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Jia-Shen decoction-medicated serum inhibits angiotensin-II induced cardiac fibroblast proliferation via the TGF-β1/Smad signaling pathway.

Cui L, Wang Y, Yu R, Li B, Xie S, Gao Y, Wang X, Zhu M - Mol Med Rep (2016)

Bottom Line: Jia-Shen decoction (JSD) is a traditional Chinese medicine, which is used widely to treat chronic heart failure.In addition, the mRNA expression levels of transforming growth factor‑β1 (TGF‑β1) and phosphorylated small mothers against decapentaplegic (p‑Smad)2/3 and their protein expression levels were analyzed.The expression levels of collagen, α‑smooth muscle actin, TGF‑β1 and p‑Smad2/3 were also increased in the Ang II‑treated group (P<0.05).

View Article: PubMed Central - PubMed

Affiliation: Central Laboratory, First Affiliated Hospital, Henan University of Traditional Chinese Medicine, Zhengzhou, Henan 450000, P.R. China.

ABSTRACT
Jia-Shen decoction (JSD) is a traditional Chinese medicine, which is used widely to treat chronic heart failure. However, the underlying mechanism remains to be elucidated. The present study aimed to investigate the mechanism underlying the effects of JSD on cardiac fibroblast (CF) proliferation and differentiation. The CFs were obtained from the hearts of neonatal (1‑3‑day old) Sprague‑Dawley rats and treated with JSD-medicated serum (JSDS) with or without angiotensin II (Ang II). Cell proliferation was assessed using Cell Counting Kit‑8 reagent. In addition, the mRNA expression levels of transforming growth factor‑β1 (TGF‑β1) and phosphorylated small mothers against decapentaplegic (p‑Smad)2/3 and their protein expression levels were analyzed. CF proliferation was significantly increased in the Ang II‑treated group, compared with the control group (P<0.05). The expression levels of collagen, α‑smooth muscle actin, TGF‑β1 and p‑Smad2/3 were also increased in the Ang II‑treated group (P<0.05). Following JSDS treatment, the increased levels of collagen and cell proliferation were inhibited, and the increased expression levels of p‑Smad2 and p‑Smad3 were also inhibited (P<0.05). These data suggested that JSDS may inhibit CF proliferation via attenuating the TGF‑β1/Smad signaling pathway.

No MeSH data available.


Related in: MedlinePlus

JSDS inhibits Ang II-induced cell proliferation and reduces collagen content in CFs. (A) Neonatal rat CFs were treated with different concentrations of JSDS and Ang II (1 µM) for 24 h. The number of cells are presented as an OD value, determined using a cell count assay. (B) Content of hydroxyproline in cell culture medium. *P<0.05, compared with the control group; #P<0.05, compared with the Ang II-treated group. Data are presented as the mean ± standard error of the mean. CFs, cardiac fibroblasts; JSDS, Jia-Shen decoction-medicated serum; Ang II, angiotensin II; OD, optical density.
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f3-mmr-14-02-1610: JSDS inhibits Ang II-induced cell proliferation and reduces collagen content in CFs. (A) Neonatal rat CFs were treated with different concentrations of JSDS and Ang II (1 µM) for 24 h. The number of cells are presented as an OD value, determined using a cell count assay. (B) Content of hydroxyproline in cell culture medium. *P<0.05, compared with the control group; #P<0.05, compared with the Ang II-treated group. Data are presented as the mean ± standard error of the mean. CFs, cardiac fibroblasts; JSDS, Jia-Shen decoction-medicated serum; Ang II, angiotensin II; OD, optical density.

Mentions: To determine whether JSDS inhibited CF proliferation, the neonatal rat CFs were incubated with different concentrations of JSDS and Ang II (1 µM) for 24 and 48 h. (Fig. 2A and B). The numbers of CFs were evaluated via cell count analysis, represented as an optical density value, and the content of hydroxyproline. Ang II significantly increased the number of CFs and the hydroxyproline concentration in the medium. JSDS effectively protected against the Ang II-induced proliferation of CFs in a concentration-dependent manner (Fig. 3A and B). Compared with the control group, the proliferation and collagen content of the Ang II-treated group were significantly increased (P<0.05). In the 10% JSDS-treated group and 5% JSDS-treated group, the increases in proliferation and collagen content were significantly decreased, compared with the Ang II-treated group (P<0.05). No significant alterations in the cell numbers or hydroxyproline levels were detected following JSDS treatment without Ang II stimulation (data not shown).


Jia-Shen decoction-medicated serum inhibits angiotensin-II induced cardiac fibroblast proliferation via the TGF-β1/Smad signaling pathway.

Cui L, Wang Y, Yu R, Li B, Xie S, Gao Y, Wang X, Zhu M - Mol Med Rep (2016)

JSDS inhibits Ang II-induced cell proliferation and reduces collagen content in CFs. (A) Neonatal rat CFs were treated with different concentrations of JSDS and Ang II (1 µM) for 24 h. The number of cells are presented as an OD value, determined using a cell count assay. (B) Content of hydroxyproline in cell culture medium. *P<0.05, compared with the control group; #P<0.05, compared with the Ang II-treated group. Data are presented as the mean ± standard error of the mean. CFs, cardiac fibroblasts; JSDS, Jia-Shen decoction-medicated serum; Ang II, angiotensin II; OD, optical density.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4940101&req=5

f3-mmr-14-02-1610: JSDS inhibits Ang II-induced cell proliferation and reduces collagen content in CFs. (A) Neonatal rat CFs were treated with different concentrations of JSDS and Ang II (1 µM) for 24 h. The number of cells are presented as an OD value, determined using a cell count assay. (B) Content of hydroxyproline in cell culture medium. *P<0.05, compared with the control group; #P<0.05, compared with the Ang II-treated group. Data are presented as the mean ± standard error of the mean. CFs, cardiac fibroblasts; JSDS, Jia-Shen decoction-medicated serum; Ang II, angiotensin II; OD, optical density.
Mentions: To determine whether JSDS inhibited CF proliferation, the neonatal rat CFs were incubated with different concentrations of JSDS and Ang II (1 µM) for 24 and 48 h. (Fig. 2A and B). The numbers of CFs were evaluated via cell count analysis, represented as an optical density value, and the content of hydroxyproline. Ang II significantly increased the number of CFs and the hydroxyproline concentration in the medium. JSDS effectively protected against the Ang II-induced proliferation of CFs in a concentration-dependent manner (Fig. 3A and B). Compared with the control group, the proliferation and collagen content of the Ang II-treated group were significantly increased (P<0.05). In the 10% JSDS-treated group and 5% JSDS-treated group, the increases in proliferation and collagen content were significantly decreased, compared with the Ang II-treated group (P<0.05). No significant alterations in the cell numbers or hydroxyproline levels were detected following JSDS treatment without Ang II stimulation (data not shown).

Bottom Line: Jia-Shen decoction (JSD) is a traditional Chinese medicine, which is used widely to treat chronic heart failure.In addition, the mRNA expression levels of transforming growth factor‑β1 (TGF‑β1) and phosphorylated small mothers against decapentaplegic (p‑Smad)2/3 and their protein expression levels were analyzed.The expression levels of collagen, α‑smooth muscle actin, TGF‑β1 and p‑Smad2/3 were also increased in the Ang II‑treated group (P<0.05).

View Article: PubMed Central - PubMed

Affiliation: Central Laboratory, First Affiliated Hospital, Henan University of Traditional Chinese Medicine, Zhengzhou, Henan 450000, P.R. China.

ABSTRACT
Jia-Shen decoction (JSD) is a traditional Chinese medicine, which is used widely to treat chronic heart failure. However, the underlying mechanism remains to be elucidated. The present study aimed to investigate the mechanism underlying the effects of JSD on cardiac fibroblast (CF) proliferation and differentiation. The CFs were obtained from the hearts of neonatal (1‑3‑day old) Sprague‑Dawley rats and treated with JSD-medicated serum (JSDS) with or without angiotensin II (Ang II). Cell proliferation was assessed using Cell Counting Kit‑8 reagent. In addition, the mRNA expression levels of transforming growth factor‑β1 (TGF‑β1) and phosphorylated small mothers against decapentaplegic (p‑Smad)2/3 and their protein expression levels were analyzed. CF proliferation was significantly increased in the Ang II‑treated group, compared with the control group (P<0.05). The expression levels of collagen, α‑smooth muscle actin, TGF‑β1 and p‑Smad2/3 were also increased in the Ang II‑treated group (P<0.05). Following JSDS treatment, the increased levels of collagen and cell proliferation were inhibited, and the increased expression levels of p‑Smad2 and p‑Smad3 were also inhibited (P<0.05). These data suggested that JSDS may inhibit CF proliferation via attenuating the TGF‑β1/Smad signaling pathway.

No MeSH data available.


Related in: MedlinePlus