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Effects of Atorvastatin on Oxidative Stress Biomarkers and Mitochondrial Morphofunctionality in Hyperfibrinogenemia-Induced Atherogenesis.

Scribano Mde L, Baez Mdel C, Florencia B, Tarán MD, Franco S, Balceda AG, Moya M - Adv Med (2014)

Bottom Line: There were no significant differences between Ctr and Ctr-Atorv in fibrinogen, NO, and SOD values.Comparing Ctr with AI an increase of fibrinogen is observed (P < 0.001), but it decreased after administration of atorvastatin in AI-Ator (P < 0.001).SOD showed an increase in AI and AI-Ator compared to Ctr (P < 0.001).

View Article: PubMed Central - PubMed

Affiliation: Cátedra de Física Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, X5000 Córdoba, Argentina.

ABSTRACT
Relationship between hyperfibrinogenemia (HF), oxidative stress, and atherogenesis was established. Effect of atorvastatin (Ator) was assessed. Wistar male (6 months) rats were studied: Ctr, control, without HF induction; Ctr-Ator, without HF treated with atorvastatin; AI, atherogenesis induced, and AI-Ator, atherogenesis induced and treated with atorvastatin. Atherogenesis was induced by daily adrenaline injection (0.1 mL/day/rat) for 90 days; treatment started 15 days after induction. Fibrinogen (mg/dL) and nitric oxide (NO) were measured in plasma (mM) and superoxide dismutase (SOD) (U/mL) in red cell lysate by spectrophotometry. Slices of aorta were analyzed by electron microscopy (EM). ANOVA and chi-square test were used; P < 0.05 was established. There were no significant differences between Ctr and Ctr-Atorv in fibrinogen, NO, and SOD values. Comparing Ctr with AI an increase of fibrinogen is observed (P < 0.001), but it decreased after administration of atorvastatin in AI-Ator (P < 0.001). NO diminished in AI relative to Ctr and increased in AI-Ator (P < 0.001). SOD showed an increase in AI and AI-Ator compared to Ctr (P < 0.001). EM revealed expansion of intermembrane space and disorganization of crests in AI. In AI-Ator mitochondrial areas and diameters were similar to control. Atorvastatin normalizes HF, stabilizes NO, increases SOD, and produces a partial regression of mitochondrial lesions.

No MeSH data available.


Related in: MedlinePlus

Enzymatic activity of SOD in rats with induced HF treated with atorvastatin (n = 12). Crt versus Ctr.Ator ND; Ctr versus AI P < 0.001; Ctr versus AI-Ator P < 0.001; Ctr-Ator versus AI P < 0.001; Ctr-Ator versus AI-Ator P < 0.001; AI versus AI-Ator P < 0.001.
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fig3: Enzymatic activity of SOD in rats with induced HF treated with atorvastatin (n = 12). Crt versus Ctr.Ator ND; Ctr versus AI P < 0.001; Ctr versus AI-Ator P < 0.001; Ctr-Ator versus AI P < 0.001; Ctr-Ator versus AI-Ator P < 0.001; AI versus AI-Ator P < 0.001.

Mentions: The results of the plasmatic variables: fibrinogen, NO, and SOD activity, are shown in Figures 1, 2, and 3 for all groups.


Effects of Atorvastatin on Oxidative Stress Biomarkers and Mitochondrial Morphofunctionality in Hyperfibrinogenemia-Induced Atherogenesis.

Scribano Mde L, Baez Mdel C, Florencia B, Tarán MD, Franco S, Balceda AG, Moya M - Adv Med (2014)

Enzymatic activity of SOD in rats with induced HF treated with atorvastatin (n = 12). Crt versus Ctr.Ator ND; Ctr versus AI P < 0.001; Ctr versus AI-Ator P < 0.001; Ctr-Ator versus AI P < 0.001; Ctr-Ator versus AI-Ator P < 0.001; AI versus AI-Ator P < 0.001.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4590975&req=5

fig3: Enzymatic activity of SOD in rats with induced HF treated with atorvastatin (n = 12). Crt versus Ctr.Ator ND; Ctr versus AI P < 0.001; Ctr versus AI-Ator P < 0.001; Ctr-Ator versus AI P < 0.001; Ctr-Ator versus AI-Ator P < 0.001; AI versus AI-Ator P < 0.001.
Mentions: The results of the plasmatic variables: fibrinogen, NO, and SOD activity, are shown in Figures 1, 2, and 3 for all groups.

Bottom Line: There were no significant differences between Ctr and Ctr-Atorv in fibrinogen, NO, and SOD values.Comparing Ctr with AI an increase of fibrinogen is observed (P < 0.001), but it decreased after administration of atorvastatin in AI-Ator (P < 0.001).SOD showed an increase in AI and AI-Ator compared to Ctr (P < 0.001).

View Article: PubMed Central - PubMed

Affiliation: Cátedra de Física Biomédica, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, X5000 Córdoba, Argentina.

ABSTRACT
Relationship between hyperfibrinogenemia (HF), oxidative stress, and atherogenesis was established. Effect of atorvastatin (Ator) was assessed. Wistar male (6 months) rats were studied: Ctr, control, without HF induction; Ctr-Ator, without HF treated with atorvastatin; AI, atherogenesis induced, and AI-Ator, atherogenesis induced and treated with atorvastatin. Atherogenesis was induced by daily adrenaline injection (0.1 mL/day/rat) for 90 days; treatment started 15 days after induction. Fibrinogen (mg/dL) and nitric oxide (NO) were measured in plasma (mM) and superoxide dismutase (SOD) (U/mL) in red cell lysate by spectrophotometry. Slices of aorta were analyzed by electron microscopy (EM). ANOVA and chi-square test were used; P < 0.05 was established. There were no significant differences between Ctr and Ctr-Atorv in fibrinogen, NO, and SOD values. Comparing Ctr with AI an increase of fibrinogen is observed (P < 0.001), but it decreased after administration of atorvastatin in AI-Ator (P < 0.001). NO diminished in AI relative to Ctr and increased in AI-Ator (P < 0.001). SOD showed an increase in AI and AI-Ator compared to Ctr (P < 0.001). EM revealed expansion of intermembrane space and disorganization of crests in AI. In AI-Ator mitochondrial areas and diameters were similar to control. Atorvastatin normalizes HF, stabilizes NO, increases SOD, and produces a partial regression of mitochondrial lesions.

No MeSH data available.


Related in: MedlinePlus