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Traditional Japanese formula kigikenchuto accelerates healing of pressure-loading skin ulcer in rats.

Kimura M, Shibahara N, Hikiami H, Yoshida T, Jo M, Kaneko M, Nogami T, Fujimoto M, Goto H, Shimada Y - Evid Based Complement Alternat Med (2011)

Bottom Line: Immunohistochemically, KKT increased CD-31-positive vessels in early phase and increased α-smooth muscle actin-(α-SMA-) positive fibroblastic cells in early phase and decreased them in late phase of wound healing.By Western blotting, KKT showed the potential to decrease inflammatory cytokines (MCP-1, IL-1β, and TNF-α) in early phase, decrease vascular endothelial growth factor in early phase and increase it in late phase, and modulate the expression of extracellular protein matrix (α-SMA, TGF-β1, bFGF, collagen III, and collagen I).These results suggested the possibility that KKT accelerates pressure ulcer healing through decreases of inflammatory cytokines, increase of angiogenesis, and induction of extracellular matrix remodeling.

View Article: PubMed Central - PubMed

Affiliation: Department of Japanese Oriental Medicine, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.

ABSTRACT
We evaluated the effect of kigikenchuto (KKT), a traditional Japanese formula, in a modified rat pressure-loading skin ulcer model. Rats were divided into three groups, KKT extract orally administered (250 or 500 mg/kg/day for 35 days) and control. KKT shortened the duration until healing. Immunohistochemically, KKT increased CD-31-positive vessels in early phase and increased α-smooth muscle actin-(α-SMA-) positive fibroblastic cells in early phase and decreased them in late phase of wound healing. By Western blotting, KKT showed the potential to decrease inflammatory cytokines (MCP-1, IL-1β, and TNF-α) in early phase, decrease vascular endothelial growth factor in early phase and increase it in late phase, and modulate the expression of extracellular protein matrix (α-SMA, TGF-β1, bFGF, collagen III, and collagen I). These results suggested the possibility that KKT accelerates pressure ulcer healing through decreases of inflammatory cytokines, increase of angiogenesis, and induction of extracellular matrix remodeling.

No MeSH data available.


Related in: MedlinePlus

Typical macroscopic view of pressure ulcer of control group on days 1, 7, 14, 21, 28, and 35. Pressure-loaded portion became necrotic after release of loading (day 1), and crust was formed in the ulcer site with redness of surrounding skin (day 7). Size of ulcer gradually decreased (days 14, 21, and 28), and disappeared (day 35).
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fig3: Typical macroscopic view of pressure ulcer of control group on days 1, 7, 14, 21, 28, and 35. Pressure-loaded portion became necrotic after release of loading (day 1), and crust was formed in the ulcer site with redness of surrounding skin (day 7). Size of ulcer gradually decreased (days 14, 21, and 28), and disappeared (day 35).

Mentions: Immediately after completion of pressure loading, the skin surface was depressed and partially colored brown or white. After day 1 the pressure-loading portion became necrotic, and the skin surrounding the ulcer edge turned red and a crust was formed at the ulcer site. Gradually the skin ulcer decreased in size and then disappeared (Figure 3).


Traditional Japanese formula kigikenchuto accelerates healing of pressure-loading skin ulcer in rats.

Kimura M, Shibahara N, Hikiami H, Yoshida T, Jo M, Kaneko M, Nogami T, Fujimoto M, Goto H, Shimada Y - Evid Based Complement Alternat Med (2011)

Typical macroscopic view of pressure ulcer of control group on days 1, 7, 14, 21, 28, and 35. Pressure-loaded portion became necrotic after release of loading (day 1), and crust was formed in the ulcer site with redness of surrounding skin (day 7). Size of ulcer gradually decreased (days 14, 21, and 28), and disappeared (day 35).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3108106&req=5

fig3: Typical macroscopic view of pressure ulcer of control group on days 1, 7, 14, 21, 28, and 35. Pressure-loaded portion became necrotic after release of loading (day 1), and crust was formed in the ulcer site with redness of surrounding skin (day 7). Size of ulcer gradually decreased (days 14, 21, and 28), and disappeared (day 35).
Mentions: Immediately after completion of pressure loading, the skin surface was depressed and partially colored brown or white. After day 1 the pressure-loading portion became necrotic, and the skin surrounding the ulcer edge turned red and a crust was formed at the ulcer site. Gradually the skin ulcer decreased in size and then disappeared (Figure 3).

Bottom Line: Immunohistochemically, KKT increased CD-31-positive vessels in early phase and increased α-smooth muscle actin-(α-SMA-) positive fibroblastic cells in early phase and decreased them in late phase of wound healing.By Western blotting, KKT showed the potential to decrease inflammatory cytokines (MCP-1, IL-1β, and TNF-α) in early phase, decrease vascular endothelial growth factor in early phase and increase it in late phase, and modulate the expression of extracellular protein matrix (α-SMA, TGF-β1, bFGF, collagen III, and collagen I).These results suggested the possibility that KKT accelerates pressure ulcer healing through decreases of inflammatory cytokines, increase of angiogenesis, and induction of extracellular matrix remodeling.

View Article: PubMed Central - PubMed

Affiliation: Department of Japanese Oriental Medicine, Graduate School of Medicine and Pharmaceutical Sciences, University of Toyama, 2630 Sugitani, Toyama 930-0194, Japan.

ABSTRACT
We evaluated the effect of kigikenchuto (KKT), a traditional Japanese formula, in a modified rat pressure-loading skin ulcer model. Rats were divided into three groups, KKT extract orally administered (250 or 500 mg/kg/day for 35 days) and control. KKT shortened the duration until healing. Immunohistochemically, KKT increased CD-31-positive vessels in early phase and increased α-smooth muscle actin-(α-SMA-) positive fibroblastic cells in early phase and decreased them in late phase of wound healing. By Western blotting, KKT showed the potential to decrease inflammatory cytokines (MCP-1, IL-1β, and TNF-α) in early phase, decrease vascular endothelial growth factor in early phase and increase it in late phase, and modulate the expression of extracellular protein matrix (α-SMA, TGF-β1, bFGF, collagen III, and collagen I). These results suggested the possibility that KKT accelerates pressure ulcer healing through decreases of inflammatory cytokines, increase of angiogenesis, and induction of extracellular matrix remodeling.

No MeSH data available.


Related in: MedlinePlus