Phlorizin is well known to inhibit
sodium/glucose cotransporters in the kidney and intestine for the treatment of diabetes,
obesity and stress hyperglycaemia. However, the effects of
phlorizin against ultraviolet B (UVB) irradiation and its molecular mechanism are still unknown. We examined the effects of
phlorizin on skin keratinocyte apoptosis,
reactive oxygen species (ROS) production, pro-inflammatory responses after UVB irradiation and the changes of some signal molecules by in vitro and in vivo assay. We observed that
phlorizin pretreatments inhibited HaCaT cell apoptosis and overproduction of ROS induced by UVB.
Phlorizin also decreased the expression of UVB-induced pro-inflammatory
cytokines, such as
interleukin-1 beta (IL-1β),
interleukin-6 (IL-6) and
interleukin-8 (IL-8) at the
mRNA level. Topical application of
phlorizin on UVB-exposed skin of nude mice prevented the formation of scaly skin and
erythema, inhibited the increase of epidermal thickness and reduced acute
inflammation infiltration in skin. Additionally, PCR, Western blot and immunohistochemical data showed that
phlorizin reversed the overexpression of
cyclooxygenase-2 (Cox-2) induced by UVB irradiation both in vitro and in vivo. The activation of p38 and
JNK mitogen-activated protein kinases (MAPK) after UVB irradiation was also inhibited by
phlorizin. These findings suggest that
phlorizin is effective in protecting skin against UVB-induced skin damage by decreasing ROS overproduction, Cox-2 expression and the subsequent excessive
inflammation reactions. It seemed that p38 and JNK MAPK signal pathways are involved in the regulation of the protective function of
phlorizin.