Role of basic fibroblast growth factor (bFGF) and platelet-derived growth factor (PDGF) in ulcer healing

Growth factors stimulate virtually all the cellular determinants of ulcer healing (e.g. angiogenesis, granulation tissue production, re-epithelialization). Oral treatment of rats with the natural bFGF-wild, acid-resistant mutein bFGF-CS23 or PDGF-BB accelerated the healing of cysteamine-induced chronic duodenal ulcers. Parallel treatment with marginally effective doses of bFGF + cimetidine or lansoprazole or sucralfate resulted in additive/synergistic ulcer healing. In the ethanol model of acute gastric haemorrhagic erosions, PDGF offered partial gastroprotection, while bFGF was not effective. To investigate the role of endogenous bFGF in the natural history of gastroduodenal ulceration, the heparin-binding fraction of protein extract from duodenal mucosa was analysed by Western blot. A transient 2-3 fold increase in the high-molecular-weight (HMW) nuclear forms of bFGF (21-25 kDa) was seen at 12 h along with the simultaneous decrease (about 50%) in the cytoplasmic 18-kDa bFGF. At 24 and 48 h, the levels of the HMW forms declined and the 18-kDa form increased when compared with 12 h samples. Thus, bFGF and PDGF may be new pharmacological and pathophysiological mediators of ulcer healing.