AI Article Synopsis
- Spinal cord injury (SCI) causes sensory and motor dysfunction, and Salvianolic acid B (Sal-B) is a promising neuroprotective compound that may help.
- Research showed that Sal-B alleviates hydrogen peroxide (HO)-induced damage in PC-12 cells by activating specific signaling pathways (PI3K/AKT and MEK/ERK).
- The protective effects of Sal-B are linked to an increase in microRNA-26a, and inhibiting this microRNA negates Sal-B's beneficial impact on injured cells.
Article Abstract
Spinal cord injury (SCI) can lead to varying degrees of sensory and motor dysfunction. Salvianolic acid B (Sal-B) is the dominating bioactive constituent of Danshen, which has been reported to alleviate liver fibrosis and exert neuroprotective effects. But, the influence of Sal-B in SCI remains mysterious. The research planned to delve the protective function of Sal-B in hydrogen peroxide (HO)-caused PC-12 cell injury. HO-caused PC-12 cells injury model was built, CCK-8, Transwell and flow cytometry experiments were enforced to assess cell proliferation, migration and apoptosis. The microRNA (miR)-26a plasmid and the matching control were transfected into PC-12 cells, subsequently, the influence of miR-26a inhibition in HO-corrupted PC-12 cells was evaluated. The cell growth-correlated factors and PI3K/AKT and MEK/ERK pathways were assayed through western blot assay. Results corroborated that Sal-B eased HO-evoked injury in PC-12 cells. Ascended miR-26a was monitored in Sal-B and HO-exposed cells. MiR-26a inhibition annulled the protective action of Sal-B in HO-corrupted cells. The protective function of Sal-B was enabled through activating PI3K/AKT and MEK/ERK pathways. These findings delineated that Sal-B protected PC-12 cells against HO-caused injury through ascending miR-26a initiating PI3K/AKT and MEK/ERK pathways. Highlights HO causes PC-12 cell injury; Sal-B eases HO-caused PC-12 cell injury; Sal-B protects PC-12 cells against HO-caused injury elevating miR-26a; Sal-B activates AKT and MEK/ERK pathways modulating miR-26a.
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| http://dx.doi.org/10.1080/21691401.2019.1673766 | DOI Listing |
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