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Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
Published on: April 6, 2017
[Effect of Panax notoginseng preparations on platelet function]
Yue Li1, Feng-Wen Yang1, Ming-Yan Zhang1
1Center for Evidence-Based Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China.
Panax notoginseng preparations (PNPs) effectively reduce platelet aggregation markers like MPAR and TXB2, especially when combined with antiplatelet or non-antiplatelet agents. However, more rigorous trials are needed due to evidence limitations.
Area of Science:
- Pharmacology and Traditional Medicine
- Cardiovascular Research
- Evidence-Based Medicine
Background:
- Platelet aggregation plays a critical role in thrombotic events.
- Panax notoginseng preparations (PNPs) are widely used in traditional medicine for cardiovascular health.
- The antiplatelet effects of PNPs require systematic evaluation.
Purpose of the Study:
- To systematically evaluate the efficacy of Panax notoginseng preparations (PNPs) on platelet function.
- To assess the impact of PNPs, alone and in combination with other agents, on platelet aggregation markers.
- To evaluate the safety profile of PNPs concerning hemorrhagic adverse events.
Main Methods:
- A systematic review and meta-analysis of randomized controlled trials (RCTs) were conducted.
- Searched six major literature databases for relevant RCTs.
- Assessed risk of bias using the Cochrane handbook and analyzed data with RevMan 5.3 software.
Main Results:
- PNPs significantly reduced the MPAR level compared to placebo and non-antiplatelet agents.
- Combination therapy with PNPs and non-antiplatelet agents reduced MPAR and TXB2.
- PNPs combined with anti-platelet agents showed enhanced effects on MPAR and TXB2, without increasing adverse events.
Conclusions:
- Panax notoginseng preparations demonstrate significant potential in reducing platelet aggregation markers, specifically MPAR and TXB2.
- Combining PNPs with anti-platelet or non-antiplatelet agents can improve therapeutic efficacy.
- High clinical heterogeneity and methodological limitations necessitate further rigorous clinical trials to strengthen the evidence base.
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