Carveol

Carveol is an orally active monoterpenoid alcohol with neuroprotective, antioxidant, anti-inflammatory, anticonvulsant, antidiabetic, hypolipidemic and hepatoprotective activities. Carveol upregulates the expression of Bcl2, downregulates the expression of caspase-3, TNF-α, IL1β and IL6, activates the Nrf2/HO-1 antioxidant signaling pathway, inhibits the RAGE/NF-κB signaling pathway, and suppresses neuroinflammation and neuronal apoptosis. Carveol inhibits α-synuclein aggregation, improves cognitive ability, and inhibits α-amylase activity. Carveol exerts neuroprotective effects in a rat model of Parkinson's disease. Carveol exhibits antidiabetic effects in alloxan-induced diabetic rats. Carveol alleviates PTZ-induced seizures in rats. Carveol can be used in research related to Parkinson's disease, epilepsy, diabetes and ischemic stroke^[1][2][3][4]. In Vitro:Carveol binds to multiple human diabetes-related target proteins with differential binding affinities, among which it shows the highest binding affinity for sodium-glucose cotransporters (ACE value = -7.3 Kcal/mol)^[3].
Carveol (0.821-65.690 μM; 30 min) inhibits the activity of purified α-amylase in a concentration-dependent manner, with an inhibition rate of 73.01% at the concentration of 65.690 μM^[3].
Carveol binds to the Nrf2-binding site of purified Keap1 protein^[4]. In Vivo:Carveol (10-20 mg/kg, i.p.; once daily; for 35 consecutive days) exerts dose-dependent neuroprotective effects in rotenone (HY-B1756)-induced Parkinson's disease rat models by restoring motor function, regulating neurotransmitter levels to normal, reducing α-synuclein aggregation, activating the Nrf2-mediated antioxidant signaling pathway, and inhibiting neuroinflammation and neuronal apoptosis^[1].
Carveol (20 mg/kg; i.p.; once daily; for 35 consecutive days) is well tolerated in healthy rats, with no adverse effects on motor function, neurochemical balance, oxidative status, inflammation or neuronal structure, while significantly upregulating the expression of BDNF mRNA^[1].
Carveol (10-20 mg/kg, i.p., administered 30 minutes prior to each pentylenetetrazol (PTZ) injection, once every 48 hours for 15 consecutive days) attenuates PTZ-induced seizures, cognitive impairment, oxidative stress, neuroinflammation and blood-brain barrier disruption in male Sprague-Dawley rats by activating the Nrf2/HO-1 signaling pathway^[2].
Carveol (65.7-394.1 µM/Kg; administered for 12 days; observed for 6 weeks) exhibits dose-dependent antidiabetic, antihyperlipidemic, and hepatoprotective effects in alloxan-induced diabetic Sprague-Dawley rats, including significant reductions in blood glucose, HbA₁C, triglycerides (TGs), low-density lipoprotein (LDL), and hepatic enzyme levels, along with an increase in high-density lipoprotein (HDL)^[3].
Carveol (10-20 mg/kg, intraperitoneally administered at 30 min and 24-72 h after MCAO) exerts a dose-dependent neuroprotective effect against MCAO-induced ischemic stroke; at the dose of 20 mg/kg, it reduces the corrected infarct size to 19.2%, restores the levels of key antioxidant enzymes, and inhibits neuroinflammation and apoptosis by activating the Nrf2 pathway^[4].