Open AccessPEG-PEI/siROCK2 inhibits Aβ42-induced microglial inflammation via NLRP3/caspase 1 pathway
Author(s) -
Yunyun Liu,
Han Zhang,
Anping Peng,
Zongwei Cai,
YuZhou Wang,
Ke Tang,
Xiuqin Wu,
Yucheng Liang,
Limin Wang,
Zhong Li
Publication year - 2021
Publication title -
neuroreport/neuroreport
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.607
H-Index - 188
eISSN - 1473-558X
pISSN - 0959-4965
DOI - 10.1097/wnr.0000000000001752
Subject(s) - microglia , pyrin domain , neuroinflammation , pharmacology , neurotoxicity , cytotoxicity , inflammation , lipopolysaccharide , inflammasome , chemistry , immunology , biology , biochemistry , medicine , toxicity , in vitro
There is an urgent need to develop therapeutic strategies to improve the treatment outcome of Alzheimer's disease. The treatment strategy of gene therapy mediated by nanocarrier systems brings new hope for the treatment of Alzheimer's disease. ROCK2 is involved in various pathological processes of Alzheimer's disease and may be a potential target for the treatment of Alzheimer's disease. Our previous study indicated that PEG-PEI/siROCK2 [polyethyleneglycol-polyethyleneimine deliver ROCK2-siRNA, (PPSR)] prevented Aβ42-induced neurotoxicity and showed a promising prospect for the treatment of Alzheimer's disease. However, whether PPSR has an effect on the microglial inflammation in Alzheimer's disease is still unclear.