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All-trans-retinoic acid ameliorated high fat diet-induced atherosclerosis in rabbits by inhibiting platelet activation and inflammation.

Zhou B, Pan Y, Hu Z, Wang X, Han J, Zhou Q, Zhai Z, Wang Y - J. Biomed. Biotechnol. (2012)

Bottom Line: All-trans-retinoic acid (atRA) is effective for many proliferative diseases.P-selectin expression and fibrinogen binding on platelets or deposition on the intima of the aorta also increased significantly as did the levels of TNF-α, IL-6, and fibrinogen in plasma.After 8 weeks of treatment with atRA, there was a significant decrease in plasma lipids and improvement in aortic lesions.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, The First Affiliated Hospital of Anhui Medical University, Anhui 230022, China.

ABSTRACT

Background: All-trans-retinoic acid (atRA) is effective for many proliferative diseases. We investigated the protective effects of atRA against atherosclerosis.

Methods: Rabbits were randomly allocated to receive basal diet or an HFD for 4 weeks. HFD group then received rosuvastatin (3 mg/day), atRA (5 mg/kg/day), or the same volume of vehicle, respectively, for next 8 weeks.

Results: HFD group showed increases in plasma lipids and aortic plaque formation. P-selectin expression and fibrinogen binding on platelets or deposition on the intima of the aorta also increased significantly as did the levels of TNF-α, IL-6, and fibrinogen in plasma. After 8 weeks of treatment with atRA, there was a significant decrease in plasma lipids and improvement in aortic lesions. AtRA also inhibited the expression of P-selectin and fibrinogen binding on platelets and deposition on the intima of the aorta.

Conclusion: AtRA can ameliorate HFD-induced AS in rabbits by inhibiting platelet activation and inflammation.

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Related in: MedlinePlus

Platelet CD62-P expressions in different groups. Isolated platelets were incubated with FITC-labelled anti-CD62P antibody, and surface CD62-P changes were monitored by flow cytometry. Representative histograms from every group are shown. (a) The expression of CD62-P on the resting platelets surface from different groups. (b) The expression of CD62-P on the thrombin-activated platelets from different groups. (c) The expression of CD62-P on the ADP-activated platelets from different groups. (d) Mean fluorescence intensity (MFI) of CD62-P expression on platelets surface in different groups. Data are mean ± standard deviation (SD). Comparisons between groups were carried out using one-way analysis of variance (ANOVA) and Student-Newman-Keuls (SNK) method (n = 6). **P < 0.01 compared to control group, ▲P < 0.05, ▲▲P < 0.01 compared to HFD group.
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fig3: Platelet CD62-P expressions in different groups. Isolated platelets were incubated with FITC-labelled anti-CD62P antibody, and surface CD62-P changes were monitored by flow cytometry. Representative histograms from every group are shown. (a) The expression of CD62-P on the resting platelets surface from different groups. (b) The expression of CD62-P on the thrombin-activated platelets from different groups. (c) The expression of CD62-P on the ADP-activated platelets from different groups. (d) Mean fluorescence intensity (MFI) of CD62-P expression on platelets surface in different groups. Data are mean ± standard deviation (SD). Comparisons between groups were carried out using one-way analysis of variance (ANOVA) and Student-Newman-Keuls (SNK) method (n = 6). **P < 0.01 compared to control group, ▲P < 0.05, ▲▲P < 0.01 compared to HFD group.

Mentions: Platelet activation was investigated by checking platelet CD62-P expression and fibrinogen binding by flow cytometry. As shown in Figures 2 and 3, the percentage and MFI of fibrinogen and CD62-P were significantly lower in resting platelets from all groups compared with findings in thrombin and ADP-stimulated platelets. Platelets from the control group (in either resting or activated states) had lower fibrinogen and CD62-P expression compared with that seen in the HFD, rosuvastatin, and atRA groups. However, when compared to HFD group, platelets from rosuvastatin and atRA groups had significantly lower expression of fibrinogen and CD62-P on platelet surfaces, suggesting that atRA suppressed platelet activation.


All-trans-retinoic acid ameliorated high fat diet-induced atherosclerosis in rabbits by inhibiting platelet activation and inflammation.

Zhou B, Pan Y, Hu Z, Wang X, Han J, Zhou Q, Zhai Z, Wang Y - J. Biomed. Biotechnol. (2012)

Platelet CD62-P expressions in different groups. Isolated platelets were incubated with FITC-labelled anti-CD62P antibody, and surface CD62-P changes were monitored by flow cytometry. Representative histograms from every group are shown. (a) The expression of CD62-P on the resting platelets surface from different groups. (b) The expression of CD62-P on the thrombin-activated platelets from different groups. (c) The expression of CD62-P on the ADP-activated platelets from different groups. (d) Mean fluorescence intensity (MFI) of CD62-P expression on platelets surface in different groups. Data are mean ± standard deviation (SD). Comparisons between groups were carried out using one-way analysis of variance (ANOVA) and Student-Newman-Keuls (SNK) method (n = 6). **P < 0.01 compared to control group, ▲P < 0.05, ▲▲P < 0.01 compared to HFD group.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3303861&req=5

fig3: Platelet CD62-P expressions in different groups. Isolated platelets were incubated with FITC-labelled anti-CD62P antibody, and surface CD62-P changes were monitored by flow cytometry. Representative histograms from every group are shown. (a) The expression of CD62-P on the resting platelets surface from different groups. (b) The expression of CD62-P on the thrombin-activated platelets from different groups. (c) The expression of CD62-P on the ADP-activated platelets from different groups. (d) Mean fluorescence intensity (MFI) of CD62-P expression on platelets surface in different groups. Data are mean ± standard deviation (SD). Comparisons between groups were carried out using one-way analysis of variance (ANOVA) and Student-Newman-Keuls (SNK) method (n = 6). **P < 0.01 compared to control group, ▲P < 0.05, ▲▲P < 0.01 compared to HFD group.
Mentions: Platelet activation was investigated by checking platelet CD62-P expression and fibrinogen binding by flow cytometry. As shown in Figures 2 and 3, the percentage and MFI of fibrinogen and CD62-P were significantly lower in resting platelets from all groups compared with findings in thrombin and ADP-stimulated platelets. Platelets from the control group (in either resting or activated states) had lower fibrinogen and CD62-P expression compared with that seen in the HFD, rosuvastatin, and atRA groups. However, when compared to HFD group, platelets from rosuvastatin and atRA groups had significantly lower expression of fibrinogen and CD62-P on platelet surfaces, suggesting that atRA suppressed platelet activation.

Bottom Line: All-trans-retinoic acid (atRA) is effective for many proliferative diseases.P-selectin expression and fibrinogen binding on platelets or deposition on the intima of the aorta also increased significantly as did the levels of TNF-α, IL-6, and fibrinogen in plasma.After 8 weeks of treatment with atRA, there was a significant decrease in plasma lipids and improvement in aortic lesions.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, The First Affiliated Hospital of Anhui Medical University, Anhui 230022, China.

ABSTRACT

Background: All-trans-retinoic acid (atRA) is effective for many proliferative diseases. We investigated the protective effects of atRA against atherosclerosis.

Methods: Rabbits were randomly allocated to receive basal diet or an HFD for 4 weeks. HFD group then received rosuvastatin (3 mg/day), atRA (5 mg/kg/day), or the same volume of vehicle, respectively, for next 8 weeks.

Results: HFD group showed increases in plasma lipids and aortic plaque formation. P-selectin expression and fibrinogen binding on platelets or deposition on the intima of the aorta also increased significantly as did the levels of TNF-α, IL-6, and fibrinogen in plasma. After 8 weeks of treatment with atRA, there was a significant decrease in plasma lipids and improvement in aortic lesions. AtRA also inhibited the expression of P-selectin and fibrinogen binding on platelets and deposition on the intima of the aorta.

Conclusion: AtRA can ameliorate HFD-induced AS in rabbits by inhibiting platelet activation and inflammation.

Show MeSH
Related in: MedlinePlus