Cigarette smoke-induced pulmonary impairment is associated with social recognition memory impairments and alterations in microglial profiles within the suprachiasmatic nucleus of the hypothalamus

• DOI: 10.1016/j.bbi.2023.02.005
• Publication Date: 2023-02-10T22:18:57Z
• Authors: Simone N. De Luca; Stanley M.H. Chan; Aleksandar Dobric; Hao Wang; Huei Jiunn Seow; Kurt Brassington; Kevin Mou; Rana Alateeq; Alina Akhtar; Steven Bozinovski; Ross Vlahos
• Keywords: Adult; Male; Inflammation; 0303 health sciences; Hypothalamus; Pneumonia; 3. Good health; Cigarette Smoking; Mice, Inbred C57BL; Mice; Pulmonary Disease, Chronic Obstructive; 03 medical and health sciences; Quality of Life; Humans; Animals; Dimethyl Sulfoxide; Suprachiasmatic Nucleus; Microglia; Lung

Chronic obstructive pulmonary disease (COPD) is a major, incurable respiratory condition that primarily caused by cigarette smoking (CS). Neurocognitive disorders including cognitive dysfunction, anxiety and depression are highly prevalent in people with COPD. It understood increased lung inflammation oxidative stress from CS exposure may 'spill over' into the systemic circulation to promote onset of these extra-pulmonary comorbidities, thus impacts quality life The precise role 'spill-over' COPD-related neurocognitive unclear. present study investigated impact chronic on anxiety-like behaviors social recognition memory, particular focus lungs. Adult male BALB/c mice were exposed either room air (sham) or (9 cigarettes per day, 5 days week) for 24 weeks daily co-administered NOX2 inhibitor, apocynin (5 mg/kg, 0.01 % DMSO diluted saline, i.p.) vehicle (0.01 saline) one hour before initial day. After 23 weeks, underwent behavioral testing physiological diurnal rhythms assessed monitoring regulation profiles. Lungs collected hallmark features Consistent its anti-inflammatory properties, treatment partially lessened function decline mice. CS-exposed displayed marked behavior impairments memory compared sham mice, which was prevented treatment. Apocynin unable restore decreased Bmal1-positive cells, key cells regulation, suprachiasmatic nucleus hypothalamus levels. treated associated restoration microglial area cell basal serum corticosterone. This data suggests we able model CS-induced seen humans preventative effects be via dependent mechanism.