Myrtenol Inhalation Mitigates Asthma-Induced Cognitive Impairments: an Electrophysiological, Behavioral, Histological, and Molecular Study.
Khadijeh EsmaeilpourElham JafariFahimeh RostamabadiMina KhaleghiFaezeh AkhgarandouzMaryam HosseiniHamid NajafipourMahdi KhodadoustVahid SheibaniMohammad-Abbas BejeshkPublished in: Molecular neurobiology (2023)
Asthma is an inflammatory disorder with significant health problems. It generally affects the lungs but can also impact brain performance via several mechanisms. Some investigations have proposed that asthma impairs cognition. This study assessed the impacts of myrtenol as a monoterpene on cognitive disorders following asthma at behavioral, molecular, and synaptic levels. Asthma was induced by injection and inhalation of ovalbumin (OVA). Male Wistar rats were allocated to five groups: control, asthma, asthma/vehicle, asthma/myrtenol, and asthma/budesonide. Myrtenol (8 mg/kg) or budesonide (160 μg/kg) was administered through inhalation once a day for 1 week, and at the end of the inhalation period, behavioral tests (MWM and Open Field), field potential recording, hippocampal brain-derived neurotrophic factor (BDNF), IL1β (ELISA), and NFκB measurement (Western blot) were performed to evaluate cognitive performance. Moreover, H&E (hematoxylin and eosin) staining was used for hippocampus histological evaluation. Myrtenol improved spatial learning, memory, LTP (long-term potentiation) impairments, and anxiety-like behaviors following asthma. Myrtenol inhalation increased the BDNF level and decreased the IL1β level and NFκB expression in the hippocampus of the asthmatic rats. The neuronal damage in the hippocampus following allergic asthma was alleviated via myrtenol administration. Myrtenol, as an herbal extract, protects the hippocampus from asthma consequences. Our observations revealed that myrtenol can improve spatial learning, memory, synaptic plasticity impairments, and anxiety-like behaviors following asthma. We believe that these ameliorating effects of myrtenol can be attributed to inflammation suppression and increased BDNF in the hippocampus.
Keyphrases
- chronic obstructive pulmonary disease
- lung function
- allergic rhinitis
- oxidative stress
- healthcare
- public health
- mental health
- cerebral ischemia
- cystic fibrosis
- physical activity
- air pollution
- clinical trial
- cognitive impairment
- immune response
- climate change
- south africa
- endothelial cells
- depressive symptoms
- white matter
- toll like receptor
- minimally invasive
- resting state
- lps induced
- mild cognitive impairment