Inflammation response after cessation of chronic arsenic exposure and post-treatment of natural astaxanthin in liver: Potential role of cytokine-mediated cell–cell interactions

Ongoing groundwater arsenic contamination throughout China was first recognized in the 1960s. Groundwater arsenic contamination was a high risk for human and animal health worldwide. Apart from the drinking water, diet is the second pathway for arsenic to enter the human body and eventually cause liver injury. Natural astaxanthin extracted from the green algae Haematococcus pluvialis has dominated nutraceutical market for potential health benefits. Nevertheless, the molecular mechanism underlying the protective effect of post astaxanthin against arsenic-induced hepatotoxicity remains largely obscure. In this study, we investigate the effect of natural astaxanthin (derived from Haemotococcus pluvialis) on oxidative stress and liver inflammatory response in rats after cessation of chronic arsenic exposure. Wistar rats were given by intragastric administration astaxanthin (250 mg/kg) daily for 2 weeks after cessation of exposure to sodium arsenite (300 µg/L, drinking water, 24 weeks). The results showed that post treatment with astaxnthin attenuated liver injury induced by long-term exposure to arsenic in rats. Most importantly, post treatment with astaxnthin decreased the increasing of inflammatory cytokine NF-κB, tumor necrosis factor-α, interleukin-1β, oxidative stress level, and total arsenic content in livers of rats exposed to arsenic. In addition, post treatment with astaxnthin reversed the increasing of protein levels of alpha-smooth muscle actin and collagen Iα1, which are activation marker of hepatic stellate cell (HSC). Collectively, these data demonstrate that post treatment with astaxnthin attenuates inflammation response in liver after cessation of chronic arsenic exposure via inhibitition of cytokine-mediated cell–cell interactions. Daily ingestion of natural astaxanthin might be a potential and beneficial candidate for the treatment of liver damage after cessation of chronic exposure to sodium arsenite.