Maria Del Carmen Baez1, Mariana Taran1, Maria de La Paz Scribano1, Ariel Balceda1, Carla Buonanotte1, Sergio Blencio1, Ismael Fonseca2, Monica Moya1.
Abstract
OBJECTIVE: The oxidative process in atherogenesis generated by proinflammatory induction and response to antioxidants vitamins in an experimental model were analyzed.
METHODS: Male rats were used: (A)Control, (B)Control+vitamin E plus C, (C)Hyperfibrinogenemia and (D)Hyperfibrinogenemia+vitamins E plus C. Hyperfibrinogenemia induced by daily injection of adrenaline (0.1mg/day/rat) for 120 days. TREATMENT: 3.42 mg/kg of vitamin E plus 2.14 mg/kg of vitamin C, fifteen days after induction. Vascular histology analyzed by optical microscopy. Fibrinogen, nitrites and superoxide dismutase analyzed by spectrophotometry. STATISTICS: MANOVA, Hotelling test for post testing, significance level p<0.05.
RESULTS: (C) group showed higher fibrinogen than (A) and (B)(p<0.001). Compared to (C) group, (D) showed a decrease of fibrinogen (p<0.001). A marked increase in nitrites was found in (C) versus (A), (B) and (D) groups (p<0.001). Superoxide dismutase activity increased in (C) group compared to groups (A) and (B) (p<0.001). In the group (D) an increase of the activity of this enzyme was observed in comparison to groups (C)(p<0.001), (A) and (B) (p<0.0001 in both). The (C) group shown endothelial denudation, thickening of the vascular intima and extracellular matrix enlargement with foam cells(p<0.001).
CONCLUSION: These results strongly suggest that vitamins E plus C produce regression of inflammatory and oxidative stress processes in this experimental model. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.
OBJECTIVE: The oxidative process in atherogenesis generated by proinflammatory induction and response to antioxidants vitamins in an experimental model were analyzed.
METHODS: Male rats were used: (A)Control, (B)Control+vitamin E plus C, (C)Hyperfibrinogenemia and (D)Hyperfibrinogenemia+vitamins E plus C. Hyperfibrinogenemia induced by daily injection of adrenaline (0.1mg/day/rat) for 120 days. TREATMENT: 3.42 mg/kg of vitamin E plus 2.14 mg/kg of vitamin C, fifteen days after induction. Vascular histology analyzed by optical microscopy. Fibrinogen, nitrites and superoxide dismutase analyzed by spectrophotometry. STATISTICS: MANOVA, Hotelling test for post testing, significance level p<0.05.
RESULTS: (C) group showed higher fibrinogen than (A) and (B)(p<0.001). Compared to (C) group, (D) showed a decrease of fibrinogen (p<0.001). A marked increase in nitrites was found in (C) versus (A), (B) and (D) groups (p<0.001). Superoxide dismutase activity increased in (C) group compared to groups (A) and (B) (p<0.001). In the group (D) an increase of the activity of this enzyme was observed in comparison to groups (C)(p<0.001), (A) and (B) (p<0.0001 in both). The (C) group shown endothelial denudation, thickening of the vascular intima and extracellular matrix enlargement with foam cells(p<0.001).
CONCLUSION: These results strongly suggest that vitamins E plus C produce regression of inflammatory and oxidative stress processes in this experimental model. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.
Entities:
Keywords:
Antioxidants; atherogenesis; atherosclerosis; hyperfibrinogenemia; oxidative stress; vitamins E plus C
Mesh:
Substances:
Year: 2017
PMID: 28618986 DOI: 10.2174/1871523016666170616121133
Source DB: PubMed Journal: Antiinflamm Antiallergy Agents Med Chem ISSN: 1871-5230