Neuroprotective effect of Bacillus subtilis in haloperidol induced rat model, targeting the microbiota-gut-brain axis.

Functional microbes regulate Parkinson's disease (PD), according to contemporary research. The mechanism by which probiotics (PBT) improve PD was not fully explored yet. We examined the antioxidant impact and mechanism of PBT (Bacillus subtilis) on PD using gut-brain axis regulation. To establish a model of PD, rats were given haloperidol (HAL) intraperitoneally (i.p.) in this study. The standard group received L-DOPA for 21 days. After that, the motor function was assessed using different neurobehavioral tests. Further estimation comprehends the build up of alpha-synuclein, the manifestation of monoamine oxidase-B (MAO-B) activity, the deterioration of dopaminergic neurons and the induction of an oxidative stress reaction. In addition, the concentration of intestinal microbes was measured. These findings demonstrated that the administration of PBT in combination with L-dopa could alleviate motor impairments caused by HAL, the deterioration of dopaminergic neurons, and the build up of α-synuclein. Furthermore, the levels of superoxide dismutase (SOD) and dopamine were considerably raised by co-administration of L-dopa and PBT in the case of HAL-treated rats, whereas the levels of alpha-synuclein, MAO-B, and malondialdehyde (MDA) were reduced. Particularly, PBT administration reduced the gut microbial dysbiosis, which in turn raised the concentration of good bacteria i.e., Bifidobacterium and reduced the concentration of E. coli in experimental animals. These findings indicated that PBT might represent a promising candidate to inhibit the progression of Parkinson's disease by targeting the gut-brain axis.