Phytochemical investigation of the butanol fraction (BUF) derived from the 70% aqueous methanolic leaf extract of Barnebydendron riedelii led to the isolation of three flavonoid glycosides; kaempferol-3-O-α-l-rhamnopyranosyl-(1 → 6)-β-d-glucopyranoside, quercetin-3-O-α-l-rhamnopyranosyl-(1 → 6)-β-d-galactopyranoside and quercetin-3-O-α-l-rhamnopyranosyl-(1 → 6)-β-d-glucopyranoside. Docking studies were fulfilled to validate the possible bio-properties of BUF toward nuclear factor kappa B (NF-κB) and nuclear factor erythroid 2-related factor 2 (Nrf2). The protective role of BUF against behavioral, biochemical, molecular, histopathological and immunohistochemical alterations in thioacetamide (TAA)-induced hepatic encephalopathy in rats was investigated. The toxicological studies indicated that BUF was safe up to 2000 mg/kg bw. Prior to TAA intoxication, rats were orally treated with either BUF at multiple doses (70, 140 and 280 mg/kg bw) or lactulose (8 mL/kg bw) for 14 consecutive days. On the 13th and the 14th day, TAA (200 mg/kg bw/day) was intraperitoneally injected. The BUF significantly improved motor impairment, ameliorated cognitive deficits and attenuated TAA-induced hepatotoxicity. Moreover, BUF controlled the inflammatory processes by suppressing the hepatic inflammatory cytokine; interleukin-6 (IL-6) as well as its pro-inflammatory mediator; NF-κB supporting the molecular docking assessment. The brain neurotransmitters; dopamine, serotonin and noradrenaline, as well as ammonia levels were improved in BUF-treated TAA-intoxicated animals in a dose-dependent manner. Furthermore, BUF administration to TAA-intoxicated rats modulated the Nrf2 and heme oxygenase 1 (HO-1) genes expression in liver and brain tissues. The histological evaluation showed that pretreatment of TAA-intoxicated rats with BUF ameliorated the degenerative effects of TAA on liver and brain tissues as well as reduced the activation of cellular apoptotic marker; caspase-3 and glial fibrillary acidic protein (GFAP⁺) astrocytes. In conclusion, the observed hepato-neuroprotective effect of BUF is attributed to its flavonoidal content through its modulatory effects on of NF-κB/IL-6 and Nrf2/HO-1 signaling pathways.

对来自Barnebydendron riedelii的70％甲醇叶提取物的丁醇级分（BUF）的植物化学研究导致分离出三种黄酮苷。山奈黄素-3- ø - α -升-rhamnopyranosyl-（1→6） - β - d吡喃葡萄糖苷，槲皮素-3- ø - α -升-rhamnopyranosyl-（1→6） - β - d -galactopyranoside和槲皮素3- O - α- l-鼠李糖基- （1→6）-β - d-吡喃葡萄糖苷。已完成对接研究，以验证BUF对核因子kappa B（NF-κB）和核因子红系2相关因子2（Nrf2）可能的生物学特性。研究了BUF在硫代乙酰胺（TAA）诱导的大鼠肝性脑病中对行为，生化，分子，组织病理学和免疫组化变化的保护作用。毒理学研究表明，BUF高达2000 mg / kg bw是安全的。在TAA中毒之前，连续14天给大鼠口服多剂量BUF（70、140和280 mg / kg bw）或乳果糖（8 mL / kg bw）。在第13和14天，腹膜内注射TAA（200 mg / kg bw /天）。BUF可以显着改善运动障碍，改善认知功能障碍，并减轻TAA诱导的肝毒性。此外，BUF通过抑制肝炎性细胞因子来控制炎性过程。白介素6（IL-6）及其促炎介质；NF-κB支持分子对接评估。脑神经递质；在BUF处理的TAA中毒动物中，多巴胺，5-羟色胺和去甲肾上腺素以及氨水平均呈剂量依赖性提高。此外，BUF给予TAA中毒的大鼠调节了肝脏和脑组织中Nrf2和血红素加氧酶1（HO-1）基因的表达。组织学评估表明，用BUF预处理TAA中毒大鼠可改善TAA对肝脏和脑组织的退行性作用，并减少细胞凋亡标记物的活化。caspase-3和神经胶质纤维酸性蛋白（GFAP NF-κB支持分子对接评估。脑神经递质；在BUF处理的TAA中毒动物中，多巴胺，5-羟色胺和去甲肾上腺素以及氨水平均呈剂量依赖性提高。此外，BUF给予TAA中毒的大鼠调节了肝脏和脑组织中Nrf2和血红素加氧酶1（HO-1）基因的表达。组织学评估表明，用BUF预处理TAA中毒大鼠可改善TAA对肝脏和脑组织的退行性作用，并减少细胞凋亡标记物的活化。caspase-3和神经胶质纤维酸性蛋白（GFAP NF-κB支持分子对接评估。脑神经递质；在BUF处理的TAA中毒动物中，多巴胺，5-羟色胺和去甲肾上腺素以及氨水平均呈剂量依赖性提高。此外，BUF给予TAA中毒的大鼠调节了肝脏和脑组织中Nrf2和血红素加氧酶1（HO-1）基因的表达。组织学评估表明，用BUF预处理TAA中毒大鼠可改善TAA对肝脏和脑组织的退行性作用，并减少细胞凋亡标记物的活化。caspase-3和神经胶质纤维酸性蛋白（GFAP 以及BUF处理的TAA中毒动物的氨水平以剂量依赖性方式得到改善。此外，BUF给予TAA中毒的大鼠调节了肝脏和脑组织中Nrf2和血红素加氧酶1（HO-1）基因的表达。组织学评估表明，用BUF预处理TAA中毒大鼠可改善TAA对肝脏和脑组织的退行性作用，并减少细胞凋亡标记物的活化。caspase-3和神经胶质纤维酸性蛋白（GFAP 以及BUF处理的TAA中毒动物的氨水平以剂量依赖性方式得到改善。此外，BUF给予TAA中毒的大鼠调节了肝脏和脑组织中Nrf2和血红素加氧酶1（HO-1）基因的表达。组织学评估表明，用BUF预处理TAA中毒大鼠可改善TAA对肝脏和脑组织的退行性作用，并减少细胞凋亡标记物的活化。caspase-3和神经胶质纤维酸性蛋白（GFAP 组织学评估表明，用BUF预处理TAA中毒大鼠可改善TAA对肝脏和脑组织的退行性作用，并减少细胞凋亡标记物的活化。caspase-3和神经胶质纤维酸性蛋白（GFAP 组织学评估表明，用BUF预处理TAA中毒大鼠可改善TAA对肝脏和脑组织的退行性作用，并减少细胞凋亡标记物的活化。caspase-3和神经胶质纤维酸性蛋白（GFAP⁺）星形胶质细胞。总之，观察到的BUF的肝神经保护作用归因于其对NF-κB/ IL-6和Nrf2 / HO-1信号通路的调节作用，其类黄酮含量。