Journal of Food and Drug Analysis

An integrated strategy was developed to promote conversion of a sugarcane bagasse cellulose-rich fraction into water-soluble cellulosic oligomers (WCOs) through phosphoric acid-mediated regeneration and enzymatic hydrolysis. Alkaline pretreatment on sugarcane bagasse powder increased glucan content from 57.6 to 93.4 g/100 g sample and lowered Klason lignin to 6.1 g/100 g sample. Phosphoric acid-mediated regeneration was subsequently capable of reorganizing the structure of cellulose from sugarcane bagasse, resulting in a decrease of crystallinity from 72.9 to 64.0% and introducing cellulose II-like features. The hydration state of regenerated cellulose strongly influenced hydrolysis performance, as the hydrated form showed significantly higher solubilization (810.4 mg/g sample) and estimated WCO yield (698.1 mg/g sample) than the dried form (448.3 and 370.1 mg/g sample, respectively). Time-course analysis indicated that the estimated WCO yield reached a plateau after 2 h, whereas prolonged hydrolysis mainly increased glucose formation and reduced WCO selectivity, suggesting secondary saccharification. Under this selected condition, the process corresponded to an estimated WCO yield of 17.4 g per 100 g dried bagasse. Positive-ion electrospray ionization mass spectrometry indicated that the hydrolysate showed prominent ions tentatively assignable to cellobiose- and cellotetraose-related species. In animal experiments, a lower starch-induced blood glucose iAUC0-150 min was observed in the high-dose WCO-rich hydrolysate group, and oral administration was associated with changes in fecal Lactobacillus spp. and Bifidobacterium spp. counts. Overall, coupling phosphoric-acid regeneration with preservation of the hydrated state and time-controlled hydrolysis enabled production of WCO-rich hydrolysate from sugarcane bagasse.

BACKGROUND  Among the spectrum of hepatopathies that pose a significant global health threat, halting the progression of hepatic fibrosis is a key therapeutic objective. Wuwei Zijin San (WWZJS) is derived from a traditional Tibetan empirical formula, yet its efficacy against hepatic fibrosis, along with the underlying mechanisms and active ingredients, remains uncertain. PURPOSE  The aim of this study was to investigate the protective effect of WWZJS against hepatic fibrosis, explore its underlying mechanisms and material basis, and evaluate the potential of direct interactions between the biologically active ingredients and their corresponding targets. METHODS Chemical profiling of the active subfraction WWZJS was performed via UHPLC-qTOF-MS/MS-based non-targeted analysis. Pharmacodynamic evaluation was conducted in a rat model of liver fibrosis induced by 50% CCl4. The underlying mechanism was predicted via transcriptomics combined with detection of relevant protein expression. Molecular docking and molecular dynamic (MD) simulation were employed to evaluate the interaction between the compounds and the target. RESULTS 30% ethanol elution product, as the active subfraction of WWZJS, can induce apoptosis in activated HSCs in vitro. In vivo, it demonstrates significant ameliorative effects on CCl4-induced hepatic fibrosis in SD rats. Transcriptomic analysis revealed its involvement in multiple pathways, including ECM-receptor interaction and the PI3K/AKT signaling pathway. Protein expression data further suggest that it may suppress ECM deposition via this signaling cascade. Molecular docking of the four major ingredients (Bergenin, Corilagin, Gallic acid and Ellagic acid) against PI3K and AKT1 showed satisfactory binding effects. Similarly, 100 active ingredients were docked with PI3K/AKT signaling pathway-related proteins from DEGs, presenting generally favorable binding performance. CONCLUSION  WWZJS ameliorates hepatic fibrosis by suppressing activated HSC proliferation and ECM deposition, a process potentially mediated through the ITGA8/PIK3R3/AKT signaling pathway. Consistently, in vitro results showing enhanced apoptosis of activated HSCs also reveal the potential capacity of WWZJS to eliminate activated HSCs. Investigation of the binding capacity between key pathway targets and active ingredients provides a theoretical basis for elucidating the mechanism through which the active subfraction of WWZJS ameliorates hepatic fibrosis via direct protein interactions.