Objective To explore the potential immunoregulatory mechanisms linking lead sulfate with cardiovascular toxicity.
Methods Wistar rats were exposed to lead sulfate via intratracheal instillation with the doses of 13.5, 67.5, and 337.5 μg/kg (body weight), respectively. The exposure was conducted once a day for 3 continuous days. Twenty-four hours after the last exposure, the rats were sacrificed. The mRNA expressions of helper T cells (Th) 1- and Th2-related transcription factors were assessed in left ventricle of rats using real-time polymerase chain reaction (PCR). Meanwhile, the levels of Th1- and Th2- related cytokines in cardiac homogenate supernatant of rats were determined using enzyme-linked immunosorbent assay (ELISA). Furthermore, the protein expressions of Th1- and Th2-related cytokines in myocardium were detected by immunohistochemistry.
Results The results of cardiac histology demonstrated significant differences in the levels of interleukin (IL)-4, IL-13, and interferon (IFN)-γ in cardiac homogenate supernatant between the exposed rats and the controls, as well as in the levels of IL-13 between the high- and low-dose groups. The mRNA expressions of Th1 and Th2 in left ventricle between the exposed rats and the controls as well as between the high- and low-dose groups were significantly different. The expressions of IL-4 protein of left ventricular were significantly increased in the exposed rats in comparison with the controls, whereas the expressions of IFN-γ protein were significantly reduced.
Conclusion These findings indicate that lead sulfate which enters into the lungs could cause inflammation and immunotoxicity in heart. The changes of Th1 and Th2-related cytokine levels might be a mechanism of cardiac injury induced by lead.
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