This meta-analysis summarizes the differences in serum lipid levels among postmenopausal women with osteopenia, osteoporosis, and normal bone mass, aiming to establish reliable lipid markers for predicting bone loss in postmenopausal women. Relevant literature published up to March 21, 2024, was sourced from databases including PubMed, Embase, Web of Science, and the Cochrane Library. Following a thorough evaluation in accordance with established inclusion and exclusion criteria, the meta-analysis incorporated 14 studies, involving a total of 12,974 postmenopausal women. The weighted mean deviation (WMD) and 95% confidence intervals (CIs) were conducted by RevMan 5.4 software. The findings indicated that serum triglyceride (TG) concentrations were significantly lower in osteopenia (WMD = -6.82, 95% CI: -9.80 to -3.83, P = 0.05, I2 = 42%) and osteoporosis (WMD = -10.28, 95% CI: -14.51 to -6.04, P < 0.001, I2 = 45%) women compared to their normal counterparts. In addition, serum high-density lipoprotein cholesterol (HDL-C) levels were notably elevated in osteoporosis women (WMD = 1.66, 95% CI: 0.75 to 2.57, P = 0.0004, I2 = 43%). However, no significant discrepancies were found in total cholesterol and low-density lipoprotein cholesterol levels among postmenopausal women with bone loss. Sensitivity analysis showed that the results of the meta-analysis were reliable. Egger's test showed no publication bias in the included studies. Consequently, our meta-analysis shows that low serum TG levels predict the onset of osteopenia in postmenopausal women, while high serum HDL-C levels suggest a potential risk for osteoporosis.

Background: Idiopathic inflammatory myopathies (IIMs), characterized by muscle weakness and chronic inflammation, currently lack highly effective therapies. This study investigated the therapeutic potential and underlying mechanism of (5R)-5-hydroxytriptolide (LLDT-8), a triptolide derivative with reduced toxicity, using an experimental autoimmune myositis (EAM) mouse model and in vitro assays. Methods: Forty female BALB/c mice were randomly assigned to five groups: normal, vehicle, methylprednisolone (MP), LLDT-8 (0.0625 mg/kg), and LLDT-8 (0.125 mg/kg). EAM mice were treated with LLDT-8 (0.0625 or 0.125 mg/kg) or methylprednisolone as a positive control. Cellular experiments and molecular docking were performed to investigate potential mechanisms of LLDT-8. Results: LLDT-8 significantly attenuated clinicopathological features, including muscle weakness and pain sensitivity, while reducing serum levels of aspartate aminotransferase and lactate dehydrogenase. Histological analysis revealed that LLDT-8 reduced inflammatory cell infiltration and the presence of CD4⁺ and CD8⁺ T cells in muscle tissues. Mechanistically, LLDT-8 inhibited the expression of nucleotide-binding oligomerization domain receptor caspase recruitment domain 5 (NLRC5), a key transcriptional regulator of major histocompatibility complex-I (MHC-I). This suppression extended to downstream antigen presentation-related molecules, including the transporter associated with antigen processing and proteasome 20S subunit beta. Molecular docking further confirmed the high binding affinity of LLDT-8 to both NLRC5 and MHC-I. Conclusions: LLDT-8 alleviates inflammatory muscle injury by targeting the NLRC5/MHC-I signaling axis, suggesting it may be a promising therapeutic candidate for IIMs.