SIRT1 attenuates blood-spinal cord barrier disruption after spinal cord injury by deacetylating p66Shc

Salidroside promotes the repair of spinal cord injury by inhibiting astrocyte polarization, promoting neural stem cell proliferation and neuronal differentiation

“…Salidroside inhibited the phosphorylation of JNK and STAT3 pathways by upregulating Sirt1 SIRT1, a histone deacetylase, plays a pivotal role in inhibiting the acetylation and phosphorylation of multiple signaling pathways [41][42][43]. Following SCI, the expression of Sirt1 typically decreases, and restoring its levels has been shown to be beneficial for SCI recovery [44]. Our investigation revealed that salidroside effectively restored Sirt1 expression levels.…”

Targeted Delivery of RGD-CD146+CD271+ Human Umbilical Cord Mesenchymal Stem Cell-Derived Exosomes Promotes Blood–Spinal Cord Barrier Repair after Spinal Cord Injury

“…The BCSB disrupts neuroremodeling and emphasizes the importance of stabilizing the BSCB for neurological recovery. ,− To investigate the association between BSCB stabilization and neurological recovery, we initially selected spinal cord specimens taken 7 days after SCI. Immunofluorescent staining of macrophages was conducted at this time point since it corresponds to the peak of macrophage aggregation .…”

Engineered Macrophage Membrane‐Coated Nanoparticles with Enhanced CCR2 Expression Promote Spinal Cord Injury Repair by Suppressing Neuroinflammation and Neuronal death

“…[ 8 ] The bEnd.3 cell is an immortalized mouse brain endothelial cell line that has been widely used to model the blood–brain barrier (BBB) or BSB in vitro. [ 54,55 ] As shown in Figure 2B, bEnd.3 cells were seeded on the upper compartment of a trans‐well system to simulate the BSB. After the cell density reached a confluent state, the medium in the upper chamber was replaced by normal astrocytes medium containing PLGA/FITC, MM@PLGA/FITC, and CCR2‐MM@PLGA/FITC respectively, and the CM from reactive astrocyte was added to the bottom chamber.…”