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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

CD-31 immunohistochemical findings of vessels at pressure ulcer edge on days 3, 7, 14, and 35. CD-31 immunopositive vessels are stained brown ((a); scale bar, 100 μm). The numbers of CD-31 immunopositive vessels per field (×200) were counted at wound tissue area including ulcer site, ulcer edge and granulation tissue (b). Values are expressed as mean ± SE (n = 4–7). *P < .05, **P < .01, versus control.
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fig6: CD-31 immunohistochemical findings of vessels at pressure ulcer edge on days 3, 7, 14, and 35. CD-31 immunopositive vessels are stained brown ((a); scale bar, 100 μm). The numbers of CD-31 immunopositive vessels per field (×200) were counted at wound tissue area including ulcer site, ulcer edge and granulation tissue (b). Values are expressed as mean ± SE (n = 4–7). *P < .05, **P < .01, versus control.

Mentions: Positive reactions to anti-CD-31 antibody were observed at the ulcer edge and just below the part of pressure loading. At the ulcer edge, CD-31-positive vessels were observed in all groups after day 3, and more CD-31-positive vessels were seen in the LD-KKT and HD-KKT groups than in the control group. The numbers of CD-31-positive vessels of day 7 demonstrated an increasing tendency compared to those of day 3 in each group, and a lot of small vessels were seen on day 7. By day 14, the numbers of CD-31-positive vessels had decreased in all groups and then decreased further by day 35, becoming equal to normal skin not having undergone pressure loading (Figure 6(a)). The number of CD-31 immunopositive vessels per field (×200) was counted in the area of damaged tissue (ulcer site, ulcer edge, and granulation tissue), and on days 3 and 7 those of the LD-KKT and HD-KKT groups increased compared to that of the control group (Figure 6(b)).


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)

CD-31 immunohistochemical findings of vessels at pressure ulcer edge on days 3, 7, 14, and 35. CD-31 immunopositive vessels are stained brown ((a); scale bar, 100 μm). The numbers of CD-31 immunopositive vessels per field (×200) were counted at wound tissue area including ulcer site, ulcer edge and granulation tissue (b). 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

fig6: CD-31 immunohistochemical findings of vessels at pressure ulcer edge on days 3, 7, 14, and 35. CD-31 immunopositive vessels are stained brown ((a); scale bar, 100 μm). The numbers of CD-31 immunopositive vessels per field (×200) were counted at wound tissue area including ulcer site, ulcer edge and granulation tissue (b). Values are expressed as mean ± SE (n = 4–7). *P < .05, **P < .01, versus control.
Mentions: Positive reactions to anti-CD-31 antibody were observed at the ulcer edge and just below the part of pressure loading. At the ulcer edge, CD-31-positive vessels were observed in all groups after day 3, and more CD-31-positive vessels were seen in the LD-KKT and HD-KKT groups than in the control group. The numbers of CD-31-positive vessels of day 7 demonstrated an increasing tendency compared to those of day 3 in each group, and a lot of small vessels were seen on day 7. By day 14, the numbers of CD-31-positive vessels had decreased in all groups and then decreased further by day 35, becoming equal to normal skin not having undergone pressure loading (Figure 6(a)). The number of CD-31 immunopositive vessels per field (×200) was counted in the area of damaged tissue (ulcer site, ulcer edge, and granulation tissue), and on days 3 and 7 those of the LD-KKT and HD-KKT groups increased compared to that of the control group (Figure 6(b)).

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