[alpha]-Solanine Isolated From Solanum Tuberosum L. cv Jayoung Abrogates LPS-Induced Inflammatory Responses Via NF-[kappa]B Inactivation in RAW 264.7 Macrophages and Endotoxin-Induced Shock Model in Mice

[alpha]-Solanine, a trisaccharide glycoalkaloid, has been reported to possess anti-cancer effects. In this study, we investigated the anti-inflammatory effects of [alpha]-solanine isolated from "Jayoung" a dark purple-fleshed potato by examining its in vitro inhibitory effects on inducible nitric-oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and pro-inflammatory cytokines in LPS-induced RAW 264.7 macrophages and its in vivo effects on LPS-induced septic shock in a mouse model. [alpha]-Solanine suppressed the expression of iNOS and COX-2 both at protein and mRNA levels and consequently inhibited nitric oxide (NO) and prostaglandin E2 (PGE2) production in LPS-induced RAW 264.7 macrophages. [alpha]-Solanine also reduced the production and mRNA expression of interleukin-6 (IL-6), tumor necrosis factor-[alpha] (TNF-[alpha]), and interleukin-1[beta] (IL-1[beta]) induced by LPS. Furthermore, molecular mechanism studies indicated that [alpha]-solanine inhibited LPS-induced activation of nuclear factor-[kappa]B (NF-[kappa]B) by reducing nuclear translocation of p65, degradation of inhibitory [kappa]B[alpha] (I[kappa]B[alpha]), and phosphorylation of I[kappa]B kinase[alpha]/[beta] (IKK[alpha]/[beta]). In an in vivo experiment of LPS-induced endotoxemia, treatment with [alpha]-solanine suppressed mRNA expressions of iNOS, COX-2, IL-6, TNF-[alpha], and IL-1[beta], and the activation of NF-[kappa]B in liver. Importantly, [alpha]-solanine increased the survival rate of mice in LPS-induced endotoxemia and polymicrobial sepsis models. Taken together, our data suggest that the [alpha]-solanine may be a promising therapeutic against inflammatory diseases by inhibiting the NF-[kappa]B signaling pathway. J. Cell. Biochem. 117: 2327-2339, 2016. © 2016 Wiley Periodicals, Inc.