The anti-inflammatory and antiapoptotic effects of probiotic on induced neurotoxicity in juvenile hamsters

Brain inflammation and apoptosis play crucial roles in the pathogenesis of various neurodevelopmental disorders. Probiotics have been shown to confer protection against many stresses, including apoptosis and inflammation, by modulating the gut function. The short-chain fatty acid, propionic acid (PPA), plays an important intermediate of cellular metabolism. Although PPA exhibits numerous beneficial biological effects, its accumulation is neurotoxic. This study focused on the therapeutic potency of probiotics against PPA-induced apoptosis and neuroinflammation in hamsters. Five groups of male golden Syrian hamsters were treated as follows: Group I as control; Group II as PPA-treated with three doses of 250 mg PPA/kg/day; Group III as clindamycin-treated with a single dose of 30 mg clindamycin/kg; Group IV as PPA-probiotic; and Group V as clindamycin-probiotic were two therapeutic groups which were treated with the same doses of PPA and clindamycin, respectively, followed by treatment with 0.2 g kg(-1) d(-1) of probiotic (Protexin (R), Probiotics International Limited) for three weeks. Proapoptotic markers, such as caspases 3 and 7; neuroinflammation markers, such as interleukins 1 beta and 8; and heat shock protein 70 were measured in the brain. Significant increase of all measured markers (p < .001) was observed in PPA and clindamycin-treated hamsters compared with controls. Probiotics significantly reduced the damages and ameliorated all the test markers in both therapeutic groups compared with the control. Our results confirmed that probiotics can be utilized as a feasible strategy for managing apoptotic and inflammation-related stresses in brain disorders by retaining the gut function.

Automated summary

This study demonstrates that probiotics can reduce apoptosis and neuroinflammation induced by propionic acid (PPA) by modulating gut function. In a hamster model, probiotics significantly decreased levels of apoptotic markers and inflammation markers, providing protection against brain damage.