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 (H 2 O 2)-caused PC-12 cell injury. H 2 O 2-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 H 2 O 2-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 H 2 O 2-evoked injury in PC-12 cells. Ascended miR-26a was monitored in Sal-B and H 2 O 2exposed cells. MiR-26a inhibition annulled the protective action of Sal-B in H 2 O 2-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 H 2 O 2-caused injury through ascending miR-26a via initiating PI3K/AKT and MEK/ERK pathways. HIGHLIGHTS H 2 O 2 causes PC-12 cell injury; Sal-B eases H 2 O 2-caused PC-12 cell injury; Sal-B protects PC-12 cells against H 2 O 2-caused injury via elevating miR-26a; Sal-B activates AKT and MEK/ERK pathways via modulating miR-26a.
Introduction: Osteoblasts and osteoclasts are cells of osteoblastic origin, and are vital in homeostasis of the skeleton. miRs are important for functioning, survival and differentiation of osteoclasts. It has been reported previously that miR-23b-3p is involved in osteoporosis and in regulation of differentiation of osteoblasts. It is also involved in the process of bone formation. However, the role of miR-23b-3p in differentiation of osteoclasts remains unexplored. Material and methods: CSF-1 and ODF induced osteoclasts were used for the study. RNA isolation was done from TIB-71 cells. TRAP staining was done for TRAP-positive osteoclast formation. PIT assay for bone resorption was performed. For in vivo studies osteoclast-specific miR-23b-3p transgenic mice were developed. Results: The levels of miR-23b-3p were upregulated in bone marrow monocytes during osteoclastogenesis with colony stimulating factor-1 and osteoclast differentiation factor induction, which suggests that miR-23b-3p plays a crucial role in differentiation of osteoclasts. Over-expression of miR-23b-3p in bone marrow monocytes leads to osteoclastogenesis, whereas the inhibition ameliorates it. We further studied the function of miR-23b-3p via PI3K/AKT targeting the PTEN pathway. In vivo, osteoclast-specific miR-23b-3p transgenic mice showed suppressed PTEN and elevated osteoclast activity, and the mice showed decreased bone mineral density. Conclusions: The results suggest that miR-23b-3p regulates the differentiation of osteoclasts by targeting PTEN through the PI3K/AKT cascade.
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