Objective To investigate the role of LncRNA-gm33782 in tubular injury in acute kidney injury (AKI) and the mechanism by which isorhamnetin ameliorates inflammatory cell apoptosis of tubular cells in AKI. Methods Forty-eight male C57BL/ 6J mice were randomly assigned to four groups: control group, AKI model group, electroporation + AKI group, and treatment group ( oral administration of 30 mg / kg isorhamnetin). AKI was induced by a one-time intraperitoneal injection of 20 mg / kg cisplatin. Chromatin isolation by RNA purification was used to capture the LncRNAgm33782 binding protein in AKI-affected kidneys for mass spectrometry, revealing the direct target protein of LncRNAgm33782. The role of LncRNA-gm33782 in AKI was evaluated by observing the renal function, pathological structure, and expression of renal inflammatory factors ( interleukin-1β, interleukin-6, and tumor necrosis factor-α) in mice after electrotransfection and isorhamnetin treatment. Nuclear factor-κB was detected as a critical mediator of inflammation. The expression levels of Bax and Bcl-2 protein were detected and flow cytometry was performed to evaluate the therapeutic effect of isorhamnetin on tubular cell apoptosis in AKI. Results Kidneys with cisplatin-induced AKI showed severe renal tubule injury, macrophage infiltration, and inflammation. Isorhamnetin treatment and LncRNA-gm33782 electrotransfection knockdown alleviated these signs of AKI. LncRNA-gm33782 was mainly expressed in renal tubular cells with AKI. LncRNA-gm33782 binding protein was detected by mass spectrometry, and complement factor H was found to have a direct binding relationship with LncRNA-gm33782. After LncRNA-gm33782 was overexpressed in vitro, the expression of complement factor-H immediately increased, and the therapeutic effect of isorhamnetin on apoptosis of AKI-affected inflammatory cells was inhibited. Conclusions Isorhamnetin alleviates apoptosis of tubular inflammatory cells in AKI by inhibiting the regulatory effect of LncRNA-gm33782 on complement factor H.