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槲皮素通过调节炎症、氧化应激和 TGF-β1/SMADs 通路预防系膜细胞模型的慢性肾脏病。

Quercetin prevents chronic kidney disease on mesangial cells model by regulating inflammation, oxidative stress, and TGF-β1/SMADs pathway.

机构信息

Faculty of Medicine, Maranatha Christian University, Bandung, West Java, Indonesia.

Biomolecular and Biomedical Research Center, Aretha Medika Utama, Bandung, West Java, Indonesia.

出版信息

PeerJ. 2022 Jun 2;10:e13257. doi: 10.7717/peerj.13257. eCollection 2022.

DOI:10.7717/peerj.13257
PMID:35673387
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9167587/
Abstract

BACKGROUND

Chronic kidney disease (CKD) happens due to decreasing kidney function. Inflammation and oxidative stress have been shown to result in the progression of CKD. Quercetin is widely known to have various bioactivities including antioxidant, anticancer, and anti-inflammatory activities.

OBJECTIVE

To evaluate the activity of quercetin to inhibit inflammation, stress oxidative, and fibrosis on CKD cells model (mouse mesangial cells induced by glucose).

METHODS AND MATERIAL

The SV40 MES 13 cells were plated in a 6-well plate with cell density at 5,000 cells/well. The medium had been substituted for 3 days with a glucose-induced medium with a concentration of 20 mM. Quercetin was added with 50, 10, and 5 µg/mL concentrations. The negative control was the untreated cell. The levels of TGF-β1, TNF-α, and MDA were determined using ELISA KIT. The gene expressions of the SMAD7, SMAD3, SMAD2, and SMAD4 were analyzed using qRT-PCR.

RESULTS

Glucose can lead to an increase in inflammatory cytokines TNF-α, TGF-β1, MDA as well as the expressions of the SMAD2, SMAD3, SMAD4, and a decrease in SMAD7. Quercetin caused the reduction of TNF-α, TGF-β1, MDA as well as the expression of the SMAD2, SMAD3, SMAD4, and increased SMAD7.

CONCLUSION

Quercetin has anti-inflammation, antioxidant, antifibrosis activity in the CKD cells model. Thus, quercetin is a promising substance for CKD therapy and further research is needed to prove this in CKD animal model.

摘要

背景

慢性肾脏病(CKD)是由于肾功能下降引起的。炎症和氧化应激已被证明会导致 CKD 的进展。槲皮素具有广泛的生物活性,包括抗氧化、抗癌和抗炎活性。

目的

评估槲皮素抑制 CKD 细胞模型(葡萄糖诱导的小鼠肾小球系膜细胞)炎症、氧化应激和纤维化的活性。

方法和材料

将 SV40 MES 13 细胞接种于 6 孔板中,细胞密度为 5,000 个/孔。用含 20mM 葡萄糖的诱导培养基代替培养基 3 天。加入 50、10 和 5μg/mL 浓度的槲皮素。未处理的细胞为阴性对照。使用 ELISA KIT 测定 TGF-β1、TNF-α 和 MDA 的水平。使用 qRT-PCR 分析 SMAD7、SMAD3、SMAD2 和 SMAD4 的基因表达。

结果

葡萄糖可导致炎症细胞因子 TNF-α、TGF-β1、MDA 以及 SMAD2、SMAD3、SMAD4 的表达增加,SMAD7 的表达减少。槲皮素可降低 TNF-α、TGF-β1、MDA 的表达,以及 SMAD2、SMAD3、SMAD4 的表达,并增加 SMAD7 的表达。

结论

槲皮素在 CKD 细胞模型中具有抗炎、抗氧化、抗纤维化活性。因此,槲皮素是治疗 CKD 的有前途的物质,需要进一步的研究来证明这一点在 CKD 动物模型中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f81f/9167587/f1e177680a45/peerj-10-13257-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f81f/9167587/18b8e72119a3/peerj-10-13257-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f81f/9167587/d88c7e5d6c05/peerj-10-13257-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f81f/9167587/ed30a3cae996/peerj-10-13257-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f81f/9167587/53e9d081b4ac/peerj-10-13257-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f81f/9167587/4c5e0c87cdd0/peerj-10-13257-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f81f/9167587/f1e177680a45/peerj-10-13257-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f81f/9167587/18b8e72119a3/peerj-10-13257-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f81f/9167587/d88c7e5d6c05/peerj-10-13257-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f81f/9167587/ed30a3cae996/peerj-10-13257-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f81f/9167587/53e9d081b4ac/peerj-10-13257-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f81f/9167587/4c5e0c87cdd0/peerj-10-13257-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f81f/9167587/f1e177680a45/peerj-10-13257-g006.jpg

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