Cinnamaldehyde (CNA) is a primary constituent found in cinnamon (Cortex cinnamomi). Although antidiabetic and anti-inflammatory activities of cinnamon extract have been investigated in recent years, whether CNA is responsible for these activities is yet to be explored. In the present study, we investigated the protective effect of CNA on streptozotocin (STZ)-induced ${eta}$-cell dysfunction in RINm5F rat insulinoma cells. CNA markedly inhibited nitric oxide (NO) and prostaglandin $E_2$ ($PGE_2$) productions in concentration-dependent manners. Parallel with these observations, the protein and mRNA levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 enzymes were inhibited by CNA in concentration-dependent manners. CNA also inhibited STZ-induced nuclear factor (NF)-${kappa}B$ activation via the prevention of inhibitory ${kappa}B{alpha}$ ($I{kappa}B{alpha}$) phosphorylation and degradation. Moreover, CNA significantly suppressed STZ-induced phosphorylations of extracellular signalregulated kinase (ERK), c-Jun NH2-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) in concentration-dependent manners. These results suggest that CNA is an active constituent of the cinnamon, and CNA protects against STZ-induced pancreatic ${eta}$-cell damage by down-regulations of iNOS and COX-2 gene expression through blocking of NF-${kappa}B$ and MAPKs activities.