The anti-osteoporosis effects of CSN1S2 protein of goat milk and yoghurt on a complete Freund's adjuvant-induced rheumatoid arthritis model in rats

Abstract

This study aimed to evaluate the anti-osteoporosis effect of CSN1S2 protein from goat milk and yoghurt on a complete Freund's adjuvant (CFA)-induced rheumatoid arthritis (RA) model in rats. Twenty-four rats were randomly divided into six groups: control (untreated) group (C), group treated with CSN1S2 (CM) protein from goat milk, group treated with CSN1S2 protein from goat yoghurt (CY), RA group, RA group treated with CSN1S2 protein from goat milk (RAM), and RA group treated with goat yoghurt (RAY). Mineral elements and mesostructure were analyzed using X-ray fluorescence and scanning electron microscopy. Bone histomorphometry was analyzed using the BoneJ software. One way analysis of variance and Tukey post hoc tests were used to analyze and compare the means of all variables between groups. The phosphorus levels were not significantly different between treatment groups relative to the control group (p > 0.05), but were significantly higher in the CM and RAY groups relative to that observed in the CY group (p < 0.05). CSN1S2 protein of goat milk repaired the collagen structure in the femur trabecular bone. The trabecular thickness and volume were significantly lower in CM and CY groups relative to the control group (p < 0.05). The trabecular volume also decreased significantly in the CM group relative to the control group (p < 0.05). The trabecular thickness was significantly lower in the CY group relative to the CM group (p < 0.05), but the trabecular separation and trabecular volume were significantly greater (p < 0.05). The trabecular volumes were significantly elevated in the RAM and RAY groups relative to the CM group (p < 0.05). The trabecular thickness was significantly higher in the RAY group relative to the CM and CY groups (p < 0.05). CSN1S2 protein of goat milk is better than goat yoghurt in repairing femur crystallization and mesostructure in CFA-induced rheumatoid arthritis in rats.