acetyl-11-ketoboswellic-acid and Peripheral-Nerve-Injuries

The existing studies by our team demonstrated the pro-recovery effect of 3-Acetyl-11-keto-beta-boswellic acid (AKBA) on a sciatic nerve injury. To further investigate the role of AKBA in peripheral nerve injury repair, The TMT quantitative proteomics technique was used to obtain differentially significant proteins in a Sham group, Model group, and AKBA group. After that, three time points (5, 14, and 28 d) and four groups (Sham + AKBA, Sham, Model, and AKBA) were set up, and immunoblotting, immunofluorescence, and cellular assays were applied to investigate the expression of CDC42, Rac1, RhoA, and Rictor in the sciatic nerve at different time points for each group in more depth. The results showed that AKBA enriched the cellular components of the myelin sheath and axon regeneration after a sciatic nerve injury and that AKBA upregulated CDC42 and Rac1 and downregulated RhoA expression 5 d after a sciatic nerve injury, promoting axon regeneration and improving the repair of a sciatic nerve injury in rats. Rictor is regulated by AKBA and upregulated in PC12 cells after AKBA action. Our findings provide a new basis for AKBA treatment of a peripheral nerve injury.

Topics: Animals; Axons; Nerve Regeneration; Peripheral Nerve Injuries; Rapamycin-Insensitive Companion of mTOR Protein; Rats; Sciatic Nerve; Sciatic Neuropathy

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.

Topics: Animals; Cell Proliferation; Extracellular Signal-Regulated MAP Kinases; Male; Nerve Fibers, Myelinated; Neurofilament Proteins; Peripheral Nerve Injuries; Rats; Rats, Sprague-Dawley; Schwann Cells; Sciatic Nerve; Signal Transduction; Triterpenes