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Journal of Dermatology Research and Skin Care | Volume 2
May 14-15, 2018 | Montreal, Canada
Spring Dermatology &
Skin Care Expo Conference
T
he central molecule in the injury pathway is the transcription
activator nuclear factor-kappa B (NF-kB) activated 30 min
after injury. NF-kB is responsible for the transcription of over
200 genes related tomultiple processes, including inflammation
and scarring. Phosphorylase kinase released 5 mins after injury
activatesdownstreamNF-kB-dependentprocesses, suchasTGF-
β1-dependent fibroblastic and myofibroblastic proliferation
responsible for scarring after injury. Curcumin, a phosphorylase
kinase inhibitor, blocks downstream NF-kB-dependent
inflammation and scarring, with minimal scarring following
burns, trauma and surgical wounds. Because of ultraviolet light,
damaged skin will make injury to the DNA, particularly double
stranded DNA breaks (DSBs), leads to increased risk of photo-
carcinogenesis. Phosphorylase kinase also phosphorylates
a family of phosphatidylinositol-3 kinases (ATR, ATM and
DNA-PK), which control the entry to the DNA Damage Repair
Pathway i.e., Cell Cycle Arrest, Nuclear Excision and DNA
replication. The repair processes are slowand often incomplete,
resulting in photo-aging and photo-carcinogenesis. By blocking
phosphorylase kinase, Curcumin induces Curcumin-induced
apoptosis, allowingnot only for the rapid removal of the severely
damaged cells, but also creates the space for replacement by
new, healthy undamaged cells. This results in rapid healing of
burns and sun-burns. In addition, the removal of premalignant
cells leads to healing of damaged skin with a decreased
tendency for malignant transformation. Psoriasis, a genetic
skin disease precipitated by injury (trauma, contact allergy and
infection), is associated with elevated levels of phosphorylase
kinase, believed to result from a defective genetic-based
switch-off mechanism. The elevated phosphorylase kinase is
associated with increased PCNA+ (proliferating cell nuclear
antigen) resulting in psoriasiform proliferation. Curcumin, by
inhibiting phosphorylase kinase, causes apoptosis of the PCNA+
cells, returning the skin to normal. We present the results of
a protocol based on suppression of phosphorylase kinase
activity with topical Curcumin, topical steroids, avoidance of
precipitating factors (contact allergens), treatment of bacterial,
fungal and viral infections, and maintenance of a strict lactose
free diet
Speaker Biography
Madalene C Y Heng is a Professor of Medicine/Dermatology, David Geffen UCLA School
of Medicine. After 25 years in full-time academia, she is currently in private practice
as a dermatologist in Camarillo, California. She is the author of over 85 publications, in
peer-reviewed journals. She is a reviewer of multiple journals with Editorial positions
in others. Her expertise includes an interest in the biochemistry and pathophysiology
of disease including acne, wound healing and psoriasis. She is the Inventor of Curcumin
gel.
e:
madaleneheng@aol.comMadalene C Y Heng
UCLA School of Medicine, USA
Phosphorylase kinase inhibition in skin disease