Y Zhang

Osteoporosis (OP) is a common chronic progressive bone disease that increases fracture risk in postmenopausal women. Research suggests that puerarin (Pue) may be an effective treatment for OP. This study examined the effects and underlying mechanisms of Pue in treating postmenopausal osteoporosis (PMOP) in rats. Sprague-Dawley (SD) rats underwent bilateral ovariectomy to simulate PMOP and were then treated with subcutaneous injections of Pue. Bone mineral density (BMD) was measured using a bone densitometer. Micro-CT scans assessed femur bone structure and various parameters were calculated: bone volume fraction (BV/TV), bone surface density (BS/TV), trabecular thickness (Tb.Th), trabecular number (Tb.N), trabecular separation (Tb.Sp), and bone surface area-to-bone volume ratio (BS/BV). Hematoxylin-eosin (HE) staining was employed to observe femoral tissue pathology. Serum levels of bone formation metabolism-related markers-osteocalcin (OC), bone alkaline phosphatase (BALP), and procollagen type I N-terminal propeptide (PINP)-were measured via enzyme-linked immunosorbent assay (ELISA). The protein expression levels of the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway in bone tissue were evaluated using Western blotting assay. The results showed improved bone density and reduced bone loss in rats treated with Pue. There were also significant increases in serum levels of OC and BALP, indicating enhanced osteogenesis. Furthermore, there was a decrease in activation of the JAK2/STAT3 pathway in femoral tissue, suggesting a pathway inhibition. These findings indicate that Pue may combat osteoporosis by promoting osteogenesis and inhibiting activation of the JAK2/STAT3 pathway activation.

Rheumatoid arthritis is an autoimmune disease characterized by the synovitis of joints and the modulation of chronic inflammation determined by increased levels of inflammatory cytokines. This study aimed to investigate the characteristics of the immunological profile of the cells of the synovial membrane and the expression of IL-10 and IL-17 in a rheumatoid arthritis rat model in order to provide a targetdirected treatment for immunological control. Eighty female Wistar rats were randomly divided into a rheumatic arthritis model group (model group) and a control group, 40 animals per group. After the successful rheumatoid arthritis rat model was obtained, 10 animals were sacrificed from each group every week starting from the third week till the sixth week and the expression levels of CD3, CD21, and CD68 in the synovial region along with the blood level of IL-10 and IL-17 were assessed. At the four stages after modeling, the expression of CD3 in the model group increased compared with the control group (P less than 0.05). The expression of CD21 was different between the model group and the control group, but the difference did not reach statistical significance (P>0.05). The expression of CD68 determined at weeks 4 and 5 after modeling was increased compared to the control group (P less than 0.05). At 6 week after modeling, IL-10 levels in the model group were higher than those in the control group (P less than 0.05). At weeks 4 and 5 after modeling, the level of IL-17 in the model group increased compared to the control group (P less than 0.05). The level of IL-17 increased with the increase of synovial inflammation in the rheumatoid arthritis-induced rats, and the level of IL-10 increased as the inflammation subsided, which shows that both cytokines are related to the occurrence and development of rheumatoid arthritis and its inflammation.