Frankincense improves motor symptoms and attenuates the progression of Paraquat (PQ)-induced Parkinson's disease in mice by attenuating oxidative stress, inflammation, and apoptotic cell death and improving nerve growth factor gene expression.

The purpose of the present investigation is to examine the neuroprotective impact of frankincense at different concentrations (10, 20, and 50 mg/kg/day) and discover its potential mechanisms associated with oxidative stress and apoptosis. To cause Parkinson's disease (PD) in mice, Paraquat (PQ) was dissolved in 0.9 % normal saline (10 mg/kg, i.p.) and administrated twice a week for three weeks. The mice were randomly divided into five cohorts ( n = 10): i) control (CON), ii) PQ (vehicle), iii) PQ + Frankincense (10 mg/kg), (iv) PQ + Frankincense (20 mg/kg), (v) PQ + Frankincense (50 mg/kg). We evaluated the effects of PQ and frankincense on behaviors using the open field test (OFT), rotarod performance test, forced swim test, and bar test. Oxidative stress factors, inflammatory markers, dopamine levels, acetylcholinesterase (AChE) activity, and apoptotic markers were assessed using ELISA and qPCR, respectively. PQ treatment caused abnormalities in motor coordination in the rotarod test, spontaneous motor activity in OFT, duration of immobility time in the forced swim test, and increased oxidative stress and apoptosis by elevating MDA level, mRNA levels of caspase3, and reducing mRNA levels of Bcl-2 and NGF. PQ treatment also reduced dopamine levels and increased AChE activity. Treatment with frankincense at different concentrations (10, 20, and 50 mg/kg/day) improved motor symptoms by inhibiting oxidative stress, inflammation, and apoptosis and elevation of dopamine levels and NGF gene expression in a dose dependent manner. In sum, frankincense exerted an inhibitory impact on the progression of PQ-induced PD model in mice by mitigating oxidative stress, neuroinflammation, and apoptotic cell death.