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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

Apoptosis in Kc and HSF determined by flow cytometry. a Apoptosis rate in Kc and HSF following SHI treatment; b Quantitative analysis of SHI-induced apoptosis in Kc and HSF. Kc and HSF were treated with 0, 1 or 3 μg/mL SHI for 12 h and then stained with annexin V and propidium iodide as per the manufacturer’s instructions. Flow cytometry was performed using FACSAria™ III Cell Sorter (Becton Dickinson). All experiments were performed three times using cells from 3 patients. Triplicate treatments were assessed in cells from each patient. Quantitative data from the 3 patients were pooled. *p < 0.05 versus the untreated control
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Fig2: Apoptosis in Kc and HSF determined by flow cytometry. a Apoptosis rate in Kc and HSF following SHI treatment; b Quantitative analysis of SHI-induced apoptosis in Kc and HSF. Kc and HSF were treated with 0, 1 or 3 μg/mL SHI for 12 h and then stained with annexin V and propidium iodide as per the manufacturer’s instructions. Flow cytometry was performed using FACSAria™ III Cell Sorter (Becton Dickinson). All experiments were performed three times using cells from 3 patients. Triplicate treatments were assessed in cells from each patient. Quantitative data from the 3 patients were pooled. *p < 0.05 versus the untreated control

Mentions: Data from flow cytometry (Fig. 2a & b) indicated that SHI at either 1 or 3 μg/mL showed no effect on Kc apoptosis compared to the untreated group. However, SHI at 3 μg/mL significantly induced 56.16 % ± 9.85 % HSF apoptosis at 12 h compared to the untreated control (p < 0.05). This data suggests that SHI at 3 μg/mL only induces apoptosis in HSF but not in Kc after 12 h of treatment.Fig. 2


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)

Apoptosis in Kc and HSF determined by flow cytometry. a Apoptosis rate in Kc and HSF following SHI treatment; b Quantitative analysis of SHI-induced apoptosis in Kc and HSF. Kc and HSF were treated with 0, 1 or 3 μg/mL SHI for 12 h and then stained with annexin V and propidium iodide as per the manufacturer’s instructions. Flow cytometry was performed using FACSAria™ III Cell Sorter (Becton Dickinson). All experiments were performed three times using cells from 3 patients. Triplicate treatments were assessed in cells from each patient. Quantitative data from the 3 patients were pooled. *p < 0.05 versus the untreated control
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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

Fig2: Apoptosis in Kc and HSF determined by flow cytometry. a Apoptosis rate in Kc and HSF following SHI treatment; b Quantitative analysis of SHI-induced apoptosis in Kc and HSF. Kc and HSF were treated with 0, 1 or 3 μg/mL SHI for 12 h and then stained with annexin V and propidium iodide as per the manufacturer’s instructions. Flow cytometry was performed using FACSAria™ III Cell Sorter (Becton Dickinson). All experiments were performed three times using cells from 3 patients. Triplicate treatments were assessed in cells from each patient. Quantitative data from the 3 patients were pooled. *p < 0.05 versus the untreated control
Mentions: Data from flow cytometry (Fig. 2a & b) indicated that SHI at either 1 or 3 μg/mL showed no effect on Kc apoptosis compared to the untreated group. However, SHI at 3 μg/mL significantly induced 56.16 % ± 9.85 % HSF apoptosis at 12 h compared to the untreated control (p < 0.05). This data suggests that SHI at 3 μg/mL only induces apoptosis in HSF but not in Kc after 12 h of treatment.Fig. 2

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