近乎完全的肝硬化。肝脏总羟脯氨酸含量增加三倍也证明了这一点。通过提高肝脏甘油三酯浓度来量化脂肪变性，通过血清酶活性（GPT、SDH）增加来量化急性坏死。每日口服马洛替酯（100 mg/kg）可完全预防CCl4-酒精诱导的肝硬化、肝脏羟脯氨酸积累以及血清酶活性增加。在西尼地醇治疗的大鼠（口服100 mg/kg）中，仅观察到门周纤维化，然而羟脯氨酸和甘油三酯积累以及血清酶活性增强并未受到抑制。在该模型中，D-青霉胺（口服300 mg/kg）和秋水仙碱（腹腔注射50微克/kg）未能保护大鼠免受CCl4-酒精诱导的纤维化、坏死和脂肪变性。
