Aim To explore the expression of proprotein convertase subtilisin kexin 9 (PCSK9) in polycystic ovary syndrome (PCOS) ovarian granulosa cells, and the relationship between PCSK9 expression and the lipid status of PCOS ovarian tissue and testosterone-treated KGN cells. Methods A rat model of PCOS was constructed by letrozole combined with high-fat diet. Oil red O staining was used to observe the lipid distribution in the ovarian tissue of PCOS rats. Transcriptome data from PCOS ovarian tissue and normal ovarian tissue was analyzed by bioinformatics, and the differentially expressed genes involved in lipid metabolism pathway were screened. Western blot and immunohistochemical techniques were used to detect the protein expression of PCSK9 in PCOS rat tissues. Immunofluorescence, qRT-PCR and Western blot techniques were used to detect the expression differences of PCSK9 and low density lipoprotein receptor (LDLR) in KGN cells treated with different concentrations of testosterone. Immunofluorescence microscope was used to observe the ability of KGN cells uptake Dil-LDL. Results The results of Oil Red O staining showed that the distribution of lipid droplets in granular cells of PCOS ovarian tissue was significantly less than that of normal ovarian tissue. The results of bioinformatics analysis showed that the up-regulated expression of PCSK9 in the ovarian tissue of PCOS rats was mainly involved in the cholesterol metabolism pathway. The results of immunohistochemistry and Western blot showed that the PCSK9 protein was mainly localized in granulosa cells and its expression increased in the granulosa cells of PCOS rats.The results of immunofluorescence, qRT-PCR and Western blot showed that PCSK9 expression was up-regulated with the increased concentration of testosterone, and LDLR expression was decreased with the increased concentration of testosterone in KGN cells. Testosterone (100 nmol/L) could reduce the uptake of Dil-LDL by KGN cells. Conclusion PCSK9 was highly expressed in PCOS ovarian granulosa cells, which could reduce the expression of LDLR protein and lead to insufficient lipid uptake of granulosa cells.