Praeruptorin E

Praeruptorin E is an orally active pyranocoumarin compound. Praeruptorin E can be isolated from the dried roots of Peucedanum praeruptorum Dunn. Praeruptorin E reduces the expression of NF-κB. Praeruptorin E upregulates the expression of PXR and CYP3A4. Praeruptorin E inhibits Th2 cytokines, TNF-α, IL6, MPO, and blocks the Ca²⁺ slow channel. Praeruptorin E promotes pulmonary tissue repair and relaxes porcine coronary artery strips. Praeruptorin E protects mice from lipopolysaccharide- and hydrochloric acid-induced acute lung injury. Praeruptorin E can be used in studies related to asthma and acute lung injury^[1][2][3]. In Vitro:Praeruptorin E (60 μM; 24 h) reduces NF-κB p65 expression and increases PXR and CYP3A4 expression in LPS-induced human L-02 fetal hepatocytes, and this effect is partially dependent on PXR expression^[1].
Praeruptorin E (60 μM) reduces the binding of NF-κB p65 to the PXR gene promoter in human L-02 fetal hepatocytes, as evidenced by a significant decrease in NF-κB enrichment at this region^[1].
Praeruptorin E (4.7 μM) acts as a calcium antagonist on potassium-depolarized swine coronary artery strips with a pD₂' value of 5.2, inhibiting Ca²⁺-induced maximum contraction and shifting the Ca²⁺ concentration-response curve rightward in a non-parallel manner^[3]. In Vivo:Praeruptorin E (administered via gavage; once daily for 7 consecutive days at doses of 2.5-40 mg/kg) enhances the anti-asthmatic effect of Aminophylline (HY-B0140) on Ovalbumin (HY-W250978)-induced asthmatic mice by alleviating airway inflammation, mucus secretion and collagen deposition, while also reducing Aminophylline-induced cardiotoxicity, with the 40 mg/kg dose exerting the strongest effect^[1].
Praeruptorin E (20-80 mg/kg; p.o.; single administration 1 hour prior to LPS challenge) dose-dependently attenuates LPS-induced acute lung injury in male BALB/c mice. At the dose of 80 mg/kg, it inhibits neutrophil (PMNs) infiltration by 53%, TNF-α release by 56%, and IL-6 release by 51%, while also suppressing the activation of the NF-κB pathway and ameliorating histopathological changes in lung tissue^[2].
Praeruptorin E (80 mg/kg; p.o.; single administration 1 h prior to hydrochloric acid challenge) protects male BALB/c mice against hydrochloric acid-induced acute lung injury by reducing polymorphonuclear neutrophil (PMNs) infiltration, IL-6 release, protein extravasation and pulmonary histopathological damage^[2].