Angelica sinensis Supercritical Fluid CO2 Extract Attenuates D-Galactose-Induced Liver and Kidney Impairment in Mice by Suppressing Oxidative Stress and Inflammation

Angelica sinensis Supercritical Fluid CO2 Extract Attenuates D-Galactose-Induced Liver and Kidney Impairment in Mice by Suppressing Oxidative Stress and Inflammation
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DOI:
10.1089/jmf.2017.4061
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发表时间:
2018-09-01
影响因子:
2.4
通讯作者:
Chen, Jian-Ping
Chen, Jian-Ping
中科院分区:
农林科学3区
文献类型:
--
作者:
Mo, Zhi-Zhun;Lin, Zhi-Xiu;Chen, Jian-Ping

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当归(Angelica sinensis,AS)是传统方剂中治疗虚损的重要中药成分,具有滋补作用。虽然AS已被证明可以改善D-半乳糖(D-gal)诱导的衰老小鼠脑的认知损伤和神经毒性,但其对肝和肾损伤的影响尚未被探索。本实验用D-半乳糖(200 mg/kg)皮下注射小鼠,并用AS(20、40或80 mg/kg)灌胃小鼠,每天1次,连续8周。结果表明,AS显着改善肝脏和肾脏功能的器官指数和功能参数评估。此外,AS预处理有效地改善了组织学恶化。AS可降低MDA水平,显著提高Cu、Zn-SOD、CAT、GPx等抗氧化酶活性及基因表达。AS还能显著抑制D-gal诱导的肝、肾组织炎症细胞因子iNOS、考克斯-2、IB、p-IB和p65表达的增加,并促进IB的表达。综上所述,AS预处理能有效保护小鼠肝脏和肾脏免受D-半乳糖诱导的损伤,其机制与减轻氧化反应和炎症应激密切相关。
Angelica sinensis (AS, Danggui in Chinese) is an important herbal component of various traditional formulae for the management of asthenia and its tonic effects. Although AS has been shown to ameliorate cognitive damage and nerve toxicity in D-galactose (D-gal)-elicited senescent mice brain, its effects on liver and kidney injury have not yet been explored. In this work, mice were subjected to hypodermic injection with D-gal (200mg/kg) and orally gavaged with AS (20, 40, or 80mg/kg) once a day for 8 successive weeks. Results revealed that AS significantly improved liver and kidney function as assessed by organ index and functional parameters. In addition, AS pretreatment effectively ameliorated the histological deterioration. AS attenuated the MDA level and markedly enhanced the activities and gene expressions of antioxidative enzymes, namely Cu, Zn-SOD, CAT, and GPx. Furthermore, AS markedly inhibited the D-gal-mediated increment of expressions of inflammatory cytokines iNOS, COX-2, IB, p-IB, and p65 and promoted the IB expression level in both hepatic and renal tissues. In sum, AS pretreatment could effectively guard the liver and kidney of mice from D-gal-induced injury, and the underlying mechanism was deemed to be intimately related to attenuating oxidative response and inflammatory stress.