The Activity of Purple Sweet Potato Extract on Antituberculosis-Induced Liver Toxicity

Abstract

BACKGROUND: The proportion of antituberculosis-induced liver injury on tuberculosis patients showed a relatively high incidence in many countries. Hepatic damage induced by antituberculosis drugs might potentially fatal. Isoniazid (INH) and rifampicin (RIF) are two main components of antituberculosis with crucial role for the incidence of liver injury. One of the herbal remedies that pose hepatoprotective action is purple sweet potato. Hepatoprotective action of purple sweet potato extract has been proved to pose antioxidant and anti-inflammatory activity. AIM: This study was designed to analyze the effect of purple sweet potato extract on rat interleukin-6 (IL-6) and tumor necrosis factor-α _(TNF-α) level, as well as liver histopathology feature in hepatic injury induced by INH-RIF. METHODS: This study was a randomized posttest-only control group design. Male Wistar rats (Rattus norvegicus), age 8–12 weeks, weight 180–220 g were included in this research (divided into three groups). Purple sweet potato extract was produced by maceration technique. IL-6 and TNF-α _level was measured by enzyme-linked immunosorbent assay, whereas liver histopathology examination was performed with hematoxylin and eosin staining. Statistical analysis was performed using one-way ANOVA and post hoc test. RESULTS: Liver IL-6 level in the normal, control, and treatment groups was 2.272±0.473, 3.315 ± 0.536, and 2.548 ± 0.304, respectively (p < 0.001). Liver TNF-α _level in the normal, control, and treatment groups was 26.476 ± 1.681, 48.584 ± 1.359, and 32.547 ± 1.528, respectively (p < 0.05). Histopathology feature of the liver in the control group showed significant liver congestion, liver degeneration, liver necrosis, and infiltration of inflammatory cell. Otherwise, histopathology feature of the liver in the treatment group showed minimal lesion. CONCLUSIONS: Purple sweet potato ethanol extract lowered the liver concentration of IL-6 and TNF-α, as well as improving liver damage in Wistar rats induced with isoniazid and rifampicin.