NSAID suppresses inflammation and causes

The pathogen enters the body and expresses some proteins on its surface, called PAMP (pathogen-associated molecular proteins). The PAMP is recognized by immune cells. The mast cells release histamines which causes vasodilation. The vascular permeability of the blood vessel increases and more gaps are formed in the endothelial layer as it contracts. This results in the entry of more blood with immune cells inside the endothelial layer. The macrophages also recognize the PAMP and release cytokinins. Cytokinins such as TNFα (tumor necrosis factor α) and IL-1 (interleukin-1). These are inflammatory mediators and cause local and systemic effects. The local effect includes inflammation and increasing fibroblast activity to trigger tissue repair. The systemic effect includes fever and leukocytosis which is the accumulation of WBC in the blood vessels, which usually happens in inflammation. When the immune cells migrate towards the affected area, the monocyte gets converted into macrophages in the affected tissue. Glucocorticoids are steroidal hormones, naturally secreted from the adrenal gland in the blood and known as cortisol hormone. They can be made synthetically and has anti-inflammatory effects.

It is a group of compounds that contribute to the inflammatory response and perception of pain. Prostaglandins are synthesized from arachidonic acid by cyclooxygenase (COX) enzyme and this prostaglandin is converted into different forms in different tissues.

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Physiological prostaglandins play an important role in temperature homeostasis, uterine contraction, renal vasodilation, sleep regulation, and allergic reactions. Their level is generally low but can go up immediately by acute stimulation.

The COX enzyme is of two types-

COX-I – It is always expressed by all the cells (constitutive nature). It also synthesizes carbonate ions (HCO3-) and thereby protects GIT (gastrointestinal tract) from acidity caused by HCL (hydrochloric acid).

COX-II – It is induced by the inflamed tissue. NSAID interferes with arachidonic acid to bind with both the enzyme forms.

The COX-II enzyme is stimulated by injury, ischemia, and seizures. The injury stimulates membrane phospholipids to form arachidonic acid. It follows the path of COX-II and forms prostaglandin.

Non-selective NSAID affects either COX-II or COX-I and inhibits prostaglandin production. Selective NSAID affects the COX-II pathway. When COX-I is inhibited by non-selective NSAID, this may cause ulcers in GIT due to excess acid.

NSAID suppresses inflammation and causes:
Inhibition of prostaglandin synthesis and chemotaxis (which is responsible for the initiation of inflammatory response).

Downregulation of IL1, because it increases the number of prostaglandin receptors in the tissue.

Free radicals stimulate the COX-II pathway for prostaglandin production, so NSAID decreases the production of free radicals.

It has antipyretic effects to restore thermoregulatory center activity.

It decreases the release of COX-II production and thereby decreasing inflammatory pain.

It also decreases the synthesis f nociceptive receptors that sense pain.

They decrease platelet aggregation and increase bleeding.

Unwanted effects of NSAID include decreased production of COX-I and causing ulcers, GIT bleeding.

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