Acetyl-11-keto-β-boswellic acid regulates the repair of rat sciatic nerve injury by promoting the proliferation of Schwann cells

This study aimed to study the effects of acetyl-11-keto-β-boswellic acid (AKBA) on the regeneration of injured peripheral nerves and the ability of the extracellular signal-regulated kinase (ERK) signaling pathway to regulate the proliferation of Schwann cells and the formation of myelin. A sciatic nerve crush injury model rats were randomly divided into the model control, low-, medium-, and high-dose AKBA groups. The repair of myelin damage was observed through Luxol Fast Blue staining and the expression of neurofilament-200 (NF200) protein was detected through immunohistochemical tests. The relative expression levels of ERK, Phosphorylated-ERK (p-ERK), c-Jun N-terminal Kinase (JNK), and Phosphorylated-JNK (p-JNK) proteins were detected in vitro in Schwann cells treated with AKBA. The effect of AKBA on P0 and P75 protein expression in Schwann cells was detected through siRNA-mediated ERK gene knockout. AKBA promotes the repair of rat sciatic nerve injury by elevating the phosphorylation of the ERK signaling pathway and by regulating the proliferation and myelination of Schwann cells. This test can provide data support for AKBA to repair sciatic nerve injury, provide a theoretical basis for further revealing AKBA repair mechanism, and provide reference for clinical development of sciatic nerve injury drugs.