Radiation-induced enterocolitis: basic and applied science

Szabó, Sándor; Sándor, Zsolt; Vincze, Áron; Gombos, Zoltán; Mohiuddin, A.; Viravathana, Thavinsakdi

doi:10.1080/11024159850191508

Cited by 10 publications

(9 citation statements)

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“…The acute effects of irradiation on the intestinal mucosa are generally ascribed to inhibition of mitosis in the crypts [25]. This loss of proliferative function results in the development of epithelium and renders the intestine permeable to luminal bacteria and antigens, which may exacerbate mucosal inflammation and dysfunction or cause bacteremia [2]. The expression of Ki-67, a proliferative marker in the jejunum, increased in the genistein-treated group; this may indicate the recovery of intestinal damage after irradiation.…”

Section: Discussionmentioning

confidence: 99%

“…Accompanying injury to the surrounding intestinal tissue may result in serious morbidity and occasional mortality. This so-called radiation enterocolitis is a major clinical problem because it is relatively unresponsive to usual therapies and because of the intractable problems it may cause to the patient [1,2]. Cancer patients undergoing radiotherapy have suffered from adverse effects related to the formation of free radicals, which cause oxidative damage to normal cells, including intestinal crypt cells [3].…”

Section: Introductionmentioning

confidence: 99%

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Protective effect of genistein on radiation-induced intestinal injury in tumor bearing mice

Son

Gong

Bae

et al. 2013

BMC Complement Altern Med

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BackgroundRadiation therapy is the most widely used treatment for cancer, but it causes the side effect of mucositis due to intestinal damage. We examined the protective effect of genistein in tumor-bearing mice after abdominal irradiation by evaluation of apoptosis and intestinal morphological changes.MethodsMouse colon cancer CT26 cells were subcutaneously injected at the flank of BALB/c mice to generate tumors. The tumor-bearing mice were treated with abdominal radiation at 5 and 10 Gy, and with genistein at 200 mg/kg body weight per day for 1 d before radiation. The changes in intestinal histology were evaluated 12 h and 3.5 d after irradiation. To assess the effect of the combination treatment on the cancer growth, the tumor volume was determined at sacrifice before tumor overgrowth occurred.ResultsGenistein significantly decreased the number of apoptotic nuclei compared with that in the irradiation group 12 h after 5 Gy irradiation. Evaluation of histological changes showed that genistein ameliorated intestinal morphological changes such as decreased crypt survival, villus shortening, and increased length of the basal lamina 3.5 d after 10 Gy irradiation. Moreover, the genistein-treated group exhibited more Ki-67-positive proliferating cells in the jejunum than the irradiated control group, and crypt depths were greater in the genistein-treated group than in the irradiated control group. The mean weight of the CT26 tumors was reduced in the group treated with genistein and radiation compared with the control group.ConclusionGenistein had a protective effect on intestinal damage induced by irradiation and delayed tumor growth. These results suggest that genistein is a useful candidate for preventing radiotherapy-induced intestinal damage in cancer patients.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Protective effect of genistein on radiation-induced intestinal injury in tumor bearing mice

Son

Gong

Bae

et al. 2013

BMC Complement Altern Med

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“…Rats were euthanized on the 7th day. Clinical parameters such as body weight changes, lethargy, and diarrhea were recorded during the treatment period, as described by Szabo et al (1998) (Table 1). The experiments were repeated two times, and data were pooled.…”

Section: Methodsmentioning

confidence: 99%

Neutralizing Anti-Vascular Endothelial Growth Factor (VEGF) Antibody Reduces Severity of Experimental Ulcerative Colitis in Rats: Direct Evidence for the Pathogenic Role of VEGF

Tolstanova¹,

Khomenko²,

Deng³

et al. 2008

J Pharmacol Exp Ther

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“…Exogenous VEGF significantly enhanced the healing of acute gastric mucosal injury induced by ethanol and duodenal ulceration elicited by cysteamine [230,231]. Stimulation of angiogenesis in granulation tissue by bFGF, PDGF dramatically accelerated healing of experimental gastric and duodenal ulcers given orally [195,196,199].…”

Section: Exogenously Applied Growth Factorsmentioning

confidence: 95%

Gastric Mucosal Protection: From Prostaglandins to Gene-Therapy

Gyires

2005

CMC

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The maintenance of gastric mucosal function and integrity highly depends on the status of microcirculation. Vasoactive agents--prostaglandins, nitric oxide and sensory neuropeptides (e.g. calcitonin gene-related peptide)--play a crucial role in mucosal defensive processes. Beside the local release of vasoactive mediators the central nervous system is also involved in regulation of gastric functions. Cerebral lesions, stimulation of different brain areas can result in gastric mucosal injury. Noxious challenge of gastric mucosa alters the sodium currents in gastric sensory neurons and induces cfos mRNA expression in nucleus tractus solitarii and area postrema. Vagal nerve has long been established to play a permissive role in the development of gastric lesions. However, several lines of evidences suggest its physiological relevance in the enhancement of gastric mucosal resistance. It was concluded that gastroprotection can be induced by low level of central vagal stimulation and the consequent release of prostaglandins, nitric oxide, and calcitonin gene-related peptide. Prostaglandins, nitric oxide and sensory neuropeptides play a role also in ulcer healing by stimulating the formation of growth factors, the epithelial proliferation and angiogenesis. Both systemic and local administration of growth factors accelerated the ulcer healing. Local, single injection of plasmid-DNA encoding vascular endothelial growth factor (VEGF) was shown to stimulate the ulcer healing in the rat. The transient, local expression of VEGF in ulcerated tissue might be a new therapeutic strategy in the treatment of gastric ulcer disease.

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Radiation-induced enterocolitis: basic and applied science

Cited by 10 publications

References 0 publications

Protective effect of genistein on radiation-induced intestinal injury in tumor bearing mice

Protective effect of genistein on radiation-induced intestinal injury in tumor bearing mice

Neutralizing Anti-Vascular Endothelial Growth Factor (VEGF) Antibody Reduces Severity of Experimental Ulcerative Colitis in Rats: Direct Evidence for the Pathogenic Role of VEGF

Gastric Mucosal Protection: From Prostaglandins to Gene-Therapy

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