Objective: To investigate the clinical efficacy of autologous platelet-rich plasma (PRP) combined with endoscopy and interventional embolization in treating refractory gastric ulcer hemorrhage in critically ill patients with systemic diseases (sepsis, uremia), and to provide a novel therapeutic option for cases failing conventional treatments. Methods: A case of a 60-year-old male patient with sepsis and uremia complicated by gastric antral ulcer (Forrest Ib) with active bleeding was reported. Autologous venous blood was collected, and PRP was prepared via a two-step centrifugation method. PRP was sprayed endoscopically followed by local injection, and then covered with a thrombin-calcium ion activator to form a gel layer. Initial treatment was performed, followed by consolidation therapy seven days later, along with selective gastroduodenal artery embolization. Results: Hemorrhage was controlled within 24 hours after the initial PRP treatment. Hemoglobin (Hb) increased from 49 g/L to 56 g/L, and coagulation function improved [activated partial thromboplastin time (APTT) decreased from>170 s to 85 s]. A stable coagulum formed on the ulcer surface after the second PRP treatment on day 7. At the 4-week follow-up endoscopic assessment, the ulcer had shrunk to approximately 0.8×1.0 cm, Hb had risen to 92 g/L, and no rebleeding occurred. Conclusion: PRP, acting through mechanical tamponade by a physical barrier and sustained release of growth factors, serves as an effective supplementary treatment for refractory gastric ulcer bleeding, offering dual mechanisms of immediate hemostasis and promotion of mucosal repair. Combining PRP with interventional embolization and multidisciplinary collaboration can further enhance efficacy and may have potential for broader application.

【Objective】 To investigate the protective effect and mechanism of platelet-rich plasma (PRP) on lipopolysaccharide (LPS) -induced inflammatory response in BV2 cells. 【Methods】 BV2 microglia were divided into normal control group, 10%PRP control group, LPS group (LPS induction), 3%PRP+ LPS group (LPS induction, 3%PRP pretreatment), 5%PRP+ LPS group (LPS induction, 5%PRP pretreatment), 10%PRP+ LPS group (LPS induction, 10%PRP pretreatment), and the proliferation of BV2 cells was measured by CCK-8. The mitochondrial membrane potential of BV2 cells was measured by confocal microscopy, ROS was measured by fluorescence method, and NO was measured by Griess method. The protein expressions of IL-6, TNF-α, BACH1, GPX4, NRF2 and HO-1 were detected by Western blot. In addition, BV2 microglia were treated with HO-1 inhibitor and divided into normal control group, LPS group, ZnPP+ LPS group, 10%PRP+ LPS group, ZnPP+ LPS+ 10%PRP group, and the protein expressions of HO-1, IL-6 and TNF-α were detected by Western blot. 【Results】 Compared with normal control group, PRP promoted the proliferation of BV2 cells (P<0.01). The mitochondrial membrane potential decreased, ROS production increased, the levels of NO, IL-6, TNF-α and BACH1 increased (P<0.01). However, the expression levels of GPX4, NRF2 and HO-1 decreased (P<0.01) in LPS group. Compared with LPS group, the proliferation activity and mitochondrial membrane potential of BV2 cells in 3%PRP+ LPS, 5%PRP+ LPS and 10%PRP+ LPS groups significantly increased. The levels of ROS, NO, IL-6, TNF-α and BACH1 significantly decreased (P<0.01). The expressions of GPX4, NRF2 and HO-1 in different concentrations of PRP (3%, 5% and 10%) increased (P<0.01). Moreover, the expression of IL-6 and TNF-α in ZnPP+ LPS group was significantly higher than that in LPS group after HO-1 inhibitor treatment. Compared with 10%PRP+ LPS+ ZnPP group, HO-1 inhibitor could reverse the effect of PRP on the expression of IL-6 and TNF-α in LPS-induced BV2 cells (P<0.01). 【Conclusion】 PRP inhibits the inflammatory response of BV2 microglia induced by LPS by activating the NRF2/HO-1 signaling pathway.