Ischemic stroke (IS) remains a leading cause of disability and mortality worldwide, and inflammation and oxidative stress play significant roles in its pathogenesis. This study investigates the effects of dihydromyricetin (DHM) on IS using RT-qPCR and western blot with SH-SY5Y cells, focusing on its effects on the small nucleolar RNA host gene 10 (SNHG10)/microRNA (miR)-665/Ras association domain family member 5 (RASSF5) axis and nuclear factor-kappa B (NF-κB) signaling. In addition, the effects of the SNHG10/miR-665/RASSF5 axis on the activity, apoptosis, oxidative stress, and inflammation levels of SH-SY5Y cells were analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, and enzyme-linked immunosorbent assays. Our results showed that, in response to oxygen-glucose deprivation/reperfusion (OGD/R), DHM treatment improved cell viability, reduced apoptosis, and attenuated neuroinflammation and oxidative stress in a dose-dependent manner. Interestingly, lncRNA SNHG10 was overexpressed during OGD/R and suppressed by DHM. Through bioinformatics analysis and experimental validation, we identified miR-665 as a direct target of SNHG10 and RASSF5 as a direct target of miR-665. The protective effect of DHM against OGD/R injury was partially reversed by SNHG10 overexpression and further enhanced by co-transfection with the miR-665 mimic and si-RASSF5. Our study provides novel insights into the neuroprotective mechanism of DHM against IS, which may act via modulation of the SNHG10/miR-665/RASSF5 axis and inactivation of NF-κB signaling, and offers a promising therapeutic target for IS.

Ischemic stroke (IS) remains a leading cause of disability and mortality worldwide, and inflammation and oxidative stress play significant roles in its pathogenesis. This study investigates the effects of dihydromyricetin (DHM) on IS using RT-qPCR and western blot with SH-SY5Y cells, focusing on its effects on the small nucleolar RNA host gene 10 (SNHG10)/microRNA (miR)-665/Ras association domain family member 5 (RASSF5) axis and nuclear factor-kappa B (NF-κB) signaling. In addition, the effects of the SNHG10/miR-665/RASSF5 axis on the activity, apoptosis, oxidative stress, and inflammation levels of SH-SY5Y cells were analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, and enzyme-linked immunosorbent assays. Our results showed that, in response to oxygen-glucose deprivation/reperfusion (OGD/R), DHM treatment improved cell viability, reduced apoptosis, and attenuated neuroinflammation and oxidative stress in a dose-dependent manner. Interestingly, lncRNA SNHG10 was overexpressed during OGD/R and suppressed by DHM. Through bioinformatics analysis and experimental validation, we identified miR-665 as a direct target of SNHG10 and RASSF5 as a direct target of miR-665. The protective effect of DHM against OGD/R injury was partially reversed by SNHG10 overexpression and further enhanced by co-transfection with the miR-665 mimic and si-RASSF5. Our study provides novel insights into the neuroprotective mechanism of DHM against IS, which may act via modulation of the SNHG10/miR-665/RASSF5 axis and inactivation of NF-κB signaling, and offers a promising therapeutic target for IS.

Ischemic stroke (IS) is an important cause of death worldwide. Dihydromyricetin (DHM) has been reported to have neuroprotective potential, but its role and mechanism in IS have not been fully elucidated. MTT assay was used to determine the safe dose of DHM in BV2 microglia and used in OGD/R-treated cells. The mechanism of action of DHM was explored by RT-qPCR, ELISA, luciferase reporter gene assay and Western blotting. DHM dose-dependently enhanced BV2 cell viability post-OGD/R and attenuated inflammation and oxidative stress. The protective effects of DHM were found to be mediated through the downregulation of SNHG17, which in turn modulated miR-452-3p expression. miR-452-3p was identified as a negative regulator of pro-inflammatory CXCR4, a direct target whose expression was inversely affected by SNHG17. The interaction between SNHG17 and miR-452-3p was further confirmed by RNA pull-down assays. Furthermore, manipulation of the SNHG17/miR-452-3p/CXCR4 axis was shown to modulate the NF-κB signaling pathway as evidenced by changes in phosphorylation levels. In conclusion, our findings elucidate a novel DHM-mediated neuroprotective mechanism in microglial cells involving the SNHG17/miR-452-3p/CXCR4 regulatory axis. This axis plays a pivotal role in attenuating OGD/R-induced inflammatory and oxidative stress responses, suggesting a therapeutic potential for DHM in conditions characterized by such pathological processes.

Ischemic stroke (IS) is an important cause of death worldwide. Dihydromyricetin (DHM) has been reported to have neuroprotective potential, but its role and mechanism in IS have not been fully elucidated. MTT assay was used to determine the safe dose of DHM in BV2 microglia and used in OGD/R-treated cells. The mechanism of action of DHM was explored by RT-qPCR, ELISA, luciferase reporter gene assay and Western blotting. DHM dose-dependently enhanced BV2 cell viability post-OGD/R and attenuated inflammation and oxidative stress. The protective effects of DHM were found to be mediated through the downregulation of SNHG17, which in turn modulated miR-452-3p expression. miR-452-3p was identified as a negative regulator of pro-inflammatory CXCR4, a direct target whose expression was inversely affected by SNHG17. The interaction between SNHG17 and miR-452-3p was further confirmed by RNA pull-down assays. Furthermore, manipulation of the SNHG17/miR-452-3p/CXCR4 axis was shown to modulate the NF-κB signaling pathway as evidenced by changes in phosphorylation levels. In conclusion, our findings elucidate a novel DHM-mediated neuroprotective mechanism in microglial cells involving the SNHG17/miR-452-3p/CXCR4 regulatory axis. This axis plays a pivotal role in attenuating OGD/R-induced inflammatory and oxidative stress responses, suggesting a therapeutic potential for DHM in conditions characterized by such pathological processes.

Ischemic stroke (IS) remains a leading cause of disability and mortality worldwide, and inflammation and oxidative stress play significant roles in its pathogenesis. This study investigates the effects of dihydromyricetin (DHM) on IS using RT-qPCR and western blot with SH-SY5Y cells, focusing on its effects on the small nucleolar RNA host gene 10 (SNHG10)/microRNA (miR)-665/Ras association domain family member 5 (RASSF5) axis and nuclear factor-kappa B (NF-κB) signaling. In addition, the effects of the SNHG10/miR-665/RASSF5 axis on the activity, apoptosis, oxidative stress, and inflammation levels of SH-SY5Y cells were analyzed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, and enzyme-linked immunosorbent assays. Our results showed that, in response to oxygen-glucose deprivation/reperfusion (OGD/R), DHM treatment improved cell viability, reduced apoptosis, and attenuated neuroinflammation and oxidative stress in a dose-dependent manner. Interestingly, lncRNA SNHG10 was overexpressed during OGD/R and suppressed by DHM. Through bioinformatics analysis and experimental validation, we identified miR-665 as a direct target of SNHG10 and RASSF5 as a direct target of miR-665. The protective effect of DHM against OGD/R injury was partially reversed by SNHG10 overexpression and further enhanced by co-transfection with the miR-665 mimic and si-RASSF5. Our study provides novel insights into the neuroprotective mechanism of DHM against IS, which may act via modulation of the SNHG10/miR-665/RASSF5 axis and inactivation of NF-κB signaling, and offers a promising therapeutic target for IS.

Ischemic stroke (IS) is an important cause of death worldwide. Dihydromyricetin (DHM) has been reported to have neuroprotective potential, but its role and mechanism in IS have not been fully elucidated. MTT assay was used to determine the safe dose of DHM in BV2 microglia and used in OGD/R-treated cells. The mechanism of action of DHM was explored by RT-qPCR, ELISA, luciferase reporter gene assay and Western blotting. DHM dose-dependently enhanced BV2 cell viability post-OGD/R and attenuated inflammation and oxidative stress. The protective effects of DHM were found to be mediated through the downregulation of SNHG17, which in turn modulated miR-452-3p expression. miR-452-3p was identified as a negative regulator of pro-inflammatory CXCR4, a direct target whose expression was inversely affected by SNHG17. The interaction between SNHG17 and miR-452-3p was further confirmed by RNA pull-down assays. Furthermore, manipulation of the SNHG17/miR-452-3p/CXCR4 axis was shown to modulate the NF-κB signaling pathway as evidenced by changes in phosphorylation levels. In conclusion, our findings elucidate a novel DHM-mediated neuroprotective mechanism in microglial cells involving the SNHG17/miR-452-3p/CXCR4 regulatory axis. This axis plays a pivotal role in attenuating OGD/R-induced inflammatory and oxidative stress responses, suggesting a therapeutic potential for DHM in conditions characterized by such pathological processes.

Ischemic stroke (IS) is an important cause of death worldwide. Dihydromyricetin (DHM) has been reported to have neuroprotective potential, but its role and mechanism in IS have not been fully elucidated. MTT assay was used to determine the safe dose of DHM in BV2 microglia and used in OGD/R-treated cells. The mechanism of action of DHM was explored by RT-qPCR, ELISA, luciferase reporter gene assay and Western blotting. DHM dose-dependently enhanced BV2 cell viability post-OGD/R and attenuated inflammation and oxidative stress. The protective effects of DHM were found to be mediated through the downregulation of SNHG17, which in turn modulated miR-452-3p expression. miR-452-3p was identified as a negative regulator of pro-inflammatory CXCR4, a direct target whose expression was inversely affected by SNHG17. The interaction between SNHG17 and miR-452-3p was further confirmed by RNA pull-down assays. Furthermore, manipulation of the SNHG17/miR-452-3p/CXCR4 axis was shown to modulate the NF-κB signaling pathway as evidenced by changes in phosphorylation levels. In conclusion, our findings elucidate a novel DHM-mediated neuroprotective mechanism in microglial cells involving the SNHG17/miR-452-3p/CXCR4 regulatory axis. This axis plays a pivotal role in attenuating OGD/R-induced inflammatory and oxidative stress responses, suggesting a therapeutic potential for DHM in conditions characterized by such pathological processes.

An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.

An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.

An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.