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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

α-SMA immunohistochemical findings on days 3, 7, 14, and 35. α-SMA immunopositive cells in skin ulcer site are shown ((a); scale bar, 100 μm). The numbers of α-SMA immunopositive cells per field were counted in the damaged area including ulcer site, ulcer edge and granulation tissue (b). All values are presented as mean ± SE (n = 4–7). *P < .05. **P < .01 versus control.
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fig8: α-SMA immunohistochemical findings on days 3, 7, 14, and 35. α-SMA immunopositive cells in skin ulcer site are shown ((a); scale bar, 100 μm). The numbers of α-SMA immunopositive cells per field were counted in the damaged area including ulcer site, ulcer edge and granulation tissue (b). All values are presented as mean ± SE (n = 4–7). *P < .05. **P < .01 versus control.

Mentions: Positive reactions to anti-α-SMA antibody were observed at the ulcer edge and just below the portion of pressure loading. At the ulcer edge, vascular smooth muscle cells showed positive reaction to anti-α-SMA antibody in all groups from day 3. On day 7, positive reaction to anti-α-SMA was observed not only at vascular smooth muscle cells of subcutaneous tissue but also at myofibroblasts around granulated areas in connective tissue. On day 14, more α-SMA-positive myofibroblasts were seen in connective tissue, but on day 35 their number had decreased (Figure 8(a)). The images of stained whole fields of injured tissue, from the epidermis to the fascia of the hamstring, were scanned into the computer system, and the area of the positive reaction to anti-α-SMA antibody was measured by image analysis software. The average of the area of the positive reaction to anti-α-SMA antibody was calculated. The result showed that, on day 3, the area of the positive reaction to anti-α-SMA antibody in the HD-KKT group was significantly higher compared to control, on day 14 that of each group reached a peak, and on day 35 those in the LD-KKT and HD-KKT groups significantly decreased compared to that in the control group (Figure 8(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)

α-SMA immunohistochemical findings on days 3, 7, 14, and 35. α-SMA immunopositive cells in skin ulcer site are shown ((a); scale bar, 100 μm). The numbers of α-SMA immunopositive cells per field were counted in the damaged area including ulcer site, ulcer edge and granulation tissue (b). All values are presented 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

fig8: α-SMA immunohistochemical findings on days 3, 7, 14, and 35. α-SMA immunopositive cells in skin ulcer site are shown ((a); scale bar, 100 μm). The numbers of α-SMA immunopositive cells per field were counted in the damaged area including ulcer site, ulcer edge and granulation tissue (b). All values are presented as mean ± SE (n = 4–7). *P < .05. **P < .01 versus control.
Mentions: Positive reactions to anti-α-SMA antibody were observed at the ulcer edge and just below the portion of pressure loading. At the ulcer edge, vascular smooth muscle cells showed positive reaction to anti-α-SMA antibody in all groups from day 3. On day 7, positive reaction to anti-α-SMA was observed not only at vascular smooth muscle cells of subcutaneous tissue but also at myofibroblasts around granulated areas in connective tissue. On day 14, more α-SMA-positive myofibroblasts were seen in connective tissue, but on day 35 their number had decreased (Figure 8(a)). The images of stained whole fields of injured tissue, from the epidermis to the fascia of the hamstring, were scanned into the computer system, and the area of the positive reaction to anti-α-SMA antibody was measured by image analysis software. The average of the area of the positive reaction to anti-α-SMA antibody was calculated. The result showed that, on day 3, the area of the positive reaction to anti-α-SMA antibody in the HD-KKT group was significantly higher compared to control, on day 14 that of each group reached a peak, and on day 35 those in the LD-KKT and HD-KKT groups significantly decreased compared to that in the control group (Figure 8(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