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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

Expressions of inflammatory cytokines in skin tissue of pressure ulcer on days 3, 7, 14, and 35 as examined by Western Blotting. (a) MCP-1, (b) IL-1β, (c) TNF-α. Values are expressed as mean ± SE (n = 4–7). *P < .05, **P < .01 versus control.
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fig9: Expressions of inflammatory cytokines in skin tissue of pressure ulcer on days 3, 7, 14, and 35 as examined by Western Blotting. (a) MCP-1, (b) IL-1β, (c) TNF-α. Values are expressed as mean ± SE (n = 4–7). *P < .05, **P < .01 versus control.

Mentions: Inflammatory cytokines: the protein levels of MCP-1 of the LD-KKT and HD-KKT groups were significantly lower than that the control group on day 3 (Figure 9(a)). The value of IL-1β in the HD-KKT group was significantly suppressed on days 3 and 7 compared to control (Figure 9(b)). TNF-α of the HD-KKT group was also significantly decreased compared to control on days 3 and 7 (Figure 9(c)).


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)

Expressions of inflammatory cytokines in skin tissue of pressure ulcer on days 3, 7, 14, and 35 as examined by Western Blotting. (a) MCP-1, (b) IL-1β, (c) TNF-α. Values are expressed as mean ± SE (n = 4–7). *P < .05, **P < .01 versus control.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig9: Expressions of inflammatory cytokines in skin tissue of pressure ulcer on days 3, 7, 14, and 35 as examined by Western Blotting. (a) MCP-1, (b) IL-1β, (c) TNF-α. Values are expressed as mean ± SE (n = 4–7). *P < .05, **P < .01 versus control.
Mentions: Inflammatory cytokines: the protein levels of MCP-1 of the LD-KKT and HD-KKT groups were significantly lower than that the control group on day 3 (Figure 9(a)). The value of IL-1β in the HD-KKT group was significantly suppressed on days 3 and 7 compared to control (Figure 9(b)). TNF-α of the HD-KKT group was also significantly decreased compared to control on days 3 and 7 (Figure 9(c)).

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