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Investigating the potential of Shikonin as a novel hypertrophic scar treatment.

Fan C, Xie Y, Dong Y, Su Y, Upton Z - J. Biomed. Sci. (2015)

Bottom Line: Our results indicate that Shikonin preferentially inhibits cell proliferation and induces apoptosis in fibroblasts without affecting keratinocyte function.In addition, we found that the proliferation-inhibiting and apoptosis-inducing abilities of SHI might be triggered via MAPK and Bcl-2/Caspase 3 signalling pathways.Furthermore, SHI has been found to attenuate the expression of TGF-β1 in Transwell co-cultured "conditioned" medium.

View Article: PubMed Central - PubMed

Affiliation: Tissue Repair and Regeneration Program, Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, 4059, Australia. c3.fan@connect.qut.edu.au.

ABSTRACT

Background: Hypertrophic scarring is a highly prevalent condition clinically and results from a decreased number of apoptotic fibroblasts and over-abundant production of collagen during scar formation following wound healing. Our previous studies indicated that Shikonin, an active component extracted from Radix Arnebiae, induces apoptosis and reduces collagen production in hypertrophic scar-derived fibroblasts. In the study reported here, we further evaluate the potential use of Shikonin as a novel scar remediation therapy by examining the effects of Shikonin on both keratinocytes and fibroblasts using Transwell® co-culture techniques. The underlying mechanisms were also revealed. In addition, effects of Shikonin on the expression of cytokines in Transwell co-culture "conditioned" medium were investigated.

Results: Our results indicate that Shikonin preferentially inhibits cell proliferation and induces apoptosis in fibroblasts without affecting keratinocyte function. In addition, we found that the proliferation-inhibiting and apoptosis-inducing abilities of SHI might be triggered via MAPK and Bcl-2/Caspase 3 signalling pathways. Furthermore, SHI has been found to attenuate the expression of TGF-β1 in Transwell co-cultured "conditioned" medium.

Conclusions: The data generated from this study provides further evidence that supports the potential use of Shikonin as a novel scar remediation therapy.

No MeSH data available.


Related in: MedlinePlus

Effects of SHI on the expression of total TGF-β1 in Kc-HSF co-culture “conditioned” media. Cells were treated with SHI for 24 and 48 h and then the “conditioned” media were collected. The concentration of TGF-β1 was measured according to the standard curve provided with the assay kit. The expression of TGF-β1 was then further converted to the percentage of the untreated control. Error bars indicate mean +/− SEM (n = 3). *p < 0.05 versus the untreated control. Statistical analysis was performed using One-way ANOVA and Tukey’s post-hoc test
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Fig7: Effects of SHI on the expression of total TGF-β1 in Kc-HSF co-culture “conditioned” media. Cells were treated with SHI for 24 and 48 h and then the “conditioned” media were collected. The concentration of TGF-β1 was measured according to the standard curve provided with the assay kit. The expression of TGF-β1 was then further converted to the percentage of the untreated control. Error bars indicate mean +/− SEM (n = 3). *p < 0.05 versus the untreated control. Statistical analysis was performed using One-way ANOVA and Tukey’s post-hoc test

Mentions: TGF-β1, produced by both Kc and HSF [30], has been broadly reported to play vital roles in wound healing processes [31]. Of particular relevance, the over-abundant expression of TGF-β1 in wound healing has been reported to result in the formation of HS [32]. The effect of SHI on total TGF-β1 expression in Kc-HSF co-culture was therefore investigated using an ELISA assay (Fig. 7). Our results suggest that total TGF-β1 expression is significantly reduced after exposed to SHI at 1 and 3 μg/mL for either 24 or 48 h compared to the untreated control (p < 0.05).Fig. 7


Investigating the potential of Shikonin as a novel hypertrophic scar treatment.

Fan C, Xie Y, Dong Y, Su Y, Upton Z - J. Biomed. Sci. (2015)

Effects of SHI on the expression of total TGF-β1 in Kc-HSF co-culture “conditioned” media. Cells were treated with SHI for 24 and 48 h and then the “conditioned” media were collected. The concentration of TGF-β1 was measured according to the standard curve provided with the assay kit. The expression of TGF-β1 was then further converted to the percentage of the untreated control. Error bars indicate mean +/− SEM (n = 3). *p < 0.05 versus the untreated control. Statistical analysis was performed using One-way ANOVA and Tukey’s post-hoc test
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4537585&req=5

Fig7: Effects of SHI on the expression of total TGF-β1 in Kc-HSF co-culture “conditioned” media. Cells were treated with SHI for 24 and 48 h and then the “conditioned” media were collected. The concentration of TGF-β1 was measured according to the standard curve provided with the assay kit. The expression of TGF-β1 was then further converted to the percentage of the untreated control. Error bars indicate mean +/− SEM (n = 3). *p < 0.05 versus the untreated control. Statistical analysis was performed using One-way ANOVA and Tukey’s post-hoc test
Mentions: TGF-β1, produced by both Kc and HSF [30], has been broadly reported to play vital roles in wound healing processes [31]. Of particular relevance, the over-abundant expression of TGF-β1 in wound healing has been reported to result in the formation of HS [32]. The effect of SHI on total TGF-β1 expression in Kc-HSF co-culture was therefore investigated using an ELISA assay (Fig. 7). Our results suggest that total TGF-β1 expression is significantly reduced after exposed to SHI at 1 and 3 μg/mL for either 24 or 48 h compared to the untreated control (p < 0.05).Fig. 7

Bottom Line: Our results indicate that Shikonin preferentially inhibits cell proliferation and induces apoptosis in fibroblasts without affecting keratinocyte function.In addition, we found that the proliferation-inhibiting and apoptosis-inducing abilities of SHI might be triggered via MAPK and Bcl-2/Caspase 3 signalling pathways.Furthermore, SHI has been found to attenuate the expression of TGF-β1 in Transwell co-cultured "conditioned" medium.

View Article: PubMed Central - PubMed

Affiliation: Tissue Repair and Regeneration Program, Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, 4059, Australia. c3.fan@connect.qut.edu.au.

ABSTRACT

Background: Hypertrophic scarring is a highly prevalent condition clinically and results from a decreased number of apoptotic fibroblasts and over-abundant production of collagen during scar formation following wound healing. Our previous studies indicated that Shikonin, an active component extracted from Radix Arnebiae, induces apoptosis and reduces collagen production in hypertrophic scar-derived fibroblasts. In the study reported here, we further evaluate the potential use of Shikonin as a novel scar remediation therapy by examining the effects of Shikonin on both keratinocytes and fibroblasts using Transwell® co-culture techniques. The underlying mechanisms were also revealed. In addition, effects of Shikonin on the expression of cytokines in Transwell co-culture "conditioned" medium were investigated.

Results: Our results indicate that Shikonin preferentially inhibits cell proliferation and induces apoptosis in fibroblasts without affecting keratinocyte function. In addition, we found that the proliferation-inhibiting and apoptosis-inducing abilities of SHI might be triggered via MAPK and Bcl-2/Caspase 3 signalling pathways. Furthermore, SHI has been found to attenuate the expression of TGF-β1 in Transwell co-cultured "conditioned" medium.

Conclusions: The data generated from this study provides further evidence that supports the potential use of Shikonin as a novel scar remediation therapy.

No MeSH data available.


Related in: MedlinePlus