Activation of protein kinase C delta (PKCδ) has been linked to the neuroinflammation but the relationship with the various neurodegenerative diseases including the Alzheimer's disease (AD) was mostly elusive. In the AD brains, the special phospholipids, ethanolamine plasmalogens (Pls), were found to be reduced and our previous study showed that these lipids possess neuroprotective and anti-inflammatory functions. In the present study, we could find that these lipids can significantly attenuate the microglial expression of PKCδ in the neuroinflammation model and in the AD model mice brains. We also show an increase of PKCδ in the human postmortem AD brains. In addition, we also report that scallop derived Pls (sPls) inhibited the p38MAPK and JNK protein expression which are involved in the expressional regulation of PKCδ in the microglial cells. In addition, the lentiviral shRNA-mediated knockdown of PKCδ attenuated the LPS-induced p65 (NF-kB) activation and inflammatory cytokine expression, suggesting that the PKCδ can induce the inflammatory response which can be inhibited by the sPls. Taken together, our recent findings suggest that the sPls can attenuate the increased expression of PKCδ associated with the neuro-inflammation in the murine brain.
|Number of pages||6|
|Journal||Biochemical and Biophysical Research Communications|
|Publication status||Published - Sep 5 2018|
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Cell Biology