Objective To investigate the role of LncRNA-33782 in AKI tubular injury and the mechanism by which Isorhamnetin ameliorates AKI tubular inflammatory cell apoptosis. Methods Twenty-four male C57BL/6J mice were randomly assigned into four groups: control group, AKI model group, electroporation + AKI group, and treatment group (30 mg/kg orally administered Isorhamnetin). Renal function, histopathological alterations, and renal inflammatory cytokines (IL-1β, IL-6, TNF-α) were evaluated to assess the role of LncRNA-33782 in AKI and the therapeutic effect of Isorhamnetin following electroporation-mediated LncRNA-33782 knockdown and Isorhamnetin treatment in mice. Subsequently, an in vitro experiment involving LncRNA-33782 overexpression was conducted to investigate the mechanism of Isorhamnetin treatment. NF-κB was considered a key signaling pathway mediating inflammation, while Bax, Bcl-2 protein expression levels, and flow cytometry apoptosis detection results were employed to assess tubular cell apoptosis. Results Renal injury and abnormal renal function significantly improved after electroporation-mediated LncRNA-33782 knockdown, accompanied by a marked decrease in inflammatory cytokine expression levels. Isorhamnetin treatment also notably attenuated AKI-induced renal injury, downregulated LncRNA-33782 expression, inhibited the NF-κB signaling pathway, and alleviated tubular cell apoptosis. However, Isorhamnetin"s therapeutic effect on AKI was suppressed after in vitro LncRNA-33782 overexpression. Conclusions LncRNA-33782 promotes AKI renal inflammatory response, while Isorhamnetin can inhibit AKI tubular inflammatory cell apoptosis mediated by LncRNA-33782-induced NF-κB activation.