Gut microbiota perturbation and motor dysfunction have been reported in steatosis patients. Rats with mild liver damage (MLD) also show motor dysfunction mediated by neuroinflammation and altered GABAergic neurotransmission in the cerebellum. The extracellular vesicles from mesenchymal stem cells (MSC-EVs) have emerged as a promising therapeutic proxy whose molecular basis rely partly upon TGFbeta action. Therefore, this study aimed to assess if MSC-EVs improve motor dysfunction in rats with MLD and analyze underlying mechanisms, including the role of EVs, TGFbeta, neuroinflammation, and gut microbiota and its metabolites. MLD rats induced by carbon tetrachloride administration were injected with EVs from normal (C-EVs) or TGFbeta-siRNA treated MSCs (T-EVs). Motor coordination, locomotor gait, neuroinflammation and TNFalpha-activated pathways modulating GABAergic neurotransmission in the cerebellum, microbiota composition in feces and microbial-derived metabolites in plasma were analyzed. C-EVs reduced glial and TNFalpha-P2X4-BDNF-TrkB pathway activation and restored GABAergic neurotransmission in the cerebellum, improving motor coordination and all the altered gait parameters. T-EVs also improved motor coordination and some gait parameters, but the mechanisms involved differed from those of C-EVs. MLD rats showed increased content of some Bacteroides species in feces, correlating with increased plasma butyrate and decreased kynurenine aside from motor alterations. These alterations were all normalized by C-EVs, whereas T-EVs only restored kynurenine levels. Our results support the role of MSC-EVs on improving motor dysfunction in rats with mild liver damage, normalizing alterations in gut microbiota and related metabolites, reducing cerebellar neuroinflammation and normalizing GABAergic neurotransmission. Some of the underlying mechanisms are TGFbeta-dependent.