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当归补血汤通过 GAS5/NF-κB 通路抑制系膜细胞增殖和细胞外基质积聚。

Danggui buxue tang inhibited mesangial cell proliferation and extracellular matrix accumulation through GAS5/NF-κB pathway.

机构信息

Department of Endocrinology, The Affiliated Hospital of Changchun University of Chinese Medicine, Changchun 130021, Jilin Province, People's Republic of China.

Department of Emergency Physicians, The Affiliated Hospital of Changchun University of Chinese Medicine, Changchun 130021, Jilin Province, People's Republic of China.

出版信息

Biosci Rep. 2019 Oct 30;39(10). doi: 10.1042/BSR20181740.

DOI:10.1042/BSR20181740
PMID:31481528
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6822488/
Abstract

Diabetic nephropathy (DN) is the common complications of diabetes mellitus, but the efficacy of available treatments for the prevention of DN is still unsatisfactory. In the present study, we aimed to explore the effect of Danggui buxue tang (DGT) on the proliferation of high glucose (HG)-induced mesangial cells and accumulation of extracellular matrix in mesangial cells. We found DGT up-regulated the expression of growth arrest specific transcript 5 (GAS5) and IκB kinase (IKK) dose-dependently in mouse mesangial cells (SV40 MES-13). We found DGT regulated the expression IKK and the activity of nuclear transcription factor-κB (NF-κB) via GAS5, and proved that long non-coding RNA (lncRNA) GAS5 was positively related with IKK. And we proved GAS5 regulated the expression of IKK and the activity of NF-κB. In addition, DGT inhibited the viability of MES-13 cells and extracellular matrix-related proteins (laminin (LN), fibronectin (FN) and collagen IV (Col IV)) via GAS5. Moreover, we proved GAS5 regulated the viability of SV40 MES-13 cells and extracellular matrix-related proteins through NF-κB pathway. DGT inhibited the proliferation of mesangial cells and accumulation of extracellular matrix via GAS5/NF-κB, therefore, DGT could be an effective treatment for the prevention of DN.

摘要

糖尿病肾病(DN)是糖尿病的常见并发症,但目前可用的预防 DN 的治疗方法的疗效仍不尽人意。在本研究中,我们旨在探讨当归补血汤(DGT)对高糖(HG)诱导的系膜细胞增殖和细胞外基质在系膜细胞中的积累的影响。我们发现 DGT 可剂量依赖性地上调小鼠系膜细胞(SV40 MES-13)中生长停滞特异性转录物 5(GAS5)和 IκB 激酶(IKK)的表达。我们发现 DGT 通过 GAS5 调节 IKK 的表达和核转录因子-κB(NF-κB)的活性,并证明长链非编码 RNA(lncRNA)GAS5 与 IKK 呈正相关。并证明 GAS5 调节 IKK 的表达和 NF-κB 的活性。此外,DGT 通过 GAS5 抑制 MES-13 细胞活力和细胞外基质相关蛋白(层粘连蛋白(LN)、纤维连接蛋白(FN)和胶原 IV(Col IV))的表达。此外,我们证明 GAS5 通过 NF-κB 途径调节 SV40 MES-13 细胞活力和细胞外基质相关蛋白的表达。DGT 通过 GAS5/NF-κB 抑制系膜细胞增殖和细胞外基质积累,因此,DGT 可有效预防 DN。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b710/6822488/3724bc8d28d3/bsr-39-bsr20181740-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b710/6822488/67502d3b0c0c/bsr-39-bsr20181740-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b710/6822488/362fb40f1581/bsr-39-bsr20181740-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b710/6822488/7b7110e0fa86/bsr-39-bsr20181740-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b710/6822488/0485579715d1/bsr-39-bsr20181740-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b710/6822488/ce2addad11df/bsr-39-bsr20181740-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b710/6822488/3724bc8d28d3/bsr-39-bsr20181740-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b710/6822488/67502d3b0c0c/bsr-39-bsr20181740-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b710/6822488/362fb40f1581/bsr-39-bsr20181740-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b710/6822488/7b7110e0fa86/bsr-39-bsr20181740-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b710/6822488/0485579715d1/bsr-39-bsr20181740-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b710/6822488/ce2addad11df/bsr-39-bsr20181740-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b710/6822488/3724bc8d28d3/bsr-39-bsr20181740-g6.jpg

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