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The core mechanism of Late-onset hypogonadism (LOH) is the deficiency of androgen due to the functional and quantitative decline of testicular Leydig cells. Here we explored the protective effect of calretinin, a Ca 2+ -binding protein, on Leydig cells. We found in MLTC-1 cells transfected with LV-calb2, the cell viability and optical density (OD) were higher ( p &lt;0.05), cells in the S phase of the cell cycle were increased ( p &lt;0.01) and p-ERK1/2 and p-AKT levels were significantly higher ( p &lt;0.01 and p &lt;0.05), while in R2C cells transfected with LV-siRNA-calb2, all of the results mentioned above were adverse ( p &lt;0.05). The cell apoptotic index after calretinin over-expressed was significantly lower ( p &lt;0.001), while the expression levels of mitochondria-related apoptotic factors such as cleaved caspase-9 and cytochrome C (cyto C) were lower and ratio of Bcl2/Bax was higher ( p&lt; 0.05). After calretinin down-regulated, the apoptotic index was higher ( p&lt; 0.05), while the expression levels of mitochondria-related apoptotic factors were higher and the ratio of Bcl2/Bax was lower ( p&lt; 0.05). Therefore, calretinin increases Leydig cell viability and proliferation, possibly via ERK1/2 and AKT pathways, and suppresses apoptosis possibly via the mitochondria-related apoptotic pathway, which could be beneficial in understanding the pathophysiology of LOH and could lead to the study of new treatments.

Protective effect of calretinin on testicular Leydig cells via the inhibition of apoptosis