酒精相关性肝病(ALD)是全球范围内的主要健康问题。近年来,由于其潜在的抗氧化和保肝特性,人们对用于预防和治疗ALD的天然产品和功能性食品越来越感兴趣。RosaroxburghiiTratt,以其丰富的生物活性化合物而闻名,已经证明了有希望的健康益处,包括抗炎和抗氧化作用。发酵已被用作增强天然产物的生物利用度和功效的策略。在本研究中,使用罗莎刺梨特拉特汁的混合物,由植物乳杆菌HH-LP56发酵的荷叶提取物和葡萄籽原花青素,一种新型的发酵刺梨(FRRT)汁被发现可以预防和调节乙醇诱导的肝细胞损伤。发酵后,pH值显著下降,VC和超氧化物歧化酶(SOD)含量显著升高,随着羟基和2,2-二苯基-1-吡喃基肼基自由基清除能力的显着增强。α小鼠肝脏12细胞暴露于乙醇24h,建立体外肝细胞损伤模型。本研究评估了FRRT对细胞损伤的影响,脂质积累和氧化应激标志物。结果表明,FRRT预处理(细胞用2.5和5mg/mlFRRT预处理2h)显着降低了肝细胞的脂质积累和氧化应激。机械上,FRRT通过影响关键基因和蛋白调节脂质代谢,如AMP激活的蛋白激酶,固醇调节元件结合转录因子1和硬脂酰辅酶A去饱和酶-1。此外,FRRT通过增加SOD活性来增强抗氧化活性,谷胱甘肽和过氧化氢酶水平,同时降低活性氧和丙二醛水平。它还逆转了乙醇诱导的氧化应激相关基因和蛋白质的表达变化。总之,一种新的功能性食品成分可能已经被发现具有广泛的潜在应用。这些发现表明,FRRT具有抗氧化特性和潜在的治疗益处,通过其对肝脏脂质代谢和氧化应激的影响来解决乙醇诱导的肝细胞损伤。
Alcohol‑related liver disease (ALD) is a major health concern worldwide. In recent years, there has been growing interest in natural products and functional foods for preventing and treating ALD due to their potential antioxidant and hepatoprotective properties.
Rosa roxburghii Tratt, known for its rich content of bioactive compounds, has demonstrated promising health benefits, including anti‑inflammatory and antioxidant effects. Fermentation has been utilized as a strategy to enhance the bioavailability and efficacy of natural products. In the present study, using a mixture of
Rosa roxburghii Tratt juice, lotus leaf extract and grape seed proanthocyanidins fermented by Lactobacillus plantarum HH‑LP56, a novel fermented
Rosa roxburghii Tratt (FRRT) juice was discovered that can prevent and regulate ethanol‑induced liver cell damage. Following fermentation, the pH was significantly decreased, and the content of VC and superoxide dismutase (SOD) were significantly increased, along with a noticeable enhancement in hydroxyl and 2,2‑diphenyl‑1‑picrylhydrazyl free radical scavenging abilities. Alpha Mouse liver 12 cells were exposed to ethanol for 24 h to establish an in vitro liver cell injury model. The present study evaluated the effects of FRRT on cell damage, lipid accumulation and oxidative stress markers. The results revealed that FRRT pretreatment (cells were pre‑treated with 2.5 and 5 mg/ml FRRT for 2 h) significantly reduced lipid accumulation and oxidative stress in liver cells. Mechanistically, FRRT regulated lipid metabolism by influencing key genes and proteins, such as AMP‑activated protein kinase, sterol regulatory element binding transcription factor 1 and Stearyl‑CoA desaturase‑1. Furthermore, FRRT enhanced antioxidant activity by increasing SOD activity, glutathione and catalase levels, while reducing reactive oxygen species and malondialdehyde levels. It also reversed the expression changes of ethanol‑induced oxidative stress‑related genes and proteins. In conclusion, a novel functional food ingredient may have been discovered with extensive potential applications. These findings indicated that FRRT has antioxidant properties and potential therapeutic benefits in addressing ethanol‑induced liver cell damage through its effects on liver lipid metabolism and oxidative stress.