الفهرس 
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Abstract
One hundred and ninety- eight male albino mice were used in this study. They were divided into the following groups: (1) Unwounded skin group: skin specimens were excised from the shaved area of the animal back of 6 mice. (2) Wounded skin group: two incision wounds of 1 cm in length were made in the dorsal skin of 192 mice. Animals were divided into the following subgroups,Group A (unmanipulated wounds –ve control): wounds of mice are left unmanipulated.Group B: DMSO was applied topically in a dose of 200μL/wound. Group C: TPA (PKCα stimulant) was applied topically in a dose of 10μg /200μL of DMSO .Group D:Go¨6976 (PKCα inhibitor) was topically applied at dose of 40μg /25μL of DMSO. At the assigned time, the wounded skins were excised. Each wound was bisected, processed for paraffin sections at 4-6 microns, and stained by histological stains: hematoxylin &eosin and Masson’s trichrome for assessment of reepithelialization. Ayoub - Shklar stain for prekeratin & keratin and immunohistochemical stain for PKCα.
Aim of the work:The present work was undertaken to study the sequence of healing of unmanipulated epidermal wound in mice during a period of (0-7) days, and to study the effect of PKCα stimulation and suppression on the epidermal wound healing.
Results
In group A and group B: the leading edge ratio increased from the 1st until the 6th day. The formation of neoepidermis started on the 6th day. By AS stain, the expression of prekeratin positive orange stain increased gradually from the 3rd day in both basal and suprabasal layers. Sections stained with anti PKCα showed positive immunoreactivity at the wound margin localized to the cell membrane of basal cells in the 1st day that progress to the suprabasal cells on the 3rd day. On the 5th day, the PKCα immunoreactivity expressed as brown granules drawing the membrane of the cells progressing to positive immunoreactivity in the cytoplasm and cell membrane on the 7th day.
In group C (TPA treated wounds): there was complete formation of neoepidermis earlier starting on 4th day. By AS stain, the epidermal cells at wound margin and newly formed cells in the leading edge and neoepidermis showed increased intensity of positive orange stained prekeratin-like substances and earlier than unmanipulated wound group on the 2nd day. They also showed increased in thickness of keratin layer from the 2nd until the 7th day. Sections stained with anti PKCα at the wound margin indicated rapid localization of PKCα to basal and suprabasal cell layers.
In group D (Go¨6976 treated wounds): There was no evidence of formation of neoepidermis completely covering the wound gap in this group. By As stain, the epidermal cells at the wound margin showed weak expression of prekeratin positive orange stain during the course of healing process as compared with the unmanipulated wound. Sections stained by PKCα revealed that expression was slower than unmanipulated wound group.
Summary and Conclusion
local augmentation of PKCα function may prove a novel future therapeutic approach to promote wound healing while inhibition of PKCα activity may result in delayed reepithelialization.