The effects of betamethasone dipropionate and fish oil on HaCaT proliferation and apoptosis

Mohd Hanif Zulfakar, Charlene M Y Ong, Charles M. Heard

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

The current work examined the effect of fish oil (FO) and betamethasone dipropionate (BD) on the growth of immortalized HaCaT keratinocytes. HaCaT cells were grown and treated with FO and/or BD, and proliferation determined using the MTT method. The cells were further probed by immunocytochemistry (ICC) techniques for apoptosis using Cleaved Caspase-3 Asp175, and inflammatory processes using cyclooxygenase-2 (COX-2). The addition of FO increased the inhibition of HaCaT cells by 27.2%, from 43.15% to 70.35% compared to BD alone (p 0.034). FO alone appeared to induce expression of Asp175 and the effect was greater in combination with BD. The net effect, however, were less than BD alone. Similar observations were seen with regards to COX-2 inhibition. The added benefits of FO to the effect of BD on the inhibition of cell growth, induction of apoptosis and inhibition of inflammation have now been demonstrated on a cellular level. Each of these activities supports beneficial effects in hyperproliferative skin disorders, such as psoriasis.

Original languageEnglish
Pages (from-to)399-405
Number of pages7
JournalInternational Journal of Pharmaceutics
Volume434
Issue number1-2
DOIs
Publication statusPublished - 15 Sep 2012

Fingerprint

Fish Oils
Apoptosis
Cyclooxygenase 2
Growth
Keratinocytes
Psoriasis
Caspase 3
betamethasone-17,21-dipropionate
Immunohistochemistry
Inflammation
Skin

Keywords

  • Apoptosis
  • Betamethasone dipropionate
  • Cell culture
  • EPA
  • Fish oil
  • HaCaT
  • Psoriasis

ASJC Scopus subject areas

  • Pharmaceutical Science

Cite this

The effects of betamethasone dipropionate and fish oil on HaCaT proliferation and apoptosis. / Zulfakar, Mohd Hanif; Ong, Charlene M Y; Heard, Charles M.

In: International Journal of Pharmaceutics, Vol. 434, No. 1-2, 15.09.2012, p. 399-405.

Research output: Contribution to journalArticle

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