Protective Effect of Andropraphis Paniculata Aqueous Extract (EAAp) Against Isoniazid and Rifampicin-Induced Rat Liver Damage

Risdawati Djohan, Ambar Harjanti, Pendrianto Pendrianto
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Abstract

Isoniazid (INH) and rifampicin (RIF) are first-line antituberculosis drugs (OAT) in tuberculosis treatment that are used for at least 6 months. The use of OAT has been associated with toxic reactions in the liver and causes hepatitis. This study aimed to determine the effect of an aqueous extract of Andrographis paniculata (EAAp) on liver damage induced by INH and RIF. Method: Male Sprague-Dawley rats weighing 250–300g were divided into 5 groups, each consisting of 6 mice. Animals were given isoniazid and rifampicin at 100 mg/kg, respectively, to induce liver damage, silymarin (25 mg/kg) for the positive control group, and Ap extract at doses of 200mg and 300 mg/kg for the test group. All treatments were given orally once daily for 28 days. Measurement of serum aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), bilirubin, and liver histopathology levels was carried out to determine the effect of EAAp on liver damage by INH and RIF. Results: Rats treated with INH+RIF were hepatotoxic, as evidenced by increased serum ALT, AST, and ALP activity, total bilirubin levels, and histopathological changes in the liver. Administration of Ap extract doses of 200 mg/kg and 300 mg/kg significantly decreased liver biochemical and histological changes caused by OAT. Conclusions: EAAp has a protective effect against hepatotoxic-induced INH and RIF in animal models.
山参水提物对异烟肼和利福平所致大鼠肝损伤的保护作用
异烟肼(INH)和利福平(RIF)是治疗结核病的一线抗结核药物(OAT),至少使用6个月。OAT的使用与肝脏毒性反应和引起肝炎有关。本研究旨在探讨穿心莲水提物(EAAp)对INH和RIF诱导的肝损伤的影响。方法:取体重250 ~ 300g的雄性sd大鼠分为5组,每组6只。小鼠分别给予异烟肼和利福平(100 mg/kg)诱导肝损伤,阳性对照组给予水飞蓟素(25 mg/kg),试验组给予Ap提取物(200mg和300 mg/kg)。所有治疗方法均为口服,每日1次,连用28天。测定血清天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、碱性磷酸酶(ALP)、胆红素及肝脏组织病理学水平,探讨EAAp对INH和RIF肝损伤的影响。结果:INH+RIF处理大鼠肝毒性,表现为血清ALT、AST和ALP活性升高,总胆红素水平升高,肝脏组织病理改变。200 mg/kg和300 mg/kg Ap提取物可显著降低OAT引起的肝脏生化和组织学变化。结论:EAAp对动物模型肝毒性诱导的INH和RIF具有保护作用。
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