عنوان مقاله [English]
Background and Purpose: Drug/chemical-induced liver injury, also known as toxic hepatopathy, is a major clinical problem. Epidemiological studies indicate that the prevalence of drug/chemical-induced hepatopathy has gone up in recent decades, especially in developing countries. Although extensive studies have been conducted for decades, the precise mechanisms underlying drug/chemical-induced liver injury are still unclear and remain controversial. Moreover, there is still a lack of effective therapeutic strategies and speciﬁc medicines for these liver diseases. Recent studies have indicated that oxidative stress might be a pivotal originating factor in the pathogenesis of liver diseases such as drug-induced hepatic damage, alcoholic hepatitis and viral hepatitis and ischemic liver injury. Carbon tetrachloride is an extensively used industrial solvent, and it is the best-characterized animal model of xenobiotic-induced free radical-mediated hepatotoxicity. Carbon tetrachloride is a toxic agent for animal experiments that induce reactive oxygen formation and depletes GSH phase II enzyme. It may reduce antioxidant enzymes and antioxidant substrates to induce oxidative stress. Carbon tetrachloride induces liver injury caused by free radicals, and it induces lipid peroxidation, which can result in hepatic cell injury. Oxidative stress is an important factor in acute and chronic liver injury. Carbon tetrachloride requires bioactivation by phase I of the cytochrome P system in the liver and yields the reactive metabolites trichloromethyl radical and proxy trichloromethyl radical. These free radicals can bind to polyunsaturated fatty acids and form alkoxy and peroxy radicals, which can generate lipid peroxides that cause damage to cell membranes, alter enzyme activity and ﬁnally induce hepatic injury and necrosis. The hepatoprotective index of a drug can be evaluated by its ability to reduce the injurious effects of a hepatotoxin or to preserve normal hepatic physiological mechanisms during hepatotoxin exposure. Descurainia sophia L. (Khaksheer) is commonly is known as flixweed, herb-Sophia, and tansy mustard. Sisymbrium sophia L. is considered as its synonym. It belongs to the Brassicaceae family. This plant is native to Asia, Africa, and Europe and is generally used as a food additive and a medicinal herb in Iranian, Chinese, and Indian traditional medicines. In traditional medicine, it is commonly used to manage cough and asthma. In Iranian traditional medicine, Descurainia sophia is used as an antipyretic, antipruritic, purgative, helminthic, aphrodisiac, appetizer, digestive tonic, cardiotonic, astringent, anti-inflammatory, analgesic, and anticancer activity. These pharmacologic properties get more interesting when it is noticed that Descurainia sophia is a highly safe herbal medicine. The purpose of this study was to evaluate the ability of hepatoprotective Descorainia sophia ethanolic extract in liver damage induced by carbon tetrachloride in male Wistar rats.
Materials and Methods: In this experimental study, 60 male Wistar rats were randomly divided into 10 groups of 6. The groups were included: normal control, toxified control (intraperitoneally injection 0.5 ml/kg of carbon tetrachloride), normal experimental (Descurainia sophia ethanolic extract at doses of 10, 50, 100 and 200 mg/kg, intragastrically), toxified experimental (intraperitoneally injection 0.5 ml/kg of carbon tetrachloride and Descurainia sophia ethanolic extract at doses of 10, 50, 100 and 200 mg/kg, intragastrically). At the end of the 28-day treatment, the rats were fasted for 12 h and killed under mild (diethyl ether) anaesthesia. Livers were immediately obtained after the animals were sacriﬁced. The liver was homogenized and centrifuged. The supernatant was used to assay the activities of antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase and level of malondialdehyde in liver homogenate. Data were analyzed using one-way ANOVA and Tukey test. The criterion was significant (p