Physiological, molecular, and histological evaluation of the effects of cobalamin on cardiac function in castrated rabbits.

BACKGROUND

Testosterone deficiency is associated with adverse cardiac remodeling, oxidative stress, and inflammation.

AIM: To investigate the physiological, biochemical, and histological effects of cobalamin (vitamin B12) supplementation on cardiac physiology in castrated rabbits.

METHODS

A total of 24 male rabbits were divided into three groups: control (C), castrated (CA), and castrated with cobalamin supplementation (CA + C). Biochemical markers, including cardiac troponin I (cTnI), heart-type fatty acid-binding protein (H-FABP), homocysteine, glutathione (GSH), interleukin-3 (IL-3), galectin-3 (Gal-3), translocator protein (TSPO), and thrombospondin-1 (TSP-1), were measured using Enzyme-Linked Immunosorbent Assay. Myocardial tissue was histologically evaluated alongside Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH) and Atrial Natriuretic Peptide (ANP) gene expression analysis using quantitative real-time reverse-transcription PCR. Statistical significance was set at p value < 0.05.

RESULTS

Castration significantly increased the levels of cardiac markers, such as cTnI, H-FABP, homocysteine, IL-3, and Gal-3, while reducing GSH levels (p < 0.001). Cobalamin supplementation significantly restored these biochemical parameters, with notable reductions in cTnI, H-FABP, homocysteine, IL-3, Gal-3, and GSH levels (p < 0.01). Histological analysis revealed myocardial contraction failure, fibrosis, and inflammation in castrated rabbits, which were mitigated by cobalamin supplementation. Gene expression analysis showed GAPDH and ANP upregulation in the castrated group, which was partially restored after cobalamin treatment. Additionally, cobalamin supplementation significantly improved the expression of other markers, such as TSPO and TSP-1, and its potential to modulate inflammatory and oxidative pathways in the heart.

CONCLUSION

Cobalamin supplementation mitigates the harmful effects of testosterone deficiency on the heart by improving oxidative stress, inflammation, and cardiac remodeling. These findings support the potential of this drug for correcting cardiovascular dysfunction associated with hormonal deficiencies.