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在一项研究中,屈青提取物对肾脏有机阴离子转运损伤具有抗氧化、抗炎和抗亚硝化应激作用。

Kützing extract exhibits antioxidant, anti-inflammation, and anti-nitrosative stress against impairment of renal organic anion transport in an study.

作者信息

Ontawong Atcharaporn, Aida Chaliya J, Vivithanaporn Pornpun, Amornlerdpison Doungporn, Vaddhanaphuti Chutima S

机构信息

Division of Physiology, School of Medical Sciences, University of Phayao, Phayao 56000, Thailand.

Office of Educational Affairs, Faculty of Abhaibhubejhr Thai Traditional Medicine, Burapha University, Chon Buri 20131, Thailand.

出版信息

Nutr Res Pract. 2024 Oct;18(5):633-646. doi: 10.4162/nrp.2024.18.5.633. Epub 2024 Jul 19.

DOI:10.4162/nrp.2024.18.5.633
PMID:39398884
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11464274/
Abstract

BACKGROUND/OBJECTIVES: extract (CGE), rich in polyphenols, was reported to exhibit antidiabetic and renoprotective effects by modulating the functions of protein kinases-mediated organic anion transporter 1 (Oat1) and 3 (Oat3) in rats with type 2 diabetes mellitus (T2DM). Nevertheless, the antioxidant effects of CGE on such renoprotection have not been investigated. This study examined the mechanisms involved in the antioxidant effects of CGE on renal organic anion transport function in an study.

MATERIALS/METHODS: Diabetes was induced in the rats through a high-fat diet combined with a single dose of 40 mg/kg body weight (BW) streptozotocin. Subsequently, normal-diet rats were supplemented with a vehicle or 1,000 mg/kg BW of CGE, while T2DM rats were supplemented with a vehicle, CGE, or 200 mg/kg BW of vitamin C for 12 weeks. The study evaluated the general characteristics of T2DM and renal oxidative stress markers. The renal organic transport function was assessed by measuring the para-aminohippurate (PAH) uptake using renal cortical slices and renal inflammatory cytokine expression in the normal diet (ND) and ND + CGE treated groups.

RESULTS

CGE supplementation significantly reduced hyperglycemia, hypertriglyceridemia, insulin resistance, and renal lipid peroxidation in T2DM rats. This was accompanied by the normalization of high expressions of renal glutathione peroxidase and nuclear factor kappa B by CGE and vitamin C. The renal anti-inflammation of CGE was evidenced by the reduction of tumor necrosis factor-1α and interleukin-1β. CGE directly blunted sodium nitroprusside-induced renal oxidative/nitrosative stresses and mediated the PAH uptake in the normally treated CGE in rats was particularly noteworthy. These data also correlated with reduced nitric oxide production, highlighting the potential of CGE as a therapeutic agent for managing T2DM-related renal complications.

CONCLUSION

These findings suggest that CGE has antidiabetic effects and directly prevents diabetic nephropathy through oxidative/nitrosative stress pathways.

摘要

背景/目的:富含多酚的肉桂提取物(CGE)据报道可通过调节蛋白激酶介导的有机阴离子转运体1(Oat1)和3(Oat3)的功能,对2型糖尿病(T2DM)大鼠发挥抗糖尿病和肾脏保护作用。然而,CGE对这种肾脏保护的抗氧化作用尚未得到研究。本研究在一项实验中探究了CGE对肾脏有机阴离子转运功能抗氧化作用的相关机制。

材料/方法:通过高脂饮食联合单次40mg/kg体重链脲佐菌素诱导大鼠患糖尿病。随后,正常饮食的大鼠补充赋形剂或1000mg/kg体重的CGE,而T2DM大鼠补充赋形剂、CGE或200mg/kg体重的维生素C,持续12周。该研究评估了T2DM的一般特征和肾脏氧化应激标志物。通过使用肾皮质切片测量对氨基马尿酸(PAH)摄取以及正常饮食(ND)和ND + CGE处理组中的肾脏炎性细胞因子表达,评估肾脏有机转运功能。

结果

补充CGE显著降低了T2DM大鼠的高血糖、高甘油三酯血症、胰岛素抵抗和肾脏脂质过氧化。同时,CGE和维生素C使肾脏谷胱甘肽过氧化物酶和核因子κB的高表达恢复正常。肿瘤坏死因子-1α和白细胞介素-1β的减少证明了CGE的肾脏抗炎作用。CGE直接减轻了硝普钠诱导的肾脏氧化/亚硝化应激,并介导了PAH摄取,在正常处理的大鼠中CGE的作用尤为显著。这些数据还与一氧化氮生成减少相关,突出了CGE作为治疗T2DM相关肾脏并发症治疗剂的潜力。

结论

这些发现表明,CGE具有抗糖尿病作用,并通过氧化/亚硝化应激途径直接预防糖尿病肾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6094/11464274/3c11ec99e66a/nrp-18-633-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6094/11464274/ec05ea76fd02/nrp-18-633-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6094/11464274/0dbfe9d3bf3d/nrp-18-633-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6094/11464274/e21d51853f87/nrp-18-633-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6094/11464274/2bc679cf7722/nrp-18-633-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6094/11464274/3c11ec99e66a/nrp-18-633-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6094/11464274/ec05ea76fd02/nrp-18-633-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6094/11464274/0dbfe9d3bf3d/nrp-18-633-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6094/11464274/e21d51853f87/nrp-18-633-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6094/11464274/2bc679cf7722/nrp-18-633-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6094/11464274/3c11ec99e66a/nrp-18-633-g005.jpg

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