After intense sound exposure, the lack of obvious degeneration in type III fibrocytes suggests that they might protect themselves against acoustic trauma. However, it is unknown whether and how type III fibrocytes play this role in other cochlear damage models. In this study, we investigated the self-protection of type III fibrocytes against severe cochlear energy failure induced by local administration of 3-nitropropionic acid to the inner ear. We detected that the type III fibrocytes did not degenerate significantly after 500 mM 3-nitropropionic acid application, and showed increased expression of proliferation marker Ki67. Moreover, low immunoreactivity for inducible nitric oxide synthase and cleaved caspase-3 was observed in type III fibrocytes 2 days after damage. These results indicate that after severe cochlear energy failure type III fibrocytes possess obvious proliferation activity, as well as strong antioxidant and antiapoptotic capacity, which can protect them from degeneration.