Extraction process optimization of alisol B 23-acetate from Alismatis Rhizoma and its protection against carbon tetrachloride-induced acute liver injury

Abstract

Alisol B 23-acetate (AB23A) is an important pharmacodynamic compound found in Alismatis Rhizoma. In this study, response surface methodology (RSM) and Box- Behnken design (BBD) were used to optimize the extraction parameters of the AB23A. The optimal conditions included a solid–liquid ratio of 1:13, a reflux extraction of 70% ethanol, an extraction time of 2 h, and an extraction cycle of 3 cycles. Furthermore, a rat model of acute liver injury was established using carbon tetrachloride (CCl4), and a comprehensive analysis combining histopathology, lipidomics, and metabolomics was conducted to elucidate the hepatoprotective effect of AB23A. The findings revealed that AB23A significantly reduced the levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP), and restored the abnormal morphology of hepatocytes. Furthermore, AB23A exhibited the ability to attenuate CCl4-induced lipid peroxidation, as evidenced by the upregulation of glutathione (GSH) and glutathione peroxidase 4 (GPX4) levels, along with a reduction in malondialdehyde (MDA) content in the liver. Omics results and immunohistochemistry analyses demonstrated a decrease in inflammatory reaction and oxidized phospholipid levels following AB23A administration, indicating an enhanced anti-inflammatory and antioxidant capacities of hepatocytes. Differential metabolite analysis revealed that AB23A improved anti-inflammatory and antioxidant capacities by modulating liver sphingolipid metabolism and purine metabolism, thereby enhancing hepatocyte recovery and counteracting acute liver injury induced by CCl4.