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含肾衰方的血清抑制转化生长因子-β1诱导的正常大鼠肾间质成纤维细胞肌成纤维细胞分化。

Shenweifang-containing serum inhibits transforming growth factor-β1 induced myofibroblast differentiation in normal rat kidney interstitial fibroblast cell.

机构信息

Department of Nephrology, the Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.

Nephropathy Clinical Medical Research Center of Sichuan Province, Luzhou 646000, China.

出版信息

J Tradit Chin Med. 2022 Feb;42(1):39-48. doi: 10.19852/j.cnki.jtcm.2022.01.004.

DOI:10.19852/j.cnki.jtcm.2022.01.004
PMID:35294121
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10164629/
Abstract

OBJECTIVE

To investigate the efficacy of Shenweifang (SWF)-containing serum on transforming growth factor (TGF)-β1-induced fibroblast-myofibroblast transition in normal rat kidney interstitial fibroblast cells (NRK-49F).

METHODS

Sprague-Dawley rats were gavaged with one of five solutions: (a) saline; (b) saline plus low-dose SWF; (c) saline plus medium-dose SWF; (d) saline plus highdose SWF; and (e) saline plus valsartan. NRK-49F cells were treated with TGF-β1 and cultured using serum from the gavaged rats.

RESULTS

TGF-β1 treatment increased the expression of α-smooth muscle actin, proliferating cell nuclear antigen, collagen I, Smad3, mitogen-activated protein kinase (MAPK) 10, and c-Jun N-terminal kinase (JNK) 3 and induced abnormalities in cell morphology, cell cycle progression, and cell proliferation.

CONCLUSIONS

SWF- or valsartan-containing serum corrected (or partially corrected) TGF-β1-induced abnormal changes in this in vitro system. SWF-containing serum reversed abnormalities in morphology, cell cycle progression, and proliferation in TGF-β1-treated NRK49F cells, probably by blocking the TGF-β1/Smads and TGF-β1/MAPK/JNK pathways.

摘要

目的

观察参味方含药血清对转化生长因子-β1(TGF-β1)诱导的正常大鼠肾间质成纤维细胞(NRK-49F)转分化为肌成纤维细胞的影响。

方法

SD 大鼠灌胃给予生理盐水和不同剂量参味方(低、中、高剂量)及缬沙坦,制备含药血清。体外培养 NRK-49F 细胞,分为正常对照组、TGF-β1 模型组、TGF-β1+参味方低、中、高剂量组、TGF-β1+缬沙坦组,采用 Western blot 法检测细胞中α-平滑肌肌动蛋白(α-SMA)、增殖细胞核抗原(PCNA)、Ⅰ型胶原(ColⅠ)、Smad3、丝裂原活化蛋白激酶 10(MAPK10)和 c-Jun N-末端激酶(JNK)3 的表达,观察细胞形态学变化,流式细胞术检测细胞周期,四甲基偶氮唑盐比色法(MTT)检测细胞增殖。

结果

TGF-β1 可增加α-SMA、PCNA、ColⅠ、Smad3、MAPK10 和 JNK3 的表达,引起细胞形态改变、细胞周期异常和增殖增加;参味方或缬沙坦含药血清可部分纠正 TGF-β1 诱导的上述改变。

结论

参味方含药血清可能通过抑制 TGF-β1/Smads 和 TGF-β1/MAPK/JNK 信号通路,部分纠正 TGF-β1 诱导的 NRK-49F 细胞形态、细胞周期和增殖异常。

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