Cadmium induced mitochondria apoptosis via the reduction of Th2 cells in pig thyroids

Abstract

Cadmium, as an environmental pollution element, is considered as a strong toxic substance of organisms. High doses of cadmium have serious cytotoxicity and induces programmed cell necrosis, autophagy, and apoptosis. Th1/Th2 balance is involved in regulating the dynamic balance of cytokine networks and is closely related to the occurrence and development of a variety of diseases. The purpose of this study was to investigate the relationship between Th1/Th2 balance and cadmium-induced apoptosis of thyroid cells. Cadmium poisoning pig model was established in which healthy 6-week-old pigs were exposed to CdCl2 for 40 days (with a dietary cadmium content of 20mg/kg). First, apoptosis was detected by TUNEL staining, and Th1/Th2 equilibrium shift was detected by immunofluorescence. Secondly, the mRNA and protein expression of related proteins were detected by qRT-PCR and Western blot. The results showed that the Th1/Th2 balance shifted towards Th1 and Th2 cells decreased；and the expression levels of Ras/Raf/MEK/ERK pathway related proteins were inhibited in group Cd. In addition, Bax, CytC, Caspase9, and Caspase3 expression increased and Bcl2 expression decreased after cadmium exposure. In brief, our experiments suggested that the pro-apoptosis-related genes expression upregulates and apoptosis induces by activating the mitochondrial pathway signaling pathway in thyroid cells after Cadmium exposure. These negative effects are in connection with the Th1/Th2 imbalance and the reduction of Th2 cytokines.