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However, the protective effects and specific mechanisms of\n                      <jats:sc>d<\/jats:sc>\n                      \u2010galactose\u2010induced testicular dysfunction in reproductively senescent rats are not fully understood.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and methods<\/jats:title>\n                    <jats:p>\n                      A\n                      <jats:sc>d<\/jats:sc>\n                      \u2010galactose\u2010induced senescence model in male rats and a\n                      <jats:sc>d<\/jats:sc>\n                      \u2010galactose\u2010induced TM3 cell model were used to investigate the effects of LBP. The protective effect on testicular spermatogenic function was assessed by histological analysis and SA\u2010\u03b2\u2010gal staining. In addition, key calcium signaling pathway alterations involved in LBP were assessed using a multi\u2010omics approach and validated by tissue. Single\u2010cell sequencing data were used to further analyze the cellular heterogeneity of calcium signaling.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      LBP significantly improved testicular structure, increased the number of spermatogonia in the seminiferous tubules, and significantly attenuated oxidative stress and testicular apoptosis. In addition, LBP restored the expression of key steroidogenic enzymes, as well as elevated levels of testosterone, follicle\u2010stimulating hormone (FSH), and estradiol (E2), and decreased levels of luteinizing hormone (LH). Mechanistically, LBP regulates key signaling pathways, including calcium homeostasis, Hippo and mTOR pathways, which play important roles in cell growth, apoptosis, and tissue regeneration. Single\u2010cell sequencing data show that calcium signaling is more active in the elderly compared to the young, mainly in Leydig cells, Round Spermatids, and Smooth Muscle Cells. In TM3 cell experiments, the LBP reduced SA\u2010\u03b2\u2010gal activity, downregulated aging markers (p16, p21, p53), and restored steroid production function. In addition, LBP regulated the Ca\n                      <jats:sup>2<\/jats:sup>\n                      \u207a\/CaM\/CaMKII signaling pathway, improved calcium homeostasis, and reduced apoptosis in rats and cells.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      LBP improves\n                      <jats:sc>d<\/jats:sc>\n                      \u2010galactose\u2010induced testicular spermatogenesis mainly by regulating calcium signaling and metabolic pathways and is closely related to elongating spermatids, round spermatids.\n                    <\/jats:p>\n                  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