Suppression of LncRNA Dlx6os1 Alleviated High Glucose‐Induced Oxidative Stress Mediated by Parkin in Cardiomyocytes
Year: 2026
Type: article
Abstract: This study aimed to evaluate the effect of lncDlx6os1 on high glucose (HG)-induced oxidative stress and the involvement of the parkin pathway. METHODS: Short hairpin RNA of lncDlx6-os1 (sh-lncDlx6os1) and small interfering RNA of Parkin (si-Parkin) were used to inhibit the expression of lncDlx6-os1 and Parkin in cardiomyocytes, respectively. qRT-PCR, western blotting, and flow cytometry were performed to investigate the underlying mechanism. RESULTS: sh-lncDlx6os1 inhibited HG-induced reactive oxygen species (ROS) generation and increased the expression of HO-1 and NRF2 in HG-treated cardiomyocytes. sh-lncDlx6os1 significantly suppressed the expression of the apoptotic molecule caspase3, and increased the expression of the anti-apoptotic molecule Bcl-2, thereby inhibiting HG-induced apoptosis. Meanwhile, sh-lncDlx6os1 increased the expression of Sirt1, PINK1, Parkin, and LC3II/LC3I in HG-treated cardiomyocytes. Suppression of Parkin by si-Parkin weakened the regulatory effect of sh-lncDlx6os1 on apoptosis and caspase3 and Bcl-2 expression. si-Parkin also attenuated the inhibitory effect of sh-lncDlx6os1 on ROS generation and increased HO-1 and NRF2 expressions in HG-treated cardiomyocytes. CONCLUSION: Our study revealed that the suppression of lncDlx6os1 significantly alleviated HG-induced oxidative stress, which was partially mediated by parkin in cardiomyocytes.
Source: Advanced Biology
Institution: Shaanxi Provincial People's Hospital
Language: English
Subfield: Epidemiology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
Awards: G2886108173, G4735502236
OpenAlex ID: W7130336924
