Cyanocobalamin (vitamin B12) ameliorates lipopolysaccharide-induced systemic and lung inflammation in rats

Considering the antioxidant and immunomodulatory properties of vitamin B12, this study aimed to evaluate the effects of cyanocobalamin (vitamin B12) on systemic and lung injury markers induced by lipopolysaccharide (LPS). Forty male Wistar rats were randomly assigned to five groups: Control; LPS (1 mg/kg, intraperitoneal injection on day 3 and from days 8 to 16); and LPS treated with cyanocobalamin at doses of 0.25, 0.5, and 1 mg/kg. Cyanocobalamin was administered orally from days 1 to 16. Finally, blood and lung tissue samples were collected to evaluate systemic and lung injury markers. Total white blood cell (WBC), neutrophil, eosinophil, and monocyte counts, as well as serum interleukin-6 (IL-6) levels, were elevated in LPS group compared to control animals. Treatment with cyanocobalamin at all doses reduced total WBC, neutrophil, and lymphocyte counts relative to the LPS group, except for total WBC at the 0.5 mg/kg dose. LPS induced upregulation of nitric oxide (NO), IL-6, tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), malondialdehyde (MDA), and the expression of Bax, p53, and the Bax/Bcl-2 ratio, along with histopathological injury. Conversely, it downregulated Bcl-2 expression, total thiol content, and catalase (CAT) and superoxide dismutase (SOD) activities in lung tissue compared to controls. Cyanocobalamin dose-dependently ameliorated LPS-induced lung alterations, including IL-6, TNF-α, MDA, thiol content, Bax, p53, Bax/Bcl-2 ratio expression, CAT activity, and injury score. These findings suggest that a synthetic form of vitamin B12, cyanocobalamin, ameliorates LPS-induced leukocytosis, lung inflammation, apoptosis, and oxidative stress.