Gryllus bimaculatus extract protects against lipopolysaccharide and palmitate-induced production of proinflammatory cytokines and inflammasome formation.

Abstract

Inflammation and the inflammasome complex formation are associated with numerous diseases, and palmitates or lipopolysaccharides (LPS) have been identified as potential links between these disorders. Recently, edible insects such as the Gryllus bimaculatus (GB) and the larva of Tenebrio molitor have emerged as alternative food sources. In the present study, the effect of GB on LPS- or palmitate-induced production of inflammatory cytokines, the formation of the inflammasome complex, reactive oxygen species (ROS) generation, endoplasmic reticulum (ER) stress and cell death was investigated in RAW264.7 cells. The results revealed that GB extract downregulated the production of inflammatory cytokines (such as TNF-α, IL-1β and IL-6). Since the role of the MAP kinase and NF-κB signalling pathways in the production of inflammatory cytokines is well established, the translocation of p65 into the nucleus and the phosphorylation of IκB and MAP kinases were further examined. Both these processes were upregulated following LPS and palmitate treatment, but they were inhibited by the GB extract. Moreover, GB extract decreased LPS/palmitate-induced inflammasome complex formation (assessed via analysing the levels of the apoptosis-associated speck-like protein containing a caspase-recruitment domain, NOD-like receptor family pyrin domain containing 3, cleaved caspase-1 and IL-1β), the generation of ROS, ER stress and cell death. Treatment with SB203580 (a p38 inhibitor), SP600125 (a JNK inhibitor) and pyrrolidinedithiocarbamate ammonium (an NF-κB inhibitor) decreased the production of inflammatory cytokines, as well as helped in the recovery of LPS/palmitate-induced cell death. Overall, GB extract served an inhibitory role in LPS/palmitate-induced inflammation via inhibiting the MAP kinase and NF-κB signalling pathways, inflammasome complex formation, ROS generation, ER stress and cell death.