The present study was conducted to evaluate the protective effects of
astaxanthin against
lipopolysaccharide (LPS)-induced inflammatory responses in Channa argus in vivo and ex vivo. Primary hepatocytes were exposed to different concentrations of LPS for 24 h to induce an inflammatory response, and the protective effects of
astaxanthin against LPS-induced
inflammation were studied ex vivo and in vivo. Hepatocytes exposed to LPS (5-20 μg mL-1) alone for 24 h resulted in a significant increase in
lactate dehydrogenase release (LDH),
Nitric oxide (NO) production and
Malondialdehyde (MDA) content, 10 μg mL-1 LPS could induced inflammatory response in hepatocytes. Gene expression of TLR4, NFkBp65, MAPKp38, TNF-α,
IL-6 and IL-1β
mRNA expression were also enhanced ex vivo (p < 0.05). In vivo test demonstrated that pretreatment with
astaxanthin prevented the LPS-induced upregulation of pro-inflammatory
cytokines TNF-α,
IL-6 and IL-1β. Besides,
astaxanthin blocked the expression of
Toll-like receptor 4 (TLR4) and then suppressed the phosphorylation of nuclear
transcription factor-kappa B (NF-κB) p65 and degradation inhibitor of NF-κBα (IκBα). Further study showed that
astaxanthin could suppress the phosphorylation of p38,
extracellular signal-regulated kinase (ERK) and c-jun NH2-terminal
kinase (JNK) in
mitogen-activated protein kinase (MAPK) signal pathway. In conclusion, our results suggest that
astaxanthin played an anti-inflammatory role by regulating TLR4 and the NF-κB and MAPK signaling pathways in C. argus.