Senkyunolide I

Senkyunolide I is an orally active, blood-brain barrier-permeable metabolite of Z-ligustilide (HY-N0401A). Senkyunolide I is isolated from Ligusticum chuanxiong. Senkyunolide I upregulates p-Erk1/2 and Nrf2/HO-1, and inhibits Caspase 3. Senkyunolide I alleviates Apoptosis. Senkyunolide I increases the pain threshold in mice and reduces acetic acid-induced writhing responses in mice. Senkyunolide I improves neurological deficits, reduces infarct volume and alleviates cerebral edema in rats with focal cerebral ischemia-reperfusion injury. Senkyunolide I protects renal function and structural integrity in a mouse model of renal ischemia-reperfusion injury. Senkyunolide I is applicable to research related to focal cerebral ischemia-reperfusion injury, migraine, and renal ischemia-reperfusion injury^[1][2][3]. In Vitro:Senkyunolide I (25-100 μM) activates the Nrf2/ARE pathway in Hek293T/pGF1-ARE cells^[1].
Senkyunolide I (100-300 μg/mL; prior to H₂O₂ treatment) protects the renal tubular epithelial cell line HK2 against H₂O₂-induced loss of viability^[3]. In Vivo:Senkyunolide I (36-72 mg/kg; i.v.; single dose at 15 minutes post-occlusion) exerts dose-dependent neuroprotective effects against focal cerebral ischemia-reperfusion injury in rats, with the 72 mg/kg dose significantly reducing neurological deficit scores to below vehicle levels, lowering infarct volume to 27.31% ± 2.40%, and enhancing anti-oxidant and anti-apoptotic pathways^[1].
Senkyunolide I (8-32 mg/kg; p.o.; single dose) dose-dependently increases thermal pain thresholds in mice, with the 32 mg/kg dose producing significant elevations as early as 20 min post-administration and the 16 mg/kg dose showing significant effects at 360 min post-administration^[2].
Senkyunolide I (32 mg/kg; p.o.; single dose) significantly reduces acetic acid-induced visceral pain in mice, while lower doses show no significant effect^[2].