Medicine:Prostaglandin E
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Prostaglandin E (PGE) is a family of naturally occurring prostaglandins involved in physiological signaling pathways, exhibiting biologically active properties for medical applications.
There are two types of prostaglandin E, which include:
- Prostaglandin E1 (PGE1), also known as alprostadil.
- Prostaglandin E2 (PGE2), also known as dinoprostone.
Among the two types, PGE₂ is the most extensively studied member of the prostaglandin E family. Both molecules are listed on the World Health Organization's List of Essential Medicines.[1]
Chemical composition
The structure of prostaglandin E contains a 20-carbon skeleton that includes a cyclopentane ring and two hydrocarbon side chains known as the α-chain and ω-chain.[2] The α-chain is identified by the terminal carboxylic acid group.[2] The classification of prostaglandin E is determined by the positioning of a ketone group at the 9th carbon position and hydroxyl at the 11th carbon position, which differs from other types of prostaglandin in the human body.[2]
Members of the prostaglandin E family are synthesized through the oxidation of polyunsaturated fatty acid substrates by cyclooxygenase (COX) enzymes.[3] PGE1 and PGE2 differ in their lipid precursors. PGE1 is derived from dihomo-r-linolenic acid, while PGE2 is derived from arachidonic acid (AA).[3] The cyclooxygenase pathway produces the intermediate prostaglandin H2 (PGH2), which can be differentiated into other prostaglandin molecules by target enzymes.[4][5] PGH2 can be converted into PGE2 by specific PGE synthases, such as microsomal prostaglandin E₂ synthase-1 (mPGES-1).[4] The pathway for PGE1 remains unclear.
Receptor binding and affinity
Members of prostaglandin E generally exhibit biological activity through binding of the E prostanoid (EP) receptor family. There are four different receptors, including subtypes EP1, EP2, EP3, and EP4, all of which are G protein-coupled receptors (GPCRs). Although PGE2 is the primary ligand, PGE1 can bind and activate these receptors with lower affinity.[5] Interactions with other prostaglandin receptor types (e.g., IP, FP receptors) can be observed due to structural similarity with other prostaglandin molecules, but with low affinity and therefore has limited physiological relevance.[5]
Medical significance
The prostaglandin E family, notably PGE2, play a central role in inflammation and regulating physiological effects such as pain, thermoregulation of the human brain, vascular permeability, and immune signaling.[3][4] PGE1 has been seen to contribute to mechanical allodynia and vasodilation.[3] Excessive or prolonged PGE production is involved in the development of chronic inflammatory diseases, making the PGE biosynthetic pathway an important target for therapeutic intervention. Common forms of treatment include the use of nonsteroidal anti-inflammatory drugs (NSAIDs), which act by inhibiting cyclooxygenase (COX) enzymes upstream in the pathway, suppressing the formation of prostaglandin E.[4] Although effective, this inhibition is non-selective, which effectively reduces production of other prostaglandin molecules involved in physiological homeostasis.[4] The use of NSAIDs, especially with long-term use, prompt adverse side effects as a result of general COX suppression, including increased cardiovascular risk and renal dysfunction.
References
- ↑ World Health Organization model list of essential medicines: 21st list 2019. Geneva: World Health Organization. 2019. WHO/MVP/EMP/IAU/2019.06. License: CC BY-NC-SA 3.0 IGO.
- ↑ 2.0 2.1 2.2 "Structural basis for prostaglandin and drug transport via SLCO2A1". Nature Communications 17 (1). March 2026. doi:10.1038/s41467-026-70227-3. PMID 41862483. Bibcode: 2026NatCo..17.2285J.
- ↑ 3.0 3.1 3.2 3.3 "The Role of Prostaglandin E1 as a Pain Mediator through Facilitation of Hyperpolarization-Activated Cyclic Nucleotide-Gated Channel 2 via the EP2 Receptor in Trigeminal Ganglion Neurons of Mice". International Journal of Molecular Sciences 22 (24). December 2021. doi:10.3390/ijms222413534. PMID 34948328.
- ↑ 4.0 4.1 4.2 4.3 4.4 "Enhanced Efficiency of the Microsomal Prostaglandin E2 Synthase-1 Inhibitor AGU661 in Human Whole Blood by Encapsulation into PLGA-Based Nanoparticles". Molecular Pharmaceutics 22 (11): 6803–6815. November 2025. doi:10.1021/acs.molpharmaceut.5c00766. PMID 41042969.
- ↑ 5.0 5.1 5.2 "A Review of Prostanoid Receptors: Expression, Characterization, Regulation, and Mechanism of Action". Journal of Cell Communication and Signaling 15 (2): 155–184. June 2021. doi:10.1007/s12079-020-00585-0. PMID 32970276.
External links
- "Alprostadil". Drug Information Portal. U.S. National Library of Medicine. https://druginfo.nlm.nih.gov/drugportal/name/alprostadil.
- "Dinoprostone". Drug Information Portal. U.S. National Library of Medicine. https://druginfo.nlm.nih.gov/drugportal/name/dinoprostone.
- Prostaglandins+E at the US National Library of Medicine Medical Subject Headings (MeSH)
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