Role of epidermal growth factor in healing of chronic gastroduodenal ulcers in rats

Konturek, S J; Dembiński, Artur; Warzecha, Zygmunt; Brzozowski, T; Gregory, H.

doi:10.1016/0016-5085(88)90667-1

Cited by 266 publications

(121 citation statements)

References 21 publications

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“…Another mechanism for EGF and other growth factors that promote wound healing include autocrine (local) production and secretion by cells at the site of a wound (24). It also has been reported that salivary gland-derived EGF enhances the healing of gastric ulcers and tongue lesions (17,19). In the partial hepatectomy model for liver regeneration (25), disruption of salivary EGF production through submandibular gland ablation results in delayed liver cell proliferation and a reduced capacity to regenerate the liver.…”

mentioning

confidence: 96%

Reduced Oral Wound Healing in the NOD Mouse Model for Type 1 Autoimmune Diabetes and Its Reversal by Epidermal Growth Factor Supplementation

Nagy

Nagashima²,

Cha³

et al. 2001

Diabetes

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Using the NOD mouse, a model for type 1 diabetes, we examined how reduced concentrations of epidermal growth factor (EGF) in the saliva, after onset of type 1 diabetes, affect oral wound healing. Diabetic NOD/LtJ mice on insulin therapy, prediabetic NOD/LtJ, and ageand sex-matched BALB/cJ mice were given a cutaneous tongue punch and allowed to undergo normal healing. With diabetes onset and a reduction in saliva-derived growth factor levels, the rate of tongue wound healing was reduced compared with nondiabetic NOD/LtJ and healthy BALB/cJ mice. Addition of exogenous EGF to the drinking water did not accelerate the rate of healing in BALB/cJ or prediabetic NOD/LtJ; however, diabetic NOD/LtJ mice exhibited accelerated wound healing similar to healthy mice. These results demonstrate that loss of growth factors from saliva is associated with profoundly reduced oral wound healing, suggesting that therapeutic treatment with topical delivery may be beneficial to patients with type 1 diabetes and oral wound complications.

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mentioning

confidence: 96%

Reduced Oral Wound Healing in the NOD Mouse Model for Type 1 Autoimmune Diabetes and Its Reversal by Epidermal Growth Factor Supplementation

Nagy

Nagashima²,

Cha³

et al. 2001

Diabetes

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“…It acts by stimulating mucosal prostaglandins, by increasing mucus secretion, by increasing alkaline secretion or by masking the mucosal cells. 5 There are many fixed dose combination (FDC) of NSAID having paracetamol in common are available in the market are extensively consumed. Rationale for such combination is not clearly defined and moreover such FDCs are not approved by WHO.…”

Section: Discussionmentioning

confidence: 99%

“…4 The minimal gastric toxicity of paracetamol and its protective role is said to be due to increase in prostaglandins production in gastric mucosa. 4,5 However, this gasto protective property of paracetamol appears to be not uniform with different NSAIDs and moreover there are controversial reports regarding gastro protective propertyof paracetamol with some NSAIDs. Gastric toxicity of aspirin, indomethacin and ibuprofen was deceased, when co administered with paracetamol in rats, but that of phenylbutazone and glafenine was not altered.…”

Section: Introductionmentioning

confidence: 99%

An experimental evaluation of gastro protective activity of paracetamol on ulcerogenicity of some NSAIDs in albino rats

Rajashekar

Shobha

2017

Int J Basic Clin Pharmacol

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Background: Fixed dose combinations (FDCs) of NSAIDs are commonly prescribed and extensively sold over the counter. An indiscriminate usage of them leads to toxicity, mainly involving gastrointestinal system. Paracetamol appears to have controversial reputation regarding its gastro protective action. In this background, the study was planned to evaluate gastro protective effect of paracetamol on the ulcerogenicity of some relatively new NSAIDs in their therapeutic and sub therapeutic doses. Methods: Gatric toxicity and gastric juice analysis-Pyloric ligation method was adopted for assessing the ulcer index of 3 NSAIDs namely aceclofenac, nimesulide and lornoxicam individually and in combination with paracetamol. Gastric juice collected was subjected for total juice volume, free acidity, combined acidity and total acid output. Results: Paracetamol produced non significant gastric damage similar to that of control. When co administered with therapeutic doses of aceclofenac, nimesulide and lornoxicam, there was significant decrease in their gastric toxicity in a uniform manner and the ulcerogenicity of these NSAIDs in sub therapeutic doses was not affected by paracetamol. This upholds the uniform gastro protective activity of paracetamol in this study and this could be explained by its anti acid secretory action on gastric juice. Conclusions: Paracetamol, itself has least gastric damaging property. When co administered with other NSAIDs, their toxicity is rather reduced than enhancing the mucosal damage by them. Thus FDCs of various NSAIDs available in market are partially justifiable.

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“…Their changes after protamine sulphate treatment were also investigated in the present study. 8,9 MATERIALS AND METHODS…”

Section: Introductionmentioning

confidence: 99%

The ulcer healing effect of protamine sulphate in rat stomach

1999

Aliment Pharmacol Ther

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INTRODUCTIONProtamine sulphate is known for its neutralizing action on the anticoagulation effect of heparin. Moreover, it was recently reported that protamine sulphate could stimulate the release of endothelium-derived relaxing factor in canine arteries, 1 and also nitric oxide production in porcine carotid artery endothelial cells. 2 It was also involved in the regulation of neuronal nitric oxide synthase (NOS) activity. 3 A protamine sulphateproduced systemic hypotension could be attenuated by nitric oxide inhibition. 4 All these re¯ect a close relationship between the protamine sulphate and nitric oxide and their action on the cardiovascular system. It was reported that nitric oxide is a pivotal factor for gastric ulcer healing. The effect of endogenous nitric oxide on the healing process of gastric ulcer was investigated by using L-arginine, a substrate for NOS, and L-N G -monomethylarginine (L-NMMA) or L-N G -nitroarginine (L-NNA), the inhibitors of NOS. The results indicated that L-arginine accelerated ulcer healing and increased gastric angiogenesis, whereas L-NMMA or L-NNA resulted in a delay in ulcer healing and a reduction in the number of capillaries. 5,6 Our preliminary study showed that heparin accelerated gastric ulcer healing in rats. 7 The drug however, prolonged bleeding time, which was detrimental to gastric ulcer formation and its healing. In order to abolish this side-effect, we used protamine sulphate to neutralize such action, so that it could promote the healing action of heparin. Interestingly, protamine sulphate not only completely neutralized the anticoagulation action of heparin, but also potentiated its ulcer SUMMARY Background: Protamine sulphate has been reported to stimulate nitric oxide production from blood vessels, which is a pivotal factor for gastric ulcer healing. Our preliminary study also showed that protamine sulphate potentiated the ulcer healing effect of heparin. Methods: Male SD rats with acetic acid-induced gastric ulcers were given protamine sulphate (40±80 mg/kg, s.c.) twice daily for 4 or 7 days. L-N G -nitroarginine methyl ester (L-NAME, 5 mg/kg), an inhibitor of nitric oxide synthase (NOS), was given s.c. prior to protamine sulphate (80 mg/kg) treatment. Ulcer healing, angiogenesis, mucosal histological changes, NOS activity and growth factors were determined.

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Role of epidermal growth factor in healing of chronic gastroduodenal ulcers in rats

Cited by 266 publications

References 21 publications

Reduced Oral Wound Healing in the NOD Mouse Model for Type 1 Autoimmune Diabetes and Its Reversal by Epidermal Growth Factor Supplementation

Reduced Oral Wound Healing in the NOD Mouse Model for Type 1 Autoimmune Diabetes and Its Reversal by Epidermal Growth Factor Supplementation

An experimental evaluation of gastro protective activity of paracetamol on ulcerogenicity of some NSAIDs in albino rats

The ulcer healing effect of protamine sulphate in rat stomach

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