Skip to main content
. Author manuscript; available in PMC: 2020 Mar 30.
Published in final edited form as: Alcohol Clin Exp Res. 2018 May 27;42(7):1206–1216. doi: 10.1111/acer.13765

Fig. 6.

Fig. 6.

Bone resorption markers in ethanol (EtOH)-fed rats following fracture and treatment with n-acetyl cysteine (NAC). (A) RANKL in the callus of NAC-treated EtOH-fed rats. EtOH had increased RANKL (NS) compared to controls. NAC treatment decreased this RANKL in the EtOH-fed rats (NS), with a significant (p < 0.05) interaction with diet. (B) Osteoprotegerin (OPG) in the tissue callus of NAC-treated EtOH-fed rats. EtOH feeding decreased (NS) the OPG in fracture callus, while NAC treatment of EtOH-fed animals significantly (**p < 0.005) increased OPG to restore it beyond control levels. However, there was no interaction with diet and treatment. (C) The RANKL/OPG ratio was significantly (**p = 0.004) decreased in the EtOH NAC-treated rats compared to EtOH alone. (D) CTX in the serum of NAC-treated EtOH-fed rats. EtOH-fed serum levels of (CTX) were higher (NS) than in controls, which was restored to control levels by NAC treatment (NS), with a significant (p < 0.01) interaction with the diet. (E) TRAP levels in the tissue callus of NAC-treated EtOH-fed rats. EtOH feeding increased (p < 0.001) TRAP5b levels in the fracture callus tissue 3.5-fold compared to controls. NAC treatment of EtOH-fed rats reduced this significantly (***p < 0.001), with a significant (p < 0.0001) interaction. N = 4 animals per group.