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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The healing process of gastric ulcers is regulated by many factors. Cytokines play a central role in the different stages of healing. In the early stage of inflammation, TNF-alpha and interleukins regulate cell-migration and -proliferation. In the ulcer's base revascularisation is stimulated by b-FGF, collagen synthesis by TGF-beta. The reepithelialization is mediated by EGF, which accelerates ulcer healing in animal models, while TGF-alpha is involved in mucosal protection. The extracellular matrix (ECM) is important for the stability and quality of the ulcer scar, as known from dermatological experiments. An increase of collagen types I and III in healing gastric ulcers was demonstrated recently, which might illuminate the particular role of ECM proteins for the gastric ulcer healing process.
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PMID:[The significance of cytokines and extracellular matrix for stomach ulcer healing]. 787 61

Transforming growth factor beta 1 (TGF-beta 1) has been shown to play a central role in wound healing. This peptide has been detected in the stomach, but no information is available at present whether TGF-beta 1 influences the healing of gastric ulcers and whether the mucosal expression of TGF-beta 1 changes in the course of this healing. In this study, gastric ulcers were induced by serosal application of acetic acid and TGF-beta 1 or vehicle saline was injected twice into the subserosa around the ulcer area, once immediately after ulcer induction and two days later. Local application of TGF-beta 1 led to significant acceleration of gastric ulcer healing. Gastric blood flow at the ulcer margin was significantly higher than that in the ulcer crater but no significant difference was found in this flow between studied groups. Immunohistochemistry showed that the expression of TGF-beta 1 reached the peak at day 2 and then declined in the course of healing. We conclude that TGF-beta 1 accelerates ulcer healing possibly by increasing the formation of granulation tissue and cell migration probably mediated by locally expressed TGF-beta 1 but the healing effects of TGF-beta 1 do not depend on the vascular factor.
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PMID:Subserosal application of transforming growth factor-beta 1 in rats with chronic gastric ulcers: effect on gastric ulcer healing and blood flow. 887

Transforming growth factor (TGF)-beta regulates cell growth and differentiation, and is known to play regulatory roles in the process of tissue repair and remodeling. However, the functional role of TGF-beta in gastric ulcer healing has not been addressed. In this study, we assayed the expression of TGF-beta and its receptors in the gastric mucosa of patients with healed or refractory gastric ulcers. Antibodies against TGF-beta and its receptors (both type I and type II) were employed to examine expression levels. Sixteen gastric ulcer patients, including four with completely healed ulcers and 12 with ulcers refractory to treatment were included in this study. All four patients with healed ulcers showed remarkable expression levels of both TGF-beta and its receptors. On the other hand, two of the 12 patients with refractory ulcers had weak or deficient TGF-beta expression in the gastric mucosa, and seven lacked expression of at least one of the TGF-beta receptors. The remaining three patients had normal (moderate to weak) expression levels of TGF-beta and its two receptors. These results suggest that both TGF-beta and its receptors are essential for gastric ulcer healing.
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PMID:Immunohistochemical studies of transforming growth factor-beta and its receptors in the gastric mucosa of patients with refractory gastric ulcer. 1056 Feb 37

In this review article we discuss the role of growth factors in gastric ulcer healing using an in vitro wound repair model with gastric epithelial and mesenchymal cells. Several growth factors accelerate gastric epithelial and mesenchymal wound healing in vitro with acceleration of cell migration and proliferation. Epidermal growth factor, transforming growth factor-alpha (TGFalpha), hepatocyte growth factor, and insulin accelerate predominantly gastric epithelial wound healing; and TGFbeta and basic fibroblast growth factor predominantly accelerate gastric mesenchymal wound healing. Platelet-derived growth factor-betabeta and insulin-like growth factor-1 (IGF-1) accelerate both significantly. Among these growth factors, IGF-1 produced from fibroblasts plays a key role in the gastric epithelial-mesenchymal interaction during the process of gastric wound healing.
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PMID:Epithelial-mesenchymal interaction in gastric mucosal restoration. 1077 21

While several autocrine/paracrine growth factors (GFs) can all stimulate epithelial regeneration in experimentally wounded primary gastric cultures, clinical relevance for their non-redundant cooperative actions in human gastric ulcer healing is suggested by the sequential pattern of GF gene induction in vivo. Using new HGE cell lines able to form a coherent monolayer with tight junctions as well as using primary human gastric epithelial cultures, we show that EGF, TGFalpha, HGF and IGFs accelerate epithelial restitution upon wounding, independently of the TGFbeta pathway (as opposed to intestinal cells). However, they differently modulate cell behavior: TGFalpha exerts strong effects (even more than EGF) on cytoplasmic spreading and non-oriented protruding activity of bordering cells whereas HGF preferentially coordinates single lamella formation, cell elongation and migration into the wound. IGF-I and IGF-II rather induce the alignment of bordering cells and maintain a compact monolayer front. The number of mitotic cells maximally increases with EGF, followed by TGFalpha and IGF-I,-II. The current study demonstrates that GFs differentially regulate the regeneration of human gastric epithelial cells through specific modulation of cell shape adaptation, migration and proliferation, further stressing that a coordination of GF activities would be necessary for the normal progression of post-wounding epithelial repair.
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PMID:Differential growth factor induction and modulation of human gastric epithelial regeneration. 1587 52

This paper reviews cellular and molecular mechanisms of gastrointestinal ulcer healing. Ulcer healing, a genetically programmed repair process, includes inflammation, cell proliferation, re-epithelialization, formation of granulation tissue, angiogenesis, interactions between various cells and the matrix and tissue remodeling, all resulting in scar formation. All these events are controlled by the cytokines and growth factors (EGF, PDGF, KGF, HGF, TGFbeta, VEGF, angiopoietins) and transcription factors activated by tissue injury in spatially and temporally coordinated manner. These growth factors trigger mitogenic, motogenic and survival pathways utilizing Ras, MAPK, PI-3K/Akt, PLC-gamma and Rho/Rac/actin signaling. Hypoxia activates pro-angiogenic genes (e.g., VEGF, angiopoietins) via HIF, while serum response factor (SRF) is critical for VEGF-induced angiogenesis, re-epithelialization and muscle restoration. EGF, its receptor, HGF and Cox2 are important for epithelial cell proliferation, migration re-epithelializaton and reconstruction of gastric glands. VEGF, angiopoietins, nitric oxide, endothelin and metalloproteinases are important for angiogenesis, vascular remodeling and mucosal regeneration within ulcer scar. Circulating progenitor cells are also important for ulcer healing. Local gene therapy with VEGF + Ang1 and/or SRF cDNAs dramatically accelerates esophageal and gastric ulcer healing and improves quality of mucosal restoration within ulcer scar. Future directions to accelerate and improve healing include the use of stem cells and tissue engineering.
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PMID:Cellular and molecular mechanisms of gastrointestinal ulcer healing. 1618 17

Zn(II)-curcumin, a mononuclear (1:1) zinc complex of curcumin was synthesized and examined for its antiulcer activities against pylorus-ligature-induced gastric ulcer in rats. The structure of Zn(II)-curcumin was identified by elemental analysis, NMR and TG-DTA analysis. It was found that a zinc atom was coordinated through the keto-enol group of curcumin along with one acetate group and one water molecule. Zn(II)-curcumin (12, 24 and 48 mg/kg) dose-dependently blocked gastric lesions, significantly reduced gastric volume, free acidity, total acidity and pepsin, compared with control group (P<0.001) and curcumin alone (24 mg/kg, P<0.05). Reverse transcriptase polymerase chain reaction (RT-PCR) analysis showed that Zn(II)-curcumin markedly inhibited the induction of nuclear factor-kappa B (NF-kappaB), transforming growth factor beta(1) (TGF-beta(1)) and interleukin-8 (IL-8), compared with control group (P<0.05). These findings suggested that Zn(II)-curcumin prevented pylorus-ligation-induced lesions in rat by inhibiting NF-kappaB activation and the subsequent production of proinflammatory cytokines, indicating a synergistic effect between curcumin and zinc. An acute toxicity study showed that mice treated with SDs of Zn(II)-curcumin (2 g/kg) manifested no abnormal signs.
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PMID:Gastroprotective effects of a new zinc(II)-curcumin complex against pylorus-ligature-induced gastric ulcer in rats. 1958 37