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葛根素通过抑制TGF-1/Smad2介导的内皮-间充质转化来预防心脏纤维化。

Puerarin Protects against Cardiac Fibrosis Associated with the Inhibition of TGF-1/Smad2-Mediated Endothelial-to-Mesenchymal Transition.

作者信息

Jin Ya-Ge, Yuan Yuan, Wu Qing-Qing, Zhang Ning, Fan Di, Che Yan, Wang Zhao-Peng, Xiao Yang, Wang Sha-Sha, Tang Qi-Zhu

机构信息

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.

Cardiovascular Research Institute of Wuhan University, Wuhan, China.

出版信息

PPAR Res. 2017;2017:2647129. doi: 10.1155/2017/2647129. Epub 2017 May 30.

DOI:10.1155/2017/2647129
PMID:28638404
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5468594/
Abstract

BACKGROUND

Puerarin is a kind of flavonoids and is extracted from Chinese herb Kudzu root. Puerarin is widely used as an adjuvant therapy in Chinese clinics. But little is known about its effects on regulating cardiac fibrosis.

METHODS

Mice were subjected to transverse aorta constriction (TAC) for 8 weeks; meanwhile puerarin was given 1 week after TAC. Cardiac fibrosis was assessed by pathological staining. The mRNA and protein changes of CD31 and vimentin in both animal and human umbilical vein endothelial cells (HUVECs) models were detected. Immunofluorescence colocalization of CD31 and vimentin and scratch test were carried out to examine TGF-1-induced changes in HUVECs. The agonist and antagonist of peroxisome proliferator-activated receptor- (PPAR-) were used to explore the underlying mechanism.

RESULTS

Puerarin mitigated TAC-induced cardiac fibrosis, accompanied with suppressed endothelial-to-mesenchymal transition (EndMT). The consistent results were achieved in HUVECs model. TGF-1/Smad2 signaling pathway was blunted and PPAR- expression was upregulated in puerarin-treated mice and HUVECs. Pioglitazone could reproduce the protective effect in HUVECs, while GW9662 reversed this effect imposed by puerarin.

CONCLUSION

Puerarin protected against TAC-induced cardiac fibrosis, and this protective effect may be attributed to the upregulation of PPAR- and the inhibition of TGF-1/Smad2-mediated EndMT.

摘要

背景

葛根素是一种黄酮类化合物，从中药葛根中提取。葛根素在中国临床中被广泛用作辅助治疗药物。但关于其对心脏纤维化调节作用的了解甚少。

方法

将小鼠进行横向主动脉缩窄（TAC）8周；同时在TAC后1周给予葛根素。通过病理染色评估心脏纤维化。检测动物模型和人脐静脉内皮细胞（HUVECs）模型中CD31和波形蛋白的mRNA和蛋白变化。进行CD31和波形蛋白的免疫荧光共定位及划痕试验，以检测转化生长因子-1（TGF-1）诱导的HUVECs变化。使用过氧化物酶体增殖物激活受体-（PPAR-）激动剂和拮抗剂探索潜在机制。

结果

葛根素减轻了TAC诱导的心脏纤维化，并伴有内皮-间充质转化（EndMT）受抑制。在HUVECs模型中也得到了一致的结果。在葛根素处理的小鼠和HUVECs中，TGF-1/Smad2信号通路减弱，PPAR-表达上调。吡格列酮可在HUVECs中重现保护作用，而GW9662可逆转葛根素施加的这种作用。

结论

葛根素可预防TAC诱导的心脏纤维化，这种保护作用可能归因于PPAR-的上调以及对TGF-1/Smad2介导的EndMT的抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/a5fb6c18f292/PPAR2017-2647129.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/f2518d3f7cd9/PPAR2017-2647129.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/7e9e65668d87/PPAR2017-2647129.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/061a2597c8f7/PPAR2017-2647129.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/a74d3d72ae2f/PPAR2017-2647129.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/c64812b7d36f/PPAR2017-2647129.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/ff233def9947/PPAR2017-2647129.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/a5fb6c18f292/PPAR2017-2647129.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/f2518d3f7cd9/PPAR2017-2647129.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/7e9e65668d87/PPAR2017-2647129.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/061a2597c8f7/PPAR2017-2647129.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/a74d3d72ae2f/PPAR2017-2647129.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/c64812b7d36f/PPAR2017-2647129.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/ff233def9947/PPAR2017-2647129.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/df28/5468594/a5fb6c18f292/PPAR2017-2647129.007.jpg

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