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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

Effects of JSDS on Ang II-induced expression of α-SMA in CFs. (A) mRNA expression levels of α-SMA in the different groups were assessed using reverse trancsription-quantitative polymerase chain reaction analysis. (B) Fluorescence intensity of the expression of α-SMA. (C) Cellular α-SMA was visualized using fluorescein isothiocyanateconjugated IgG by immunofluorescence staining. Representative images of the (a) control group, the (b) AngII-treated group and the (c) JSDS-treated group. 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. Original magnification, ×20, with representative images shown; n=3. CFs, cardiac fibroblasts; JSDS, Jia-Shen decoction-medicated serum; α-SMA, α-smooth muscle actin; Ang II, angiotensin II.
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f5-mmr-14-02-1610: Effects of JSDS on Ang II-induced expression of α-SMA in CFs. (A) mRNA expression levels of α-SMA in the different groups were assessed using reverse trancsription-quantitative polymerase chain reaction analysis. (B) Fluorescence intensity of the expression of α-SMA. (C) Cellular α-SMA was visualized using fluorescein isothiocyanateconjugated IgG by immunofluorescence staining. Representative images of the (a) control group, the (b) AngII-treated group and the (c) JSDS-treated group. 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. Original magnification, ×20, with representative images shown; n=3. CFs, cardiac fibroblasts; JSDS, Jia-Shen decoction-medicated serum; α-SMA, α-smooth muscle actin; Ang II, angiotensin II.

Mentions: As CFs can transform into myofibroblasts (MFs), the present study determined whether JSDS can affect the phenotypic switching of CFs following treatment with Ang II. The mRNA and protein expression levels of α-SMA were detected using RT-qPCR analyses and immunofluorescence. The results showed that the expression of α-SMA was significantly increased following Ang II stimulation at the mRNA and protein levels, which were decreased following JSDS treatment (Fig. 5A–C).


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)

Effects of JSDS on Ang II-induced expression of α-SMA in CFs. (A) mRNA expression levels of α-SMA in the different groups were assessed using reverse trancsription-quantitative polymerase chain reaction analysis. (B) Fluorescence intensity of the expression of α-SMA. (C) Cellular α-SMA was visualized using fluorescein isothiocyanateconjugated IgG by immunofluorescence staining. Representative images of the (a) control group, the (b) AngII-treated group and the (c) JSDS-treated group. 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. Original magnification, ×20, with representative images shown; n=3. CFs, cardiac fibroblasts; JSDS, Jia-Shen decoction-medicated serum; α-SMA, α-smooth muscle actin; Ang II, angiotensin II.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f5-mmr-14-02-1610: Effects of JSDS on Ang II-induced expression of α-SMA in CFs. (A) mRNA expression levels of α-SMA in the different groups were assessed using reverse trancsription-quantitative polymerase chain reaction analysis. (B) Fluorescence intensity of the expression of α-SMA. (C) Cellular α-SMA was visualized using fluorescein isothiocyanateconjugated IgG by immunofluorescence staining. Representative images of the (a) control group, the (b) AngII-treated group and the (c) JSDS-treated group. 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. Original magnification, ×20, with representative images shown; n=3. CFs, cardiac fibroblasts; JSDS, Jia-Shen decoction-medicated serum; α-SMA, α-smooth muscle actin; Ang II, angiotensin II.
Mentions: As CFs can transform into myofibroblasts (MFs), the present study determined whether JSDS can affect the phenotypic switching of CFs following treatment with Ang II. The mRNA and protein expression levels of α-SMA were detected using RT-qPCR analyses and immunofluorescence. The results showed that the expression of α-SMA was significantly increased following Ang II stimulation at the mRNA and protein levels, which were decreased following JSDS treatment (Fig. 5A–C).

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