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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 relative mRNA and protein levels of TGF-β1 in CFs. (A) mRNA expression levels of TGF-β1 were assessed using reverse transcription-quantitative polymerase chain reaction analysis. Data were normalized to GAPDH mRNA. (B) Cell lysates were analyzed to determine the protein expression levels of TGF-β1 using western blot analysis. Values are expressed as the mean ± standard error of the mean (n=3). *P<0.05, compared with the control group; #P<0.05, compared with the Ang II-treated group. CFs, cardiac fibroblasts; JSDS, Jia-Shen decoction-medicated serum; TGF-β1, transforming growth factor-β1; Ang II, angiotensin II.
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f6-mmr-14-02-1610: JSDS inhibits Ang II-induced relative mRNA and protein levels of TGF-β1 in CFs. (A) mRNA expression levels of TGF-β1 were assessed using reverse transcription-quantitative polymerase chain reaction analysis. Data were normalized to GAPDH mRNA. (B) Cell lysates were analyzed to determine the protein expression levels of TGF-β1 using western blot analysis. Values are expressed as the mean ± standard error of the mean (n=3). *P<0.05, compared with the control group; #P<0.05, compared with the Ang II-treated group. CFs, cardiac fibroblasts; JSDS, Jia-Shen decoction-medicated serum; TGF-β1, transforming growth factor-β1; Ang II, angiotensin II.

Mentions: Following stimulation with Ang II, the mRNA levels of TGF-β1 in the CFs were significantly increased (P<0.05). The administration of JSDS prevented this by downregulating the mRNA level of TGF-β1 stimulated by Ang II (P<0.05; Fig. 6A). The protein levels of TGF-β1 and p-Smad2/3 were significantly increased when the cells were treated with Ang II. The administration of JSDS prevented this, downregulating the protein levels of TGF-β1 and p-Smad2/3 stimulated by Ang II (P<0.05; Figs. 6B, 7A and B).


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 relative mRNA and protein levels of TGF-β1 in CFs. (A) mRNA expression levels of TGF-β1 were assessed using reverse transcription-quantitative polymerase chain reaction analysis. Data were normalized to GAPDH mRNA. (B) Cell lysates were analyzed to determine the protein expression levels of TGF-β1 using western blot analysis. Values are expressed as the mean ± standard error of the mean (n=3). *P<0.05, compared with the control group; #P<0.05, compared with the Ang II-treated group. CFs, cardiac fibroblasts; JSDS, Jia-Shen decoction-medicated serum; TGF-β1, transforming growth factor-β1; Ang II, angiotensin II.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f6-mmr-14-02-1610: JSDS inhibits Ang II-induced relative mRNA and protein levels of TGF-β1 in CFs. (A) mRNA expression levels of TGF-β1 were assessed using reverse transcription-quantitative polymerase chain reaction analysis. Data were normalized to GAPDH mRNA. (B) Cell lysates were analyzed to determine the protein expression levels of TGF-β1 using western blot analysis. Values are expressed as the mean ± standard error of the mean (n=3). *P<0.05, compared with the control group; #P<0.05, compared with the Ang II-treated group. CFs, cardiac fibroblasts; JSDS, Jia-Shen decoction-medicated serum; TGF-β1, transforming growth factor-β1; Ang II, angiotensin II.
Mentions: Following stimulation with Ang II, the mRNA levels of TGF-β1 in the CFs were significantly increased (P<0.05). The administration of JSDS prevented this by downregulating the mRNA level of TGF-β1 stimulated by Ang II (P<0.05; Fig. 6A). The protein levels of TGF-β1 and p-Smad2/3 were significantly increased when the cells were treated with Ang II. The administration of JSDS prevented this, downregulating the protein levels of TGF-β1 and p-Smad2/3 stimulated by Ang II (P<0.05; Figs. 6B, 7A and B).

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