21.7 : 消化性潰瘍疾患の薬：粘膜保護剤としてのプロスタグランジン類似体

The gastric mucosa majorly produces prostaglandin E₂ and I₂ to protect cells from mucosal injury.

These bind to EP₃ receptors, which couple with inhibitory G proteins, decreasing gastric acid. Interaction with EP_1/2 and EP₄ receptors stimulate bicarbonate and mucus secretion, while EP_2/4 promotes mucosal blood flow. These actions collectively form protective barriers for the gastric mucosa.

Nonsteroidal anti-inflammatory drugs or NSAIDs, commonly used to manage fever and pain, inhibit the enzyme cyclooxygenase, blocking the synthesis of prostaglandins. This increases gastric acid and causes peptic ulcers.

Misoprostol, a synthetic prostaglandin agonist, lowers gastric acid secretion and enhances mucus and bicarbonate production, mitigating NSAID-induced mucosal injury.

Upon oral administration, misoprostol is rapidly absorbed and metabolized into its active metabolite.

It can cause diarrhea and abdominal cramps. It may also stimulate uterine contractions and is contraindicated during pregnancy.