Levodopa attenuates cellular apoptosis in steroid-associated necrosis of the femoral head

Xi, Hongbo; Tao, Weijian; Jian, Zhengguang; Sun, Xuefeng; Gong, Xiaohong; Huang, Lixin; Dong, Tianhua

Since the 1950s, glucocorticoids had been widely used in clinical practice as an effective means of treating diseases such as systemic lupus erythematosus, severe acute respiratory syndrome, and those caused by kidney transplantation, resulting in an increase in the number of steroid-associated necrosis of the femoral head (SANFH) cases (1) (2) (3) . SANFH is the most common cause of non-traumatic osteonecrosis (2) . For the past 40 years, Chinese and foreign researchers have investigated SANFH; however, its pathogenesis remains unclear. There are a variety of theories as to what is associated with the pathogenesis SANFH, including dyslipidemia, intravascular coagulation, immune complex deposition-induced arterial inflammation, osteoporosis, venous stasis-induced intra-bone high pressure and hormonal toxicity of bone cells. The above theories also did not clearly prove that the bone cells exhibited necrosis, because no necrosis-specific inflammatory responses cell swelling were found (4) (5) (6) (7) (8) . Therefore, SANFH lacks effective prevention and early treatment strategies (9) . Previous studies have shown that hormones not only promote the apoptosis of bone cells, osteoblasts and cartilage cells, but are involved in the pathological process of femoral head necrosis (10, 11) . The present study utilized single low-dose lipopolysaccharide (LPS) plus methylprednisolone (MPS) to establish a rabbit model of SANFH. The roles of levodopa (LEV) in cellular apoptosis were observed in the rabbit model of SANFH, with the aim of providing a basis for the prevention and early treatment of femoral head necrosis.