Songklanakarin Journal of Science and Technology (SJST) (Aug 2015)

Young coconut juice accelerates cutaneous wound healing by downregulating macrophage migration inhibitory factor (MIF) in ovariectomized rats: Preliminary novel findings

  • Nisaudah Radenahmad,
  • Saowaros Suwansa-ard,
  • Ibrahim Sayoh

Journal volume & issue
Vol. 37, no. 4
pp. 417 – 423

Abstract

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Estrogens play a crucial role in cutaneous wound healing by down-regulating macrophage migration inhibitory factor (MIF). We had previously reported the effect of young coconut juice (YCJ) known to contain the phytoestrogen, -sitosterol, on cutaneous wound healing in ovariectomized (ovx) rats. This research investigated the possible mechanisms of YCJ on cutaneous wound healing and it was found that it down regulated macrophage migration inhibitory factor (MIF). This resulted in ultrastructural changes that were observed using transmission electron microscopy (TEM). Four groups of female rats (6 in each group) were included in this study: sham-operated, ovariectomized (ovx), ovx that received estradiol benzoate (EB) injections intraperitoneally, and ovx that received YCJ orally. Two weeks after ovariectomy, two equidistant 1-cm full-thickness skin incisional wounds were made. At the end of the third week (7 day treatment) and the fourth week (14 day treatment) of study the rats were sacrificed, and their serum estradiol (E2) levels were measured by a chemiluminescent immunoassay. The skin from the wound was excised and examined by TEM and MIF immunohistochemical staining. The TEM study after 14 days of treatment showed that the size of the keratinocyte cells from the ovx+YCJ group was larger and these cells contained many more cytoplasmic processes than those of the ovx group. The MIF immunoreactivity was also lowest in the ovx+YCJ group. This study showed that there was an increased intercellular exchange via the cytoplasmic processes of the keratinocytes that could account for the promotion of cutaneous wound healing in the ovx rats receiving YCJ, and that the possible mechanism for this was via the down-regulation of MIF.

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