Most patients with large hiatal hernia and Cameron lesions presented with overt GI bleeding. Patients with Cameron lesions tend to be older females. In patients with anemia and GI bleeding, large hiatal hernia and Cameron erosions should also be considered.
Purpose: To evaluate the effects of an angiotensin-converting enzyme (ACE) inhibitor, captopril, on pentylenetetrazole (PTZ)-induced seizures and post-seizure hippocampal injury.
Materials: Thirty-five male Balb-c mice weighing 30 - 33 g were divided into control, saline PTZ, s(erum physiologic 1 ml/kg as solvent), positive control (valproic acid 200 mg/kg), captopril (25 mg/kg/day for 7 days), and captopril (50 mg/kg/day for 7 days) groups. PTZ (60 mg/kg) was administered thirty minutes after medication administration to induce epileptic seizures. The animals were observed for 30 min to record Racine stages, the time of the first myoclonic jerk (FMJ), and the occurrence of the first generalized tonic-clonic seizure (GTCS). Cornu Ammonis (CA)1, CA2, CA3, and the dentate gyrus (DG) of the hippocampus underwent histopathological examinations. The levels of total oxidant status (TOS), oxidative stress markers (total antioxidant status, TAS), and oxidative stress index (OSI) were measured in the brain tissue.
Results: Compared to PTZ group, 25 mg/kg captopril decreased seizure scores and delayed FMJ and GTCS (p < 0.05). Histopathological assessment demonstrated that both 25 and 50 mg/kg captopril alleviated neuronal injury in CA1, CA2, CA3, and DG compared to PTZ (p < 0.05). Also, TOS and OSI levels in the brain tissue were reduced by both 25 and 50 mg/kg doses of captopril (p < 0.05).
Conclusion: Captopril favorably improves epileptic seizure parameters and acts against post-seizure neuronal injury in the hippocampus. Captopril may be a drug of choice in epileptic individuals with hypertension.
Keywords: Captopril, Angiotensin-converting enzyme, Epilepsy, Pentylenetetrazole, Neuronal damage
Purpose: An inverse association between serum lycopene levels and risk of cancers has been pointed out by many prospective and retrospective epidemiological studies which prompted more studies to be performed on animal models and cell cultures in order to test this hypothesis. The aim of the present study was to evaluate the antiproliferative and pro-apoptotic effect of lycopene on colon cancer HT-29 cell lines.Materials and Methods: The effect of lycopene on the viability of HT-29 cell line was investigated using XTT assay. the levels of BCL-2, cleaved caspase 3, BAX, cleaved PARP and 8-oxo-dG in lycopene-treated HT-29 cells were measured using ELISA. gamma-H2AX and cytochrome C expression was assessed semiquantitatively using immuno uorescence staining.Results: Lycopene at doses of 10 and 20 μM produced a signi cant antiproliferative effect on HT-29 cells compared to the control (p < 0.05). The IC50 value of lycopene in HT-29 cells was found to be 4.382 μM for 24 hours. Lycopene (4.382 μM) signi cantly elevated cleaved caspase 3 (p <0.01), BAX, and cleaved PARP, 8-oxo-dG levels (p<0.05). the levels of γ-H2AX foci are signi cantly higher while the levels of cytochrome-C are lower (p<0.05) in lycopene treated HT-29 cells.
Conclusion:These results indicate that lycopene has an antiproliferative apoptotic and genotoxic effect on HT-29 colon cancer cell lines.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.