Nocodazole treatment interrupted Brucella abortus invasion in RAW 264.7 cells, and successfully attenuated splenic proliferation with enhanced inflammatory response in mice
Nocodazole directly inhibited the growth of B. abortus in a dose-dependent manner. Nocodazole reduced bacterial invasion with F-actin polymerization inhibition. Nocodazole inhibited ERK and p38α phosphorylation after bacterial infection. Nocodazole treatment increased cytokines production and inhibited bacterial proliferation in the spleens. Nocodazole can be useful for therapeutic application in animal brucellosis.