Research of PDGF-BB gel on the wound healing of diabetic rats and its pharmacodynamics.
BACKGROUND
One of the leading causes of impaired wound healing is diabetes mellitus. In diabetic patients, a minor skin wound often leads to serious complications. Many experiments had demonstrated that the expression of platelet-derived growth factor (PDGF) and its receptor was decreased in wounds of healing-impaired diabetic mice, indicating that a certain expression level of PDGF is essential for normal repair.


METHODS
The diabetic rats was induced by a single i.p. injection of streptozotocin and a 1.8 cm diameter full-thickness wound was made on each side of the rat mid-back. Then the rats were randomly divided into five groups, with eight animals in each group as follows: blank control, vehicle control, 3.5 microg PDGF-BB/cm(2) treatment group, 7 microg PDGF-BB/cm(2) treatment group and 14 microg PDGF-BB/cm(2) treatment group for either 7 or 14 consecutive days after wounding. Re-epithelialization area was measured by computerized planimetry, percentage wound closure and percentage wound contraction was calculated, granulation tissue and collagen formation was assessed by Masson trichrome, cell proliferation (proliferating cell nuclear antigen staining) and angiogenesis (Factor VIII related antigen staining) was assessed by immunohistological methods.


RESULTS
PDGF-BB treatment improved healing quality, enhanced angiogenesis, cell proliferation and epithelialization, and formed thicker and more highly organized collagen fiber deposition in full-thickness excisional wound of diabetic rats. The effects of topically applied PDGF-BB were dose-dependent.


CONCLUSIONS
PDGF-BB is an important future clinical tool, particularly for stimulating soft tissue repair in patients with an impaired capacity for wound healing.
Li
Haihong
H
Mental Health Center, ShanTou University Medical College, ShanTou, People's Republic of China.
Fu
Xiaobing
X
Zhang
Lei
L
Huang
Qingjun
Q
Wu
Zhigu
Z
Sun
Tongzhu
T
D043925:Angiogenesis Inducing Agents / Q000493:pharmacokinetics* / Q000494:pharmacology*; D000818:Animals; D000077214:Becaplermin; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D003094:Collagen / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000503:physiopathology*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005782:Gels; D008297:Male; D018919:Neovascularization, Physiologic / Q000187:drug effects; D010982:Platelet-Derived Growth Factor / Q000493:pharmacokinetics* / Q000494:pharmacology*; D020574:Proto-Oncogene Proteins c-sis; D051381:Rats; D017208:Rats, Wistar; D013311:Streptozocin; D014945:Wound Healing / Q000187:drug effects*
D043925:Angiogenesis Inducing Agents; D001786:Blood Glucose; D005782:Gels; D010982:Platelet-Derived Growth Factor; D020574:Proto-Oncogene Proteins c-sis; D000077214:Becaplermin; D013311:Streptozocin; D003094:Collagen