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The pathogenesis of Parkinson’s disease (PD) is closely related to mitophagy, a process regulated by miRNAs and long non-coding RNAs (lncRNAs). In this study, we investigated the role of the lncRNA-CasC7/miR-30c/BNIP3L (BCL2 Interacting Protein 3 Like) signaling pathway in PD.    Material and methods  A 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD was generated and treated by hydrogen sulfide (H2S) inhalation. The SH-SY5Y cell model of PD was generated by MPP+ and the treatment was NaHS. The open field, rotarod and tail suspension tests were performed to assess motor deficits. TUNEL and immunofluorescence assays were used to evaluate neuronal apoptosis in mice and in SH-SY5Y cell culture. Real-time PCR was performed to measure the expression level of the lncRNA-CasC7, miR-30c and BNIP3L, and western blotting was used to assess the protein levels of CBS, BNIP3L and PINK1. Luciferase assays were conducted to examine the regulatory relationship between miR-30c and lncRNA-CasC7/BNIP3L.    Results  H2S inhalation alleviated the motor disorder and neuronal apoptosis in PD mice, and NaHS treatment inhibited apoptosis in the SH-SY5Y cell culture model of PD. The sulfide compounds also ameliorated the dysregulated expression of CasC7, miR-30c, BNIP3L, and PINK1 in the PD models. Furthermore, miR-30c significantly inhibited the expression of lncRNA-CasC7 and BNIP3L, as assessed with the luciferase assays.    Conclusions  Our findings suggest that the lncRNA-CasC7/miR-30c/BNIP3L mitophagy signaling pathway is involved in the pathogenesis of PD.

H2S alleviates Parkinson-like phenotypes by modulating lncRNA-CasC7/miR-30c/BNIP3L signaling pathway