Separation Of NSAIDs By Capillary Electrophoresis

Separation Of NSAIDs By Capillary Electrophoresis

Separation Of NSAIDs By Capillary Electrophoresis


Discuss about the Separation of NSAIDs by Capillary Electrophoresis.



Non Steroidal Anti-inflammatory drugs or NSAIDs as the name suggests are drugs, which are non steroidal in nature. It helps to fight back against the inflammatory reactions and hence they are known as anti-inflammatory drugs. They act as an analgesic and helps to treat pain. It also has anti pyretic actions and suppress the signs and symptoms of inflammation.

The classification of NSAIDs on the basis of their chemical nature (Conaghan 2012)

  • Salicylates: Aspirin Sodium salicylate and diflunisal
  • Propionic acid derivatives: ibuprofen, ketoprofen and naproxen
  • Aryl acetic acid derivatives: diclofenac and ketorolac
  • Indole derivatives: indomethacin and sulindac
  • Alkanones: Nabumetone
  • Oxicams: piroxicam and tenoxicam
  • Anthranilic acid derivatives (fenamates): Mefenamic acid and flufenamic acid
  • Pyrazolone derivatives: phenylbutazone, oxyphenbutazone and azapropazone (apazone) & dipyrone (novalgine)
  • Aniline derivatives (analgesic only): paracetamol

Properties Of Salicylates

Aspirin is the most important example of Salicylates. It is gets readily absorbed from the stomach and during its passage from the upper part of the small intestine. Upon absorption, it gets distributed all over the body via diffusion in the body fluid, blood. Nearly 50?80% of the salicylate moves via binding with the plasma protein (albumin). Salicylate an active metabolite at times remains conjugated with glucuronic acid and glycine and gets excreted through the kidney and this excretion is further increased via the alkalinization of the urine (Rainsford 2013).

Aspirin Mechanism Of Action

A family of very potent biological signaling molecule, Eicosanoids, acts as short-range messengers. It causes the localized action that is, it affects tissues near the cells that produce them. In response to the hormonal stimulation or other stimuli, Phospholipase A2 (an outer membrane protein of mammalian cell) cleaves membrane glycerophospholipids, releasing Arachidonate from the middle carbon of glycerol. Following this reaction, the enzymes present in the smooth endoplasmic reticulum (ER) converts arachidonate into prostaglandins (prostaglandin H2 or PGH2). The peroxides then convert PH2 into the other precursors of prostaglandins and thromboxanes (Lehninger 2012). A bifunctional enzyme, cyclooxygenase (COX) (also known as prostaglandin H2 synthase) promotes the conversion of the arachidonate into PGH2.

Prostaglandin is a secondary mediator of type I hypersensitivity reactions. It is produced after the mast cell degranulation and thus causes more pronounced and long lasting effect. Prostaglandin D2 causes broncho constriction. The other prostaglandins caused vasodilatation, contraction of the pulmonary smooth muscles and platelet aggregation (Owen, Punt and Stranford 2013). In order to treat such inflammatory reactions caused by the secondary mediators, Aspirin is prescribed. Aspirin (acetylsalicylate) irreversibly inactivates the activity of the COX. It acetylates the Ser residue present at the active site of the enzyme and thus blocking the enzymes activity and this in turn inhibits the synthesis of prostaglandins and thromboxanes (Dovizio et al. 2013).

NSAIDs like indomethacin and ibuprofen, inhibits the action of cyclooxygenases via the mechanism of competitive inhibition. They compete with the arachidonate with the active substrate binding site of COX and thus inhibiting the action of the enzyme on Arachidonate.