Reactive astrocytes contribute to neuroinflammation and synaptic dysfunction, but it remains unclear whether transient inflammatory stimulation causes a persistent reactive state after the initial inflammatory stimulus is removed. Here, we investigated whether transient exposure to a defined inflammatory cytokine/complement cocktail induces a persistent reactive astrocyte state and examined the signaling mechanism underlying its maintenance. Human astrocytes were exposed to the inflammatory stimulus and subsequently subjected to stimulus washout, followed by time-course analyses to compare the reversibility of inflammatory gene expression after stimulus removal. Following washout, the expression of several inflammatory response genes, including CXCL10 and NF-κB-associated genes such as NFKBIA, TNFAIP3, and RELB, returned toward baseline levels. In contrast, C3 expression remained elevated, indicating persistence of a post-inflammatory C3-high astrocyte state after withdrawal of the inflammatory stimulus. Pharmacological inhibition of JAK signaling reduced persistent C3 expression to near-baseline levels, supporting the involvement of JAK-dependent signaling in maintenance of this persistent state. Together, these findings suggest that transient inflammatory stimulation induces a post-inflammatory persistent C3-high astrocyte state that is maintained even after broader inflammatory gene responses have subsided. This persistent C3-high component is pharmacologically attenuated by JAK inhibition, identifying JAK-dependent pathways as modulators of persistent astrocyte inflammatory reactivity.