Previous studies suggested that oxidative stress is related to the onset and development of
osteoporosis. Moreover, it was demonstrated that
berberine has a protective effect against oxidative stress-induced
injuries. In this study, we aimed to investigate the effect and mechanism of action of
berberine on rats with induced
osteoporosis. Sixty 8-week-old female Wistar rats were randomly divided into the following 6 groups: control saline-treated,
osteoporosis saline-treated, 3
osteoporosis berberine-treated groups (Ber 5, 10, and 20 mg/kg/
body weight, respectively), and
osteoporosis alendronate-treated (ALD) group.
Osteoporosis was induced by
bilateral ovariectomy. All treatments were performed for 8 weeks. The bone mineral density (BMD), serum
alkaline phosphatase (ALP),
osteocalcin,
calcium,
phosphorus,
superoxide dismutase (SOD), methylenedioxyamphetamine (MDA), and
glutathione peroxidase (GSH-Px) level was determined in the rat femur tissue. The gene and
protein expression of
osteoprotegerin (OPG) and
receptor activator of nuclear factor kappa-B ligand (RANKL) was analyzed by quantitative reverse transcription PCR and Western blot, respectively. The BMD, SOD and GSH⁃Px levels, and the expression of OPG were significantly lower in
osteoporosis compared to control group (all p < 0.05). The serum levels of
osteocalcin, ALP, and MDA, and the expression of RANKL were significantly higher in
osteoporosis compared to control group (all p < 0.05).
Berberine, especially the high doses of
berberine, effectively increased SOD, GSH⁃Px, and OPG levels as well as decreased serum
osteocalcin, ALP, MDA and RANKL levels in
berberine-treated
osteoporosis groups (all p < 0.05). To conclude, oxidative stress may promote the development of
osteoporosis in rats through the RANK/RANKL/OPG pathway. The antioxidative effect of
berberine reduces the development of
osteoporosis in rats to some extent.