Cyclopentenone prostaglandins

Cyclopentenone prostaglandins are a type of prostaglandin, which are lipid compounds that have hormone-like effects in the body. They are derived from fatty acids and have a cyclopentenone structure, which is a five-membered ring with one double bond and a ketone group.

Cyclopentenone prostaglandins are produced in the body from arachidonic acid through the cyclooxygenase pathway. They are involved in a variety of physiological and pathological processes, including inflammation, pain, fever, and the regulation of blood pressure.

Structure and Synthesis[edit | edit source]

The structure of cyclopentenone prostaglandins is characterized by a five-membered ring with a double bond and a ketone group. This structure is formed from arachidonic acid through a series of enzymatic reactions involving cyclooxygenase and prostaglandin synthase enzymes.

The synthesis of cyclopentenone prostaglandins begins with the conversion of arachidonic acid to prostaglandin H2 by the enzyme cyclooxygenase. Prostaglandin H2 is then converted to prostaglandin E2 by the enzyme prostaglandin E synthase. Finally, prostaglandin E2 is converted to a cyclopentenone prostaglandin by the enzyme 15-hydroxyprostaglandin dehydrogenase.

Function[edit | edit source]

Cyclopentenone prostaglandins have a variety of functions in the body. They are involved in the regulation of inflammation, pain, and fever, and they also play a role in the regulation of blood pressure.

In inflammation, cyclopentenone prostaglandins act as pro-inflammatory mediators, promoting the recruitment of immune cells to the site of injury or infection. They also enhance the production of other pro-inflammatory molecules, such as cytokines and chemokines.

In pain and fever, cyclopentenone prostaglandins act on the central nervous system to increase the body's temperature and sensitivity to pain. They do this by binding to prostaglandin receptors in the brain and spinal cord.

In the regulation of blood pressure, cyclopentenone prostaglandins act on the vascular smooth muscle to cause vasodilation, which lowers blood pressure. They also inhibit the release of vasoconstrictor substances, such as angiotensin II and norepinephrine, further contributing to the reduction of blood pressure.