Inhibitory effect of capsaicin on fibroblast proliferation and its molecular mechanism

doi:10.3969/j.issn.2095-4344.0574

Abstract

Abstract:

Abstract
BACKGROUND: Capsaicin has been reported to inhibit fibrosis and the proliferation and collagen synthesis of hypertrophic fibroblasts. However, the underlying mechanism is unclear.
OBJECTIVE: To investigate the effect of capsaicin on inhibiting the proliferation of fibroblasts and the corresponding molecular mechanism.
METHODS: Neonatal Sprague-Dawley rat epidermal fibroblasts were cultured in vitro, and were treated with capsaicin at different concentrations (0.5, 1, 2, 4, 8 mg/L) for 24 hours. The cells without treatment of capsaicin were included in the negative control group. Morphological changes of the epidermal fibroblasts were observed under phase-contrast microscope. The cell viability and IC50 value were detected by MTT assay. The cell apoptosis was detected by Hoechst 33258 staining and AnnexinV-FITC/PI staining. The cell cycle distribution was determined by flow cytometry. The protein expression levels of FoxO1, p-FoxO1, Akt and p-Akt were detected by western blot assay.
RESULTS AND CONCLUSION: With capsaicin concentration increasing, cell survival rate decreased gradually in a concentration-dependent manner, and IC50 value was 3.55 mg/L. Compared with the negative control group, after 24 hours, capsaicin treated fibroblasts stopped in G1 phase and the apoptosis rate increased. Meanwhile, capsaicin could decrease the expression of P-Akt and P-FoxO1. Therefore, capsaicin can inhibit the proliferation of fibroblasts, promote cell apoptosis, and present a concentration-dependent effect. The Akt-FoxO1 signaling pathway may be involved in the inhibition of capsaicin on fibroblast proliferation.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

Key words: Fibroblasts, Cicatrix, Signal Transduction, Tissue Engineering

CLC Number:

R446
R318

Zhou Yanxing1, Peng Xinsheng2, Hou Gan1, Li Jiangbin1, Zhang Hua1, Zhou Zhikun2, Zhou Yanfang3 . Inhibitory effect of capsaicin on fibroblast proliferation and its molecular mechanism[J]. Chinese Journal of Tissue Engineering Research, 2019, 23(7): 1018-1022.

Figures/Tables 3

References

[1] Xu X, Lai L, Zhang X,et al. Autologous chyle fat grafting for the treatment of hypertrophic scars and scar-related conditions. Stem Cell Res Ther.2018;9(1): 64.

[2] Tang M, Wang W, Cheng L,et al.The inhibitory effects of 20(R)-ginsenoside Rg3 on the proliferation, angiogenesis, and collagen synthesis of hypertrophic scar derived fibroblastsin vitro. Iran J Basic Med Sci. 2018;21(3):309-317.

[3] Austin E, Koo E, Jagdeo J. The Cellular Response of Keloids and Hypertrophic Scars to Botulinum Toxin A: A Comprehensive Literature Review. Dermatol Surg. 2018;44(2):149-157.

[4] Ouyang HW, Li GF, Lei Y, et al. Comparison of the effectiveness of pulsed dye laser vs pulsed dye laser combined with ultrapulse fractional CO2 laser in the treatment of immature red hypertrophic scars. J Cosmet Dermatol. 2018; 17(1):54-60.

[5] Ghazawi FM, Zargham R, Gilardino MS,.et al.Insights into the Pathophysiology of Hypertrophic Scars and Keloids: How Do They Differ? . Adv Skin Wound Care. 2018;31(1):582-595.

[6] Samaras DJ, Kingsford AC.Surgical management of extensive hypertrophic scarring of the halluces secondary to a decade of untreated onychocryptosis: An illustrative case report. SAGE Open Med Case Rep. 2017 Nov 6;5:2050313X17740514.

[7] Huang XF, Xue JY, Jiang AQ, et al.Capsaicin and its analogues: structure-activity relationship study. Curr Med Chem. 2013;20(21):2661-2672.

[8] Prodromidou A, Frountzas M, Vlachos DE, et al. Botulinum toxin for the prevention and healing of wound scars: A systematic review of the literature. Plast Surg (Oakv). 2015; 23(4):260-264.

[9] Joshi RS. In-the-bag decentration of an intraocular lens in a patient with a tendency to hypertrophic scarring. Digit J Ophthalmol. 2016;22(1):28-31.

[10] Finnerty CC, Jeschke MG, Branski LK,et al. Hypertrophic scarring: the greatest unmet challenge after burn injury. Lancet. 2016;388(10052):1427-1436

[11] Akhtar F, Muhammad Sharif H, Arshad Mallick M,et al.Capsaicin: Its biological activities and in silico target fishing. Acta Pol Pharm. 2017;74(2):321-329.

[12] Ma D, Li S, Cui Y, et al. Paclitaxel increases the sensitivity of lung cancer cells to lobaplatin via PI3K/Akt pathway. Oncol Lett. 2018;15(5):6211-6216.

[13] Liu Q, Zhang FG, Zhang WS, et al.Ginsenoside Rg1 Inhibits Glucagon-Induced Hepatic Gluconeogenesis through Akt-FoxO1 Interaction. Theranostics. 2017;7(16):4001-4012.

[14] Gao Y, Liao G, Xiang C, et al.Effects of Phycocyanin on INS-1 Pancreatic β-Cell Mediated by PI3K/Akt/FoxO1 signaling pathway. Int J Biol Macromol. 2016;83:185-194.

[15] Hao F, Kang J, Cao Y, et al.Curcumin attenuates palmitate-induced apoptosis in MIN6 pancreatic β-cells through PI3K/Akt/FoxO1 and mitochondrial survival pathways. Apoptosis. 2015;20(11):1420-1432.