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  • Title: Penehyclidine hydrochloride suppresses inflammation response and reduces podocyte injury in diabetic nephropathy by targeting fibrinogen-like protein 2.
    Author: Tan HB, Zhao Q, Chen L.
    Journal: Int Immunopharmacol; 2022 Jun; 107():108680. PubMed ID: 35303505.
    Abstract:
    BACKGROUND: Diabetic nephropathy (DN) is one of the main complications of diabetes. Penehyclidine hydrochloride (PHC) has anti-inflammatory, anti-apoptotic and anti-oxidative stress effects. Nevertheless, whether PHC can be used to prevent podocyte injury has not been reported. OBJECTIVES: This present study aimed to identify the functional role of PHC in DN as well as its underlying mechanism. METHODS: The high-glucose (HG)-induced podocyte damage in vitro model was established. The proliferation, apoptotic rate, inflammatory factors, and gene/protein expressions of HG-induced MPC5 cells were determined using CCK-8 assay, flow cytometry, ELISA, real-time PCR, and Western blot upon PHC treatment. Co-immunoprecipitation experiments and pull-down assay were performed to verify the interactions between fibrinogen-like protein 2 (Fgl2) and toll-like receptor 4 (TLR4) as well as TLR4 and NLRP3. A rat in vivo model was used to confirm the effect of PHC treatment. RESULTS: PHC treatment reduced Fgl2 expression and inhibited HG-induced podocyte injury and DN-induced kidney damage. Flg2 was associated with TLR4 and NLRP3. It was further proved that PHC treatment suppressed the TLR4-NF-кB and NLRP3-Caspase-1 pathways through Fgl2, which eventually inhibited inflammatory cytokines and prevented HG-induced podocyte injury both in vitro and in vivo. CONCLUSION: PHC treatment possibly ameliorates DN by preventing podocyte injury via inactivating the TLR4-NF-кB and NLRP3-Caspase-1 signaling pathways by Flg2.
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