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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

Characterization of primary cultured neonatal rat CFs. (A) Cell morphology of the first passage of neonatal rat CFs under an optical microscope. Original magnification, ×20. (B) Primary cultured CFs were subjected to immunofluorescence staining for vimentin to determine their purity. Red shows vimentin staining; DAPI is shown in blue (nuclear). Original magnification, ×40. CFs, cardiac fibroblasts.
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f1-mmr-14-02-1610: Characterization of primary cultured neonatal rat CFs. (A) Cell morphology of the first passage of neonatal rat CFs under an optical microscope. Original magnification, ×20. (B) Primary cultured CFs were subjected to immunofluorescence staining for vimentin to determine their purity. Red shows vimentin staining; DAPI is shown in blue (nuclear). Original magnification, ×40. CFs, cardiac fibroblasts.

Mentions: The first passage of neonatal rat CFs cultured in the present study had the typical morphological characteristics of fibroblasts, as evidenced by their spindle or polygonal shape and large ovoid nucleus (Fig. 1A). The results of the immunofluorescence staining revealed that these cells were positive for vimentin, a marker of fibroblasts (Fig. 1B).


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)

Characterization of primary cultured neonatal rat CFs. (A) Cell morphology of the first passage of neonatal rat CFs under an optical microscope. Original magnification, ×20. (B) Primary cultured CFs were subjected to immunofluorescence staining for vimentin to determine their purity. Red shows vimentin staining; DAPI is shown in blue (nuclear). Original magnification, ×40. CFs, cardiac fibroblasts.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f1-mmr-14-02-1610: Characterization of primary cultured neonatal rat CFs. (A) Cell morphology of the first passage of neonatal rat CFs under an optical microscope. Original magnification, ×20. (B) Primary cultured CFs were subjected to immunofluorescence staining for vimentin to determine their purity. Red shows vimentin staining; DAPI is shown in blue (nuclear). Original magnification, ×40. CFs, cardiac fibroblasts.
Mentions: The first passage of neonatal rat CFs cultured in the present study had the typical morphological characteristics of fibroblasts, as evidenced by their spindle or polygonal shape and large ovoid nucleus (Fig. 1A). The results of the immunofluorescence staining revealed that these cells were positive for vimentin, a marker of fibroblasts (Fig. 1B).

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