Main Article Content

Probiotic Strains Alleviate Lipopolysaccharide-Induced Depressive-Like Symptoms via Attenuation of Neuroinflammatory Signaling in Rats


Olusegun A. Adeoluwa
Abiola O. Obisesan
Gladys O. Adeoluwa
Elizabeth T. Akinluyi
Safiyyah A. Shehu
Deborah E. Ereh
Lily O. Otomewo

Abstract

A growing body of evidence has linked mental health to the gut microbiome. This has led to the investigation of the gastrointestinal tract  as a possible source of novel treatments and probiotic supplements for depressive disorders. Thus, this study aims to evaluate the  antidepressant effect of a multi-strain probiotics against lipopolysaccharide (LPS)-induced depression in rats. Twentyfour male Wistar  rats were randomly grouped into four groups of 6 animals each. Groups 1 and 2 received vehicle (distilled water, 10 mL/kg), group 3  received a probiotic cocktail (10 mL/kg), while group 4 received fluoxetine (10 mg/kg). All treatments were administered orally for seven consecutive days. One hour after treatment on day seven, LPS (0.85 mg/kg, i.p.) was given to all the animals except group 1 animals.  Twenty-four hours later, all the animals were subjected to behavioural tests [Forced Swim Test (FST), Sucrose Splash Test (SST), and Open  Field Test (OFT)]. Thereafter, the animals were sacrificed, and brain samples were collected for bioassay of central pro-inflammatory  mediators; tumour necrosis factor-alpha (TNF-α), interleukin-6, and interleukin-17 (IL-6 and IL-17) using enzyme-linked immunosorbent  assay. The LPS significantly increased immobility of rats in the FST and decreased grooming in the SST which is indicative of depressive- like behaviours. These behaviours were significantly attenuated by probiotics compared to control. LPS caused marked increase in TNF-α,  IL-6, and IL-17 concentration in the hippocampus. The elevated cytokine levels were attenuated by pretreatment with probiotics. Therefore, probiotics exhibited antidepressant-like activity which may be due to the inhibition of neuroinflammatory signalling pathways. 


Journal Identifiers


eISSN: 2616-0692
print ISSN: 2616-0684