Aspirin vs Plavix (Clopidogrel Bisulfate), use San Qi (Notoginseng) to replace them when people have severe side effects from these drugs

1 Jan , 2024
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What is aspirin? How does it work?

Aspirin is a nonsteroidal anti-inflammatory drug (NSAID) used to treat feverpain, and inflammation in the body. It also prevents blood clots and is used to prevent heart attack and stroke. Other NSAIDs include ibuprofen (AleveMotrin), indomethacin (Indocin), and nabumetone (Relafen).

NSAIDs block the enzyme that makes prostaglandins (cyclooxygenase), resulting in lower concentrations of prostaglandins, and reducing levels of inflammation, pain, and fever. Inhibition of prostaglandins also reduces the function of platelets and the ability of blood to clot. Aspirin inhibits the function of platelets in a manner different from other NSAIDs and its antithrombotic effects last longer than other NSAIDs.

What is Plavix? How does it work?

Plavix (clopidogrel bisulfate) is an anti-platelet drug used to prevent blood clots. Plavix is used to reduce the risk of heart attacks and strokes, particularly in people with a recent history of stroke or heart attack, and those with peripheral vascular disease.

Plavix works by binding to the P2Y12 receptor on platelets, preventing adenosine diphosphate (ADP) from activating platelets. It belongs to a class of drugs called P2Y12 inhibitors. Other P2Y12 inhibitors include ticagrelor (Brilinta) and prasugrel (Effient). Clopidogrel is similar to ticlopidine (Ticlid) in chemical structure and in the way it works.


Aspirin side effects

Most people benefit from aspirin and other NSAIDs with few side effects. However, serious side effects can occur and generally tend to be dose-related. Therefore, it is advisable to use the lowest effective dose to minimize side effects.

The most common side effects of aspirin involve the gastrointestinal system and ringing in the ears.

Gastrointestinal side effects of aspirin

  • Ulcers
  • Abdominal burning
  • Pain
  • Cramping
  • Nausea
  • Gastritis
  • Serious gastrointestinal bleeding
  • Liver toxicity
  • Rach
  • Kidney Impairment
  • Vertigo
  • Dizziness

Plavix side effects

The tolerability of clopidogrel is similar to that of aspirin. Common side effects of clopidogrel are:

Side effects of Plavix that are more serious include:

But ....

Clinical trial shows that San Qi (notoginseng) has the solution. (https://www.thrombosisresearch.com/article/S0049-3848(16)30082-2/pdf)

This study was designed to investigate the effect of Panax notoginseng saponin (PNS) on platelet adhesion to injured endothelial cells (ECs) and platelet activation induced by injured ECs, and to explore its underlying mechanisms.

Methods

Human umbilical vein endothelial cells (HUVECs) pretreated with aspirin (ASA,15 μg/mL) or PNS (160 μg/mL), or neither, were exposed to oxidized low-density lipoprotein (ox-LDL,80 mg/L) for 16 h. Platelets were then added and co-cultured with HUVECs for 5 min. Platelet adhesion to ECs, platelet CD62p expression, and HUVEC apoptosis were assessed by fluorescence activated cell sorting (FACS)·Supernatant concentration of 6-keto-PGF1α and thromboxane 2 (TXB2) were measured by radioimmunoassay. Cyclooxygenase-1 (COX-1) and COX-2 protein expression were measured by western blotting.

Results

The inhibitory effect of PNS on platelet activation was similar to ASA, but the inhibitory effect of PNS on platelet adhesion to ECs was superior to ASA. PNS modulated COX-2 expression, and increased 6-keto-PGF1α concentration in HUVECs, while down-regulated COX-1 expression and decreased supernatant TXB2 concentration in platelets. Co-culturing of injured HUVECs with platelets increased HUVEC apoptosis induced by ox-LDL compared with HUVECs cultured without platelets; ASA increased HUVEC apoptosis induced by ox-LDL when cultured without platelets, while decreased the apoptosis when co-cultured with platelets.

Conclusions

EC protection by ASA is closely associated with its inhibitory effect on platelet activation. PNS is superior to ASA in protecting ECs and in inhibiting platelet adhesion to injured ECs, and the regulation of COX pathway in both ECs and platelets might be the underlying mechanisms of PNS.