Bilobalide Improves Steroid-Induced Avascular Necrosis of the Femoral Head through PI3K/AKT Pathway

Abstract

Steroid-induced avascular necrosis of the femoral head is a metabolic disease that results from the use of glucocorticoid drugs, leading to impaired blood supply to the femoral head and death of bone cells and altered bone marrow composition, which in turn lead to structural changes, collapse of the femoral head, and articular dysfunction. It is a challenging disorder to manage due to frequent collapse of the femoral head and dysfunction of the hip joint often requiring joint arthroplasty surgery. Therefore, there is a critical need to develop effective strategies to prevent and treat this condition. Bilobalide, an intermediate metabolite of ginkgolide, is known to inhibit apoptosis, protects damaged cells, and protects the brain from injury. However, the role of bilobalide in steroid-induced avascular necrosis of the femoral head is poorly understood. In this study, we investigated the role of bilobalide in steroid-induced avascular necrosis of the femoral head in rats. Our data show that bilobalide reduced femoral head inflammation and oxidative stress in steroid-induced avascular necrosis of the femoral head in rats. Bilobalide reduced the apoptosis of femoral head cells in steroid-induced avascular necrosis of the femoral head in rats. In addition, bilobalide improved bone tissue injury in steroid-induced avascular necrosis of the femoral head in rats. Mechanically, bilobalide improved steroid-induced avascular necrosis of the femoral head through PI3K/AKT pathway. We therefore suggest that bilobalide may serve as a promising drug for steroid-induced avascular necrosis of the femoral head.