system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Antioxidants, COS Cells, Cercopithecus aethiops, Dose-Response Relationship, Drug, Flavanones, Membrane Potentials, Neuroprotective Agents, Patch-Clamp Techniques, Potassium Channels, Tandem Pore Domain, Rats, Riluzole.
user
Are baicalein and wogonin activators of rat TREK-2 two-pore domain K+ channel? Context: Earlier studies have shown that TREK-1 and TREK-2 (TREKs), members of the two-pore domain K(+) (K(2P)) channel family that are highly expressed under pathological conditions, are activated by neuroprotective agents. Baicalein and wogonin, oriental flavonoids originating from the root of the medicinal herb Scutellaria baicalensis, are known to have beneficial effects for neuroprotection. However, little is known about the effects of baicalein and wogonin on ion channels including TREKs. We investigated whether baicalein and wogonin modulate the TREK-2 channel, which has been less studied than TREK-1. Single-channel recordings were performed in COS-7 cells transfected with rat TREK-2 and analyzed baicalein- or wogonin-induced channel activity. We found that baicalein and wogonin activated the TREK-2 current by increasing the opening frequency (channel activity: from 0.05 ± 0.01 to 0.17 ± 0.06 in baicalein treatment and from 0.03 ± 0.01 to 0.29 ± 0.09 in wogonin treatment, P < 0.05), while leaving the single-channel conductance and mean open time unchanged. Baicalein continuously activated TREK-2, whereas wogonin transiently activated TREK-2. Application of baicalein and wogonin activated TREK-2 in both cell attached and excised patches, suggesting that baicalein and wogonin may modulate TREK-2 either directly or indirectly with different mechanisms.
assistant
These results suggest that baicalein- and wogonin-induced TREK-2 activation help set the resting membrane potential of cells exposed to pathological conditions and thus may give beneficial effects in neuroprotection. Final Decision: yes