Protective effect of polypeptide from Chlamys farreri on hairless mice damaged by ultraviolet A.
Abstract
AIM: To study the protective effect of the polypeptide isolated from Chlamys
farreri (PCF) on hairless mice skin damaged by ultraviolet A.
METHODS: Enzymes and malondialdehyde (MDA) were determined by biochemical
methods; the expressions of Bcl-2 protein and NOS protein were examined by
immunohistochemical technique. The ultra-structure of the skin was observed
through electronic microscope.
RESULTS: PCF could enhance the activities of glutathione peroxidase (GSH-px),
superoxide dismutase (SOD), and total anti-oxidative capacity (T-AOC). Also PCF
could reduce the amount of MDA, increase the expression of Bcl-2 protein, and
inhibit the expression of NOS protein. The ultra-structure of epidermis and
fibroblasts remained normal in 20 % PCF groups; there were vacuoles in smooth
endoplasm reticulum in epidermis of mice and the number of rough endoplasm
reticulum in fibroblasts was decreased in model group.
CONCLUSION: PCF had the protective effects on hairless mice skin damaged by
ultraviolet A via its anti-oxidative mechanisms.
Keywords:
farreri (PCF) on hairless mice skin damaged by ultraviolet A.
METHODS: Enzymes and malondialdehyde (MDA) were determined by biochemical
methods; the expressions of Bcl-2 protein and NOS protein were examined by
immunohistochemical technique. The ultra-structure of the skin was observed
through electronic microscope.
RESULTS: PCF could enhance the activities of glutathione peroxidase (GSH-px),
superoxide dismutase (SOD), and total anti-oxidative capacity (T-AOC). Also PCF
could reduce the amount of MDA, increase the expression of Bcl-2 protein, and
inhibit the expression of NOS protein. The ultra-structure of epidermis and
fibroblasts remained normal in 20 % PCF groups; there were vacuoles in smooth
endoplasm reticulum in epidermis of mice and the number of rough endoplasm
reticulum in fibroblasts was decreased in model group.
CONCLUSION: PCF had the protective effects on hairless mice skin damaged by
ultraviolet A via its anti-oxidative mechanisms.