Hydrangea macrophylla and Thunberginol C Attenuate Stress-Induced Anxiety in Mice.
Jihye LeeHuiyoung KwonEunbi ChoJieun JeonIn-Kyu LeeWan-Seob ChoSe Jin ParkSeungheon LeeDong Hyun KimJi Wook JungPublished in: Antioxidants (Basel, Switzerland) (2022)
Stress is an important neurological input for successful life. However, chronic stress and stress hormones could be a cause of various neurological disorders including anxiety disorders. Therefore, there have been many efforts to find effective materials for curing stress-induced neurological disorders. In this study, we examined the effect of Hydrangea macrophylla (HM) on corticosterone-induced neurotoxicity, stress-induced anxiety in mice and suggested a possible active ingredient of HM. HM protected cortical neurons against neurotoxicity of corticosterone (CORT), a stress hormone. HM also blocked CORT-induced hippocampal synaptic deficit via regulating Akt signaling. Oral administration of HM improved chronic restraint stress-induced anxiety in Elevated Plus maze test along with reduction of plasma corticosterone and TNF-α levels. Moreover, HM reduced stress-induced neuroinflammation and oxidative stress. Thunberginol C, an active ingredient of HM, also prevented CORT-induced neuronal cell death and restraint stress-induced anxiety. Moreover, thunberginol C reduced plasma TNF-α level and neuroinflammation and oxidative stress. Collectively, HM could be a good candidate for preventing stress-induced neurological disorders and thunberginol C may be an active ingredient of HM for this purpose.
Keyphrases
- stress induced
- diabetic rats
- oxidative stress
- cerebral ischemia
- cell death
- high glucose
- drug induced
- rheumatoid arthritis
- sleep quality
- signaling pathway
- lipopolysaccharide induced
- type diabetes
- cell proliferation
- ischemia reperfusion injury
- induced apoptosis
- high fat diet induced
- subarachnoid hemorrhage
- endothelial cells
- physical activity
- adipose tissue
- blood brain barrier
- insulin resistance
- quality improvement
- skeletal muscle
- heat stress
- heat shock
- pi k akt
- prefrontal cortex
- heat shock protein