Protective Effects of Ticlopidine and Aspirin, Administered Alone and in Combination, on Thrombus Formation in Rat Cerebral Vessels

Sasaki, Yasuto; Ishii, Izumi; Giddings, J. C.; Yamamoto, Junichiro

doi:10.1159/000217200

Cited by 8 publications

(5 citation statements)

References 18 publications

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“…Ticlopidine was used in the present study as a pharmacological tool, with the higher dose selected because it is effective in terms of inhibiting platelet aggregation in the rat (19,22,23). Further studies to evaluate the effects of therapeutic doses of ticlopidine on the production of angiogenesis-related growth factors in humans seem warranted.…”

Section: Discussionmentioning

confidence: 99%

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Platelets modulate gastric ulcer healing: Role of endostatin and vascular endothelial growth factor release

Elliott

Cirino

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

227

193

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Bleeding and delayed healing of ulcers are well recognized clinical problems associated with the use of aspirin and other nonsteroidal antiinflammatory drugs, which have been attributed to their antiaggregatory effects on platelets. We hypothesized that antiplatelet drugs might interfere with gastric ulcer healing by suppressing the release of growth factors, such as vascular endothelial growth factor (VEGF), from platelets. Gastric ulcers were induced in rats by serosal application of acetic acid. Daily oral treatment with vehicle, aspirin, or ticlopidine (an ADP receptor antagonist) was started 3 days later and continued for 1 week. Ulcer induction resulted in a significant increase in serum levels of VEGF and a significant decrease in serum levels of endostatin (an antiangiogenic factor). Although both aspirin and ticlopidine markedly suppressed platelet aggregation, only ticlopidine impaired gastric ulcer healing and angiogenesis as well as reversing the ulcerassociated changes in serum levels of VEGF and endostatin. The effects of ticlopidine on ulcer healing and angiogenesis were mimicked by immunodepletion of circulating platelets, and ticlopidine did not influence ulcer healing when given to thrombocytopenic rats. Incubation of human umbilical vein endothelial cells with serum from ticlopidine-treated rats significantly reduced proliferation and increased apoptosis, effects reversed by an antibody directed against endostatin. Ticlopidine treatment resulted in increased platelet endostatin content and release. These results demonstrate a previously unrecognized contribution of platelets to the regulation of gastric ulcer healing. Such effects likely are mediated through the release from platelets of endostatin and possibly VEGF. As shown with ticlopidine, drugs that influence gastric ulcer healing may do so in part through altering the ability of platelets to release growth factors.angiogenesis ͉ ticlopidine ͉ aspirin ͉ proliferation ͉ endothelium

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Section: Discussionmentioning

confidence: 99%

“…These doses of ticlopidine and aspirin have been shown to inhibit platelet aggregation and thrombus formation in the rat (18)(19)(20)(21)(22)(23). Aspirin's inhibitory effects on thromboxane (TX) synthesis were confirmed by taking blood before sacrifice, allowing it to clot at 37°C for 45 min, and then measuring TXB 2 levels by ELISA (20).…”

Section: Methodsmentioning

confidence: 99%

Platelets modulate gastric ulcer healing: Role of endostatin and vascular endothelial growth factor release

Elliott

Cirino

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

227

193

View full text Add to dashboard Cite

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“…Control rats were treated with the same volume of vehicle (NaCl 0.9%). Previously, these doses have been shown to cause effective inhibition of platelet aggregations and thrombus formation in rats 16‐21 . At the end of the experimental period (15 days) and before 8:00 AM , each rat was anesthetized with 1 mg/kg body weight of ketamine # and 0.4 mL/kg of xylazine ** and 3‐mL blood samples were collected into K3EDTA‐containing vacuum tubes †† by cardiac puncture.…”

Section: Methodsmentioning

confidence: 99%

Influence of Antiplatelet Drugs in the Pathogenesis of Experimental Periodontitis and Periodontal Repair in Rats

Coimbra

Rossa

Guimarães

et al. 2011

Journal of Periodontology

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“…One day after placement of ligatures, animals were administered daily doses of intragastric aspirin (Asp; 30 mg/kg), clopidogrel (Clop; 75 mg/kg) or the same volume of vehicle (NaCl 0.9%), this treatment was performed for the remaining 9 days of the study. These doses were previously shown to cause effective inhibition of platelet aggregation and thrombus formation in mice (Sasaki, Ishii, Giddings, & Yamamoto, ; Taka, Okano, Seiki, & Yamamoto, ). Mice in the other three groups were negative controls with no ligature‐induced experimental periodontitis; these mice were treated with Asp, Clop and NaCl 0.9%, as described above.…”

Section: Methodsmentioning

confidence: 98%

Platelets as inflammatory mediators in a murine model of periodontitis

Zhan

Meng

et al. 2020

J Clinic Periodontology

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Aim To investigate the role of platelets during the development of ligature‐induced experimental periodontitis in mice. Materials and Methods Experimental periodontitis was induced by placement of sterilized 5‐0 cotton ligatures around the maxillary and mandibular second molars of C57BL/6 wild‐type mice. Flow cytometry was used to analyse platelet activation and platelet–leucocyte aggregate formation, and histologic analysis was used to evaluate inflammation and localization of platelets and leucocytes in periodontal tissues during the development of experimental periodontitis and in experimental periodontitis with and without antiplatelet drug treatment. Results Experimental periodontitis induced platelet activation and platelet–leucocyte interaction. Platelets and leucocytes gradually infiltrated in inflammatory gingival tissues during the development of experimental periodontitis. The inhibition of platelet activation via drug therapy led to significant inhibition of leucocyte migration and marked reduction in periodontal inflammation. Conclusion This study revealed that platelets are critical for inflammation and tissue injury in periodontitis and serve as mediators of inflammation in periodontal tissue.

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Protective Effects of Ticlopidine and Aspirin, Administered Alone and in Combination, on Thrombus Formation in Rat Cerebral Vessels

Cited by 8 publications

References 18 publications

Platelets modulate gastric ulcer healing: Role of endostatin and vascular endothelial growth factor release

Platelets modulate gastric ulcer healing: Role of endostatin and vascular endothelial growth factor release

Influence of Antiplatelet Drugs in the Pathogenesis of Experimental Periodontitis and Periodontal Repair in Rats

Platelets as inflammatory mediators in a murine model of periodontitis

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