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无刺蜂()蜂蜜及其富含酚类的提取物通过 KEAP1-NRF2 信号通路改善氧化应激-抗氧化平衡。

Stingless Bee () Honey and Its Phenolic-Rich Extract Ameliorate Oxidant-Antioxidant Balance via KEAP1-NRF2 Signalling Pathway.

机构信息

Natural Medicines and Products Research Laboratory, Institute of Bioscience, Universiti Putra Malaysia, Serdang 43400, Selangor, Malaysia.

Department of Food Science, Faculty of Food Science and Technology, Universiti Putra Malaysia, Serdang 43400, Selangor, Malaysia.

出版信息

Nutrients. 2023 Jun 22;15(13):2835. doi: 10.3390/nu15132835.

DOI:10.3390/nu15132835
PMID:37447162
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10343317/
Abstract

Diabetes is associated with an imbalance between oxidants and antioxidants, leading to oxidative stress. This imbalance contributes to the development and progression of diabetic complications. Similarly, renal and liver diseases are characterised by oxidative stress, where an excess of oxidants overwhelms the antioxidant defense mechanisms, causing tissue damage and dysfunction. Restoring the oxidant-antioxidant balance is essential for mitigating oxidative stress-related damage under these conditions. In this current study, the efficacy of stingless bee honey (SBH) and its phenolic-rich extract (PRE) in controlling the oxidant-antioxidant balance in high-fat diet- and streptozotocin/nicotinamide-induced diabetic rats was investigated. The administration of SBH and PRE improved systemic antioxidant defense and oxidative stress-related measures without compromising liver and renal functioning. Analyses of the liver, skeletal muscle and adipose tissues revealed differences in their capacities to scavenge free radicals and halt lipid peroxidation. Transcriptional alterations hypothesised tissue-specific control of KEAP1-NRF2 signalling by upregulation of and in a tissue-specific manner. In addition, hepatic translational studies demonstrated the stimulation of downstream antioxidant-related protein with upregulated expression of SOD-1 and HOD-1 protein. Overall, the results indicated that PRE and SBH can be exploited to restore the oxidant-antioxidant imbalance generated by diabetes via regulating the KEAP1-NRF2 signalling pathway.

摘要

糖尿病与氧化剂和抗氧化剂之间的失衡有关,导致氧化应激。这种失衡导致糖尿病并发症的发展和进展。同样,肾脏和肝脏疾病的特征是氧化应激,其中氧化剂过多会破坏抗氧化防御机制,导致组织损伤和功能障碍。在这些情况下,恢复氧化剂-抗氧化剂平衡对于减轻与氧化应激相关的损伤至关重要。在本研究中,研究了无刺蜜蜂蜂蜜(SBH)及其富含酚类的提取物(PRE)在控制高脂肪饮食和链脲佐菌素/烟酰胺诱导的糖尿病大鼠氧化应激中的功效。SBH 和 PRE 的给药改善了全身抗氧化防御和氧化应激相关措施,而不会损害肝脏和肾脏功能。对肝脏、骨骼肌和脂肪组织的分析表明,它们清除自由基和阻止脂质过氧化的能力存在差异。转录分析假设 KEAP1-NRF2 信号的组织特异性控制通过以组织特异性方式上调 和 。此外,肝翻译研究表明,通过上调 SOD-1 和 HOD-1 蛋白的表达,刺激下游抗氧化相关蛋白。总的来说,结果表明 PRE 和 SBH 可以通过调节 KEAP1-NRF2 信号通路来恢复糖尿病引起的氧化应激失衡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2061/10343317/68ef164c2de4/nutrients-15-02835-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2061/10343317/ca861ed227ca/nutrients-15-02835-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2061/10343317/3577f4279c8d/nutrients-15-02835-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2061/10343317/cb7ce56fc99c/nutrients-15-02835-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2061/10343317/e66d2b41986a/nutrients-15-02835-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2061/10343317/68ef164c2de4/nutrients-15-02835-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2061/10343317/ca861ed227ca/nutrients-15-02835-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2061/10343317/3577f4279c8d/nutrients-15-02835-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2061/10343317/cb7ce56fc99c/nutrients-15-02835-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2061/10343317/e66d2b41986a/nutrients-15-02835-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2061/10343317/68ef164c2de4/nutrients-15-02835-g005.jpg

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