MiR-182-5p/TLR4/NF-κB axis contributes to the protective effect of caffeic acid phenethyl ester against cadmium-induced spleen toxicity and associated damage in mice

Cadmium (Cd) is a toxic heavy metal pollutant that can be accumulated in organs including the spleen, thereby threatening human health. In this study, the effect of caffeic acid phenethyl ester (CAPE, a bioactive component of honeybee propolis) on CdCl2-induced spleen toxicity and underlying mechanisms were examined in mice. Histological examinations revealed that CAPE (10 mu mol/kg/day b.w.) could mitigate spleen damage induced by CdCl2 (1.5 mg/kg/day b.w.) in mice. Compared to the mice treated only by CdCl2, CAPE administration increased the body weight while decreasing the spleen weight, spleen Cd content and spleen to body ratio of the CdCl2-treated mice. Western blot and ELISA tests revealed that CAPE suppressed CdCl2-induced inflammation (indicated by the decreases in the levels of inflammatory indictors). TUNEL and Western blot results showed that CAPE suppressed CdCl2-induced apoptosis through reducing the percentage of TUNEL-positive cells and regulating apoptosis factors. The antagonistic effect of CAPE against CdCl2-induced spleen toxicity was realized by increasing miR-182-5p expression to regulate the TLR4/NF-kappa B pathway. Therefore, CAPE could be a food-derived spleen protector to counteract Cd-induced spleen toxicity through alleviating apoptosis and inflammation via the miR-182-5p/TLR4/NF-kappa B axis.

Automated summary

The study demonstrated that CAPE mitigates CdCl2-induced spleen damage by reducing spleen weight and Cd content, and by regulating inflammation and apoptosis pathways. The protective effect is achieved through the miR-182-5p/TLR4/NF-κB axis.