Ligustrazine (hydrochloride)

Ligustrazine hydrochloride is an orally active, blood-brain barrier-permeable alkaloid. It can be isolated from Ligusticum striatum DC. Ligustrazine hydrochloride reduces ROS, upregulates the levels of p-Akt/Akt and p-eNOS/eNOS, and decreases ALT and AST. It inhibits glutamate excitotoxicity, calcium overload, oxidative stress, ischemia-reperfusion injury and atherosclerotic plaque progression, enhances synaptic plasticity, and improves neurological function, cerebral infarct volume and brain water content. Ligustrazine hydrochloride possesses anti-inflammatory, antioxidant, lipid-lowering, endothelial protective and hepatoprotective activities. It can be used in studies related to ischemic stroke, cerebral ischemia-reperfusion injury and atherosclerosis^[1][2][3]. In Vitro: Ligustrazine (1-100 μM) hydrochloride dose-dependently increases NO production in OGD-treated human amniotic epithelial cells by activating the PI3K/Akt pathway, with no significant effect on NO production in normal HAECs^[2].
Ligustrazine (0.1-10 μM) hydrochloride dose-dependently increases p-Akt/Akt and p-eNOS/eNOS in OGD-treated human amniotic epithelial cells by activating the PI3K/Akt pathway, with no significant effect on these factors in normal HAECs^[2].
Ligustrazine hydrochloride protects endothelial cells against LDL-induced damage in an in vitro cell-based system^[3]. In Vivo: Ligustrazine (10-120 mg/kg; intraperitoneal injection; intravenous injection; oral administration) hydrochloride exerts protective effects on rat models of ischemic stroke, significantly improves neurological function, reduces the levels of brain injury markers, regulates inflammatory and oxidative stress pathways, inhibits cell apoptosis, and repairs blood-brain barrier permeability^[1].
Ligustrazine (20 mg/kg; i.p.; 15 min after model establishment) hydrochloride improves neurological function in male C57BL/6 mouse models of ischemic stroke^[1].
Ligustrazine (1-10 mg/kg; i.p.; administered once at 2 h and 12 h post-operation) hydrochloride protects Wistar rats against cerebral ischemia-reperfusion injury in a dose-dependent manner by activating the PI3K/Akt pathway, which increases the levels of p-Akt and p-eNOS, improves neurological function, and alleviates brain tissue damage^[2].
Ligustrazine (20-80 mg/kg; p.o.; 6 weeks) hydrochloride dose-dependently inhibits the progression of atherosclerosis and hepatic lipid accumulation in Sprague-Dawley rats, with the daily oral dose of 80 mg/kg reducing the aortic lesion area by 49.0% compared with the untreated atherosclerotic control group^[3].