Expression of miR-106b-25 induced by salvianolic acid B inhibits epithelial-to-mesenchymal transition in HK-2 cells

Tang, Qiong; Zhong, Haizhen A.; Xie, Fengyan; Xie, Jianyong; Yao, Gang

doi:10.1016/j.ejphar.2014.07.051

Cited by 40 publications

(29 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has been reported that SAB could effectively reverse liver fibrosis in patients suffering from chronic hepatitis B16. Furthermore, SAB could possibly facilitate the repair of tubular epithelial structures and the regression of renal fibrosis in injured kidneys21. Therefore, we carried out further in vivo and in vitro studies to examine the effect as well as the mechanism of SAB on pulmonary fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Salvianolic Acid B Attenuates Experimental Pulmonary Fibrosis through Inhibition of the TGF-β Signaling Pathway

Liu

Chu

et al. 2016

Sci Rep

View full text Add to dashboard Cite

Pulmonary fibrosis is a progressive and fatal disorder. In our previous study, we found that the Yiqihuoxue formula (YQHX), a prescription of Traditional Chinese Medicine, had a curative effect on scleroderma, a typical fibrotic disease. The aim of this study was to determine the key ingredient mediating the therapeutic effects of YQHX and to examine its effect on pulmonary fibrosis, including its mechanism. Luciferase reporter assays showed that the most important anti-fibrotic component of the YQHX was Salviae miltiorrhiza (SM). Experiments performed using a bleomycin-instilled mouse model of pulmonary fibrosis showed that Salvianolic acid B (SAB), the major ingredient of SM, had strong anti-inflammatory and anti-fibrotic effects through its inhibition of inflammatory cell infiltration, alveolar structure disruption, and collagen deposition. Furthermore, SAB suppressed TGF-β-induced myofibroblastic differentiation of MRC-5 fibroblasts and TGF-β-mediated epithelial-to-mesenchymal transition of A549 cells by inhibiting both Smad-dependent signaling and the Smad-independent MAPK pathway. Taken together, our results suggest that SM is the key anti-fibrotic component of the YQHX and that SAB, the major ingredient of SM, alleviates experimental pulmonary fibrosis both in vivo and in vitro by inhibiting the TGF-β signaling pathway. Together, these results suggest that SAB potently inhibits pulmonary fibrosis.

show abstract

Section: Discussionmentioning

confidence: 99%

Salvianolic Acid B Attenuates Experimental Pulmonary Fibrosis through Inhibition of the TGF-β Signaling Pathway

Liu

Chu

et al. 2016

Sci Rep

View full text Add to dashboard Cite

show abstract

“…ShenKang injection (SKI), a Chinese Material Medica‐standardized product extracted from Rhubarb, Astragalus, Radix Salviae miltiorrhizae and Carthami Flos, is formulated base on TCM theory and widely applied in clinical treatment of CKD. Its four components have been widely reported their protection of kidney [14–17]. However, unclearness of functional mechanism of SKI limits its modernization and acceptance by Western medicine.…”

Section: Introductionmentioning

confidence: 99%

“…Its four components have been widely reported their protection of kidney. [14][15][16][17] However, unclearness of functional mechanism of SKI limits its modernization and acceptance by Western medicine. In the present study, we first studied the therapeutic potential of SKI, and indicated its ability of antifibrosis.…”

Section: Introductionmentioning

confidence: 99%

ShenKang injection suppresses kidney fibrosis and oxidative stress via transforming growth factor-β/Smad3 signalling pathway in vivo and in vitro

Guan

Yan

et al. 2015

Journal of Pharmacy and Pharmacology

View full text Add to dashboard Cite

show abstract

“…Salvianolic acid, an active compound present in Salvia miltiorrhiza, can suppress CCL-20 expression in TNF-α-treated macrophages [264]. Salvianolic acid B (1-100 µM)-induced expression of miR-106b-25 can suppress EMT of HK-2 cells [265]. Salvianolic acid B (1-10 µM) can prevent EMT through the TGF-1 signal transduction pathway [266].…”

Section: Reversal Of Emt By Anti-inflammatory Natural Compoundsmentioning

confidence: 99%

Reversal of Epithelial–Mesenchymal Transition by Natural Anti-Inflammatory and Pro-Resolving Lipids

Lee

2019

Cancers

View full text Add to dashboard Cite

Epithelial mesenchymal transition (EMT) is a key process in the progression of malignant cancer. Therefore, blocking the EMT can be a critical fast track for the development of anticancer drugs. In this paper, we update recent research output of EMT and we explore suppression of EMT by natural anti-inflammatory compounds and pro-resolving lipids.A typical signaling pathway of EMT is the transforming growth factor-β1 (TGF-β1) pathway. TGF-β1 induces EMT via SMAD-dependent or non-SMAD signaling pathway [7]. Growth factors including FGF, HGF, IGF1, EGF, and PDGF via receptor tyrosine kinase can induce EMT via signaling pathway of PI3K-AKT and ERK MAPK [8][9][10][11]. Wnt signaling, hedgehog signaling, Notch signaling, hypoxia, and inflammatory tumor microenvironment also involves in EMT [5]. Recently, it has been shown that hippo signaling is also involved in EMT [12]. YAP and TAZ can enhance EMT through upregulation of EMT transcription factors such as forkhead box C2 (FOXC2), snail family zinc finger 1/2 (SNAIL1, SLUG), twist-related protein 1 (TWIST1), and ZEB1 [12-15]. Transcription Factors Involved in EMTNovel players are newly recognized as regulatory transcription factor in the EMT. Brachyury, the T-box transcription factor, is a novel transcription factor implicated in the EMT of cancer cells [16]. Brachyury is known as the target gene of WNT, one of the m ajor signaling pathways of EMT [17]. Foxq1, one of forkhead transcription factor, has also regarded as a novel transcription factor mediating the EMT of gastric cancer [6,18]. Runt-related transcription factor 2 (Runx2) belongs to the runt-related transcription factor family [19]. Runx2 plays a key role in EMT of hepatocellular carcinoma (HCC) [20]. GATA transcription factors are also implicated in the EMT of cancer cells [21].A typical signaling pathway of EMT is the transforming growth factor-β1 (TGF-β1) pathway. TGF-β1 induces EMT via SMAD-dependent or non-SMAD signaling pathway [7]. Growth factors including FGF, HGF, IGF1, EGF, and PDGF via receptor tyrosine kinase can induce EMT via signaling pathway of PI3K-AKT and ERK MAPK [8][9][10][11]. Wnt signaling, hedgehog signaling, Notch signaling, hypoxia, and inflammatory tumor microenvironment also involves in EMT [5]. Recently, it has been shown that hippo signaling is also involved in EMT [12]. YAP and TAZ can enhance EMT through upregulation of EMT transcription factors such as forkhead box C2 (FOXC2), snail family zinc finger 1/2 (SNAIL1, SLUG), twist-related protein 1 (TWIST1), and ZEB1 [12-15]. Transcription Factors Involved in EMTNovel players are newly recognized as regulatory transcription factor in the EMT. Brachyury, the T-box transcription factor, is a novel transcription factor implicated in the EMT of cancer cells [16]. Brachyury is known as the target gene of WNT, one of the major signaling pathways of EMT [17]. Foxq1, one of forkhead transcription factor, has also regarded as a novel transcription factor mediating the EMT of gastric cancer [6,18]. Runt-related transcription factor 2 (Runx2...

show abstract

Expression of miR-106b-25 induced by salvianolic acid B inhibits epithelial-to-mesenchymal transition in HK-2 cells

Cited by 40 publications

References 38 publications

Salvianolic Acid B Attenuates Experimental Pulmonary Fibrosis through Inhibition of the TGF-β Signaling Pathway

Salvianolic Acid B Attenuates Experimental Pulmonary Fibrosis through Inhibition of the TGF-β Signaling Pathway

ShenKang injection suppresses kidney fibrosis and oxidative stress via transforming growth factor-β/Smad3 signalling pathway in vivo and in vitro

Reversal of Epithelial–Mesenchymal Transition by Natural Anti-Inflammatory and Pro-Resolving Lipids

Contact Info

Product

Resources

About